Clinical Review

Spironolactone is increasingly used off label for acne treatment and is now being prescribed for women with acne at a frequency similar to oral antibiotics.^1,2 In this article, we provide an overview of spironolactone use for acne treatment and discuss recent clinical trials and practical strategies for patient selection, dosing, adverse effect management, and monitoring (Table).

History and Mechanism of Action

Because sebaceous gland activity is an important component of acne pathogenesis and is regulated by androgens,³ there has long been interest in identifying treatment strategies that can target the role of hormones in activating the sebaceous gland. In the 1980s, it became apparent that spironolactone, originally developed as a potassium-sparing diuretic, also might possess antiandrogenic properties that could be useful in the treatment of acne.⁴ Spironolactone has been found to decrease testosterone production, inhibit testosterone and dihydrotestosterone binding to androgen receptors,^5-8 and block 5α-reductase receptors of the sebaceous glands of skin.⁹

In 1984, Goodfellow et al¹⁰ conducted a trial in which 36 male and female patients with severe acne were randomized to placebo or spironolactone doses ranging from 50 to 200 mg/d. They found that spironolactone resulted in dose-dependent reductions of sebum production as well as improvement in patient- and clinician-reported assessments of acne. In 1986, another placebo-controlled crossover trial by Muhlemann et al¹¹ provided further support for the effectiveness of spironolactone for acne. This trial randomized 21 women to placebo or spironolactone 200 mg/d and found that spironolactone was associated with statistically significant (P<.001) improvements in acne lesion counts.

Recent Observational Studies and Trials

Following these early trials, several large case series have been published describing the successful use of spironolactone for acne, including a 2020 retrospective case series from the Mayo Clinic describing 395 patients.¹² The investigators found that almost 66% of patients had a complete response and almost 85% had a complete response or a partial response greater than 50%. They also found that the median time to initial response and maximal response were 3 and 5 months, respectively, and that efficacy was observed across acne subtypes, including for nodulocystic acne.¹² In addition, a 2021 case series describing 403 patients treated with spironolactone found that approximately 80% had reduction or complete clearance of acne, with improvements observed for both facial and truncal acne. In this cohort, doses of 100 to 150 mg/d typically were the most successful.¹³ A case series of 80 adolescent females also highlighted the efficacy of spironolactone in younger populations.¹⁴

Adding to these observational data, the multicenter, phase 3, double-blind Spironolactone for Adult Female Acne (SAFA) trial included 410 women (mean age, 29.2 years) who were randomized to receive either placebo or intervention (spironolactone 50 mg/d until week 6 and 100 mg/d until week 24).¹⁵ At 24 weeks, greater improvement in quality of life and participant self-assessed improvement were observed in the spironolactone group. In addition, at 12 weeks, rates of success were higher in the spironolactone group using the Investigator Global Assessment score (adjusted odds ratio 5.18 [95% CI, 2.18- 12.28]). Those randomized to receive spironolactone also had lower rates of oral antibiotic use at 52 weeks than the placebo group did (5.8% vs 13.5%, respectively).

In the SAFA trial, spironolactone was well tolerated; the most common adverse effects relative to placebo were lightheadedness (19% for spironolactone vs 12% for placebo) and headache (20% for spironolactone vs 12% for placebo). Notably, more than 95% of patients were able to increase from 50 mg/d to 100 mg/d at week 6, with greater than 90% tolerating 100 mg/d. As observational data suggest that spironolactone takes 3 to 5 months to reach peak efficacy, these findings provide further support that starting at a dose of at least 100 mg/d is likely optimal for most patients.¹⁶

A Potential Alternative to Oral Antibiotics

Oral antibiotics such as tetracyclines have long played a central role in the treatment of acne and remain a first-line treatment option.¹⁷ In addition, many of these antibiotic courses exceed 6 months in duration.¹ In fact, dermatologists prescribe more antibiotics per capita than any other specialty^1,18-20; however, this can be associated with the development of antibiotic resistance,^21,22 as well as other antibiotic-associated complications, including inflammatory bowel disease,²³ pharyngitis,²⁴Clostridium difficile infections, and cancer.^25-29

In addition to these concerns, many patients may prefer nonantibiotic alternatives to oral antibiotics, with more than 75% preferring a nonantibiotic option if available. For female patients with acne, antiandrogens such as spironolactone have been suggested as a potential alternative.³⁰ A 10-year retrospective study of female patients with acne found that those who had ever received hormonal therapy (ie, spironolactone or a combined oral contraceptive) received fewer cumulative days of oral antibiotics than those who did not (226 days vs 302 days, respectively).³¹ In addition, while oral antibiotics were the most common initial therapy prescribed for patients, as they progressed through their treatment course, more patients ended up on hormonal therapy than oral antibiotics. This study suggests that hormonal therapy such as spironolactone could represent an alternative to the use of systemic antibiotics.³¹

Further supporting the role of spironolactone as an alternative to oral antibiotics, a 2018 analysis of claims data found that spironolactone may have similar effectiveness to oral antibiotics for the treatment of acne.32 After adjusting for age and topical retinoid and oral contraceptive use, this study found that there was no significant difference in the odds of being prescribed a different systemic treatment within 1 year (ie, treatment failure) among those starting spironolactone vs those starting oral tetracycline-class antibiotics as their initial therapy for acne.

A multicenter, randomized, double-blind trial (Female Acne Spironolactone vs doxyCycline Efficacy [FASCE]) also evaluated the comparative effectiveness of doxycycline 100 mg/d for 3 months followed by an oral placebo for 3 months vs spironolactone 150 mg/d for 6 months among 133 adult women with acne. This study found that spironolactone had statistically significantly greater rates of Investigator Global Assessment treatment success after 6 months (odds ratio 2.87 [95% CI, 1.38-5.99; P=.007]).³³ Since spironolactone historically has been prescribed less often than oral antibiotics for women with acne, these findings support spironolactone as an underutilized treatment alternative. The ongoing Spironolactone versus Doxycycline for Acne: A Comparative Effectiveness, Noninferiority Evaluation trial—a 16-week, blinded trial comparing 100 mg/d doses of both drugs—should provide additional evidence regarding the relative role of spironolactone and oral antibiotics in the management of acne.³⁴

Ultimately, the decision to use spironolactone or other treatments such as oral antibiotics should be based on shared decision making between clinician and patient. Spironolactone has a relatively slow onset of efficacy, and other options such as oral antibiotics might be preferred by those looking for more immediate results; however, as women with acne often have activity that persists into adulthood, spironolactone might be preferable as a long-term maintenance therapy to avoid complications of prolonged antibiotic use.³⁵ Comorbidities also will influence the optimal choice of therapy (eg, spironolactone might be preferred in someone with inflammatory bowel disease, and oral antibiotics might be preferred in someone with orthostatic hypotension).

Patient Selection

Acne occurring along the lower face or jawline in adult women sometimes is referred to as hormonal acne, but this dogma is not particularly evidence based. An observational study of 374 patients found that almost 90% of adult women had acne involving multiple facial zones with a spectrum of facial acne severity similar to that in adolescents.³⁶ Only a small subset of these patients (11.2%) had acne localized solely to the mandibular area. In addition, acne along the lower face is not predictive of hyperandrogenism (eg, polycystic ovary syndrome).³⁷ Antiandrogen therapies such as spironolactone and clascoterone are effective in both men and women with acne^10,38 and in adolescents and adults, suggesting that hormones play a fundamental role in all acne and that addressing this mechanism can be useful broadly. Therefore, hormonal therapies such as spironolactone should not be restricted to only adult women with acne along the lower face.

While spironolactone can be effective for acne treatment in any age group, it may be most effective for adult women with acne. In the SAFA trial, prespecified subgroup analyses showed a statistically significant (P=.005) interaction term for age (categorized as <25 years and ≥25 years), which suggested that spironolactone might be a more effective treatment for women 25 years and older.¹⁵ In addition, subgroup analyses in the aforementioned 2018 analysis of claims data found that spironolactone was more effective relative to oral antibiotics in adults vs adolescents.³² Despite these limitations, several case series have highlighted that spironolactone is effective among adolescent populations with acne. A case series of spironolactone use in 73 patients aged 19 years or younger found that 68% of patients demonstrated resolution or improvement in their acne after spironolactone treatment.³⁹ Another case series among 80 adolescent females reported 80% of patients experiencing improvement of their acne.¹⁴

For those with more severe acne, spironolactone can be combined with other complementary treatment approaches such as topicals, oral antibiotics, or procedural modalities.⁴⁰

Dosing

We recommend starting spironolactone at a dose of 100 mg/d (the patient can take 50 mg/d for 1 week, then increase to 100 mg/d if there are no adverse effects at the lower dose). In the 1984 trial by Goodfellow et al,¹⁰ participants were randomized to doses of 50 mg/d, 100 mg/d, 150 mg/d, and 200 mg/d. In this trial, efficacy assessed by objective and subjective outcomes did not plateau until doses of 100 mg/d to 150 mg/d. In addition, a case series of 403 patients found that the most successful dosage of spironolactone generally was 100 mg/d or higher.¹³ Most of the patients who were started at this dosage either stayed at this level or escalated, whereas patients who started at lower dosages (25-75 mg/d) frequently increased their dosage over time. The SAFA trial also highlighted that most patients can tolerate a spironolactone dose of 100 mg/d.¹⁵ For specific populations, such as patients with polycystic ovary syndrome, a higher dose (mean dosage of 143 mg/d) may be required for efficacy.⁴¹ Given the slow onset of efficacy, typically taking 3 to 5 months, and the low rate of adverse effects, we believe the optimal starting dose is 100 mg/s to 150 mg/d. If adverse effects occur or lesions clear, then the dosage may be reduced.

Adverse Effects

Spironolactone generally is well tolerated; in the SAFA and FASCE trials, fewer than 1% of participants discontinued due to adverse effects.^15,33 Rates of discontinuation due to adverse effects typically have been less than 5% in case series of patients treated in routine clinical practice.^12-14

Because spironolactone is a diuretic and antihypertensive, the most common adverse effects are related to these characteristics. In the SAFA trial, dizziness, lightheadedness, and vertigo were reported more commonly in the spironolactone group than in the placebo group (19% vs 12%, respectively). Similarly, headaches also were reported more frequently in the spironolactone group than in the placebo group (20% vs 12%, respectively).¹⁵ One case series found that, among the 267 patients on spironolactone whose blood pressure was monitored, the mean reduction in systolic blood pressure was 3.5 mm Hg and the mean reduction in diastolic blood pressure was 0.9 mm Hg.¹³ For those with baseline orthostasis or in those who experience adverse effects related to hypotension, reducing the dose often can be helpful. Of note, while doses of 100 mg/d to 150 mg/d often are the most effective, randomized trials have found that spironolactone still can be effective for acne at doses as low as 25 mg/d to 50 mg/d.^10,38

Menstrual irregularities are another commonly cited adverse effect of spironolactone. While a systematic review found that 15% to 30% of patients treated with spironolactone experience menstrual irregularities, it has been difficult to evaluate whether this is due to the medication or other comorbidities, such as polycystic ovary syndrome.⁴² Notably, in the SAFA trial, rates of menstrual irregularities were equivalent between the spironolactone and placebo groups at a dose of 100 mg/d (32% vs 35%, respectively).¹⁵ In contrast, in the FASCE trial, menstrual irregularities were more commonly reported at a dose of 150 mg/d.³³ These findings are consistent with observational data suggesting that menstrual irregularities are much more common at spironolactone doses greater than 100 mg/d.⁴² Additionally, some evidence supports that for some patients these menstrual irregularities may resolve within 2 to 3 months of continued treatment.⁴³ It has been noted in several studies that menstrual irregularities are less likely to occur in patients who are using combined oral contraceptives; therefore, for patients who are amenable and have no contraindications, combined oral contraceptives can be considered to prevent or address menstrual irregularities.^13,42,44

More generally, combined oral contraceptives can be an excellent combination with spironolactone, as they have complementary characteristics. Spironolactone primarily blocks the effects of androgens, while combined oral contraceptives predominantly block the production of androgens. Whereas spironolactone typically causes hypotension and menstrual irregularities, combined oral contraceptives cause hypertension and help to regulate the menstrual cycle.

Spironolactone carries an official US Food and Drug Administration warning regarding possible tumorigenicity that is based on animal studies that used up to 150 times the normal dose of spironolactone used in humans⁴⁵; however, observational studies in humans have not identified such an association when spironolactone is used in normal clinical settings. A systematic review and metanalysis in 2022 reviewed data from a total population of more than 4 million individuals and found that there was no statistically significant association between spironolactone use and the risk for breast, ovarian, bladder, kidney, gastric, or esophageal cancers.⁴⁶ Additional studies also found no association between spironolactone use and cancers.⁴⁸ A more recent cohort study specifically among patients treated with spironolactone for acne also found no significant increased risk for breast cancer.⁴⁹

Combined oral contraceptives are associated with an increased risk for venous thromboembolisms, and there have been concerns that this risk may be greater in combined oral contraceptives that contain drospirenone.⁵⁰ Drospirenone is molecularly related to spironolactone, which has prompted the consideration of whether spironolactone use also conveys a risk for venous thromboembolism. Reassuringly, a retrospective study of claims data found that individuals on spironolactone were not more likely to develop a pulmonary embolism or a deep venous thrombosis than matched controls treated with tetracycline antibiotics, with a point estimate favoring decreased risk.⁵¹

Monitoring

Given that one of spironolactone’s mechanisms of action is aldosterone antagonism and thus the inhibition of potassium excretion, there have been concerns regarding risk for hyperkalemia. A retrospective study analyzing data from 2000 to 2014 found that, among 974 young women receiving spironolactone therapy, the rate of hyperkalemia was 0.72%, which is equivalent to the 0.76% baseline rate of hyperkalemia in the same population.⁵² Subsequent studies also have found that spironolactone does not appear to be associated with a meaningful risk for hyperkalemia among young healthy patients treated for acne.^38,53 These studies suggest that routine potassium monitoring is of low usefulness for healthy young women taking spironolactone for acne. The 2024 American Academy of Dermatology guidelines on the management of acne also state that potassium monitoring is not needed in healthy patients but that potassium testing should be considered for those with risk factors for hyperkalemia (eg, older age, medical comorbidities, medications).⁴⁰ Clinicians should still engage in shared decision making with patients to determine whether to check potassium. If potassium is to be monitored, it should be checked 1 to 2 weeks after spironolactone is started.^45,54

Since drospirenone also has aldosterone antagonistic properties,⁵⁵ there have been concerns about whether concomitant use of spironolactone and drospirenone-containing combined oral contraceptives might increase the risk for hyperkalemia.⁵⁶ However, a retrospective cohort study analyzing data from more than 1 million women found that drospirenone is not any more likely than levonorgestrel to cause hyperkalemia and that there is no interaction between drospirenone and spironolactone for hyperkalemia.⁵⁷ A subsequent prospective study of 27 women treated with combined oral contraceptives containing ethinyl estradiol/drospirenone and spironolactone also did not find any significant elevations in potassium.⁵⁸ Data from these studies suggest that spironolactone can safely be co-administered with drospirenone-containing combined oral contraceptives.

Reproductive Risks

Despite its utility in treating acne, spironolactone should not be used during pregnancy, and appropriate pregnancy prevention is recommended. Spironolactone crosses the placenta, and some animal studies have shown feminization of male fetuses.⁵⁹ While human data are limited to a few case reports that did not demonstrate an association of major malformations,⁶⁰ it generally is recommended to avoid spironolactone during pregnancy. Small studies have found that spironolactone has minimal transfer to breastmilk and is not associated with adverse effects in breastfed infants.^61-63 Accordingly, the World Health Organization considers spironolactone to be compatible with breastfeeding.⁶⁴ Notably, spironolactone may be associated with lactation suppression^65,66; therefore, it may be best if lactating patients ensure that their milk production is established prior to starting spironolactone and to increase their water intake to offset the diuretic effects.

Spironolactone also can result in gynecomastia in men and therefore typically is not prescribed for the treatment of acne in this population in oral form¹⁰; however, topical antiandrogens such as clascoterone can be used in both women and men with acne.⁶⁷

Conclusion

Spironolactone is a well-tolerated and effective treatment for women with acne, both in adult and adolescent populations. It is a potentially underutilized alternative to oral antibiotics. Spironolactone also is affordable, fully covered without any requirements in almost 90% of states under Medicaid and with a monthly cost of only $4.00 when obtained through major retailers in the United States, making it an optimal long-term treatment option for many patients.^52,68 We recommend a starting dose of 100 mg/d, which can be increased to 150 mg/d to 200 mg/d if needed for better acne control or decreased if adverse effects occur or acne clears. Potassium monitoring is of low usefulness in young healthy women, and studies have not identified an association between spironolactone use and increased risk for cancer.

Spironolactone is increasingly used off label for acne treatment and is now being prescribed for women with acne at a frequency similar to oral antibiotics.^1,2 In this article, we provide an overview of spironolactone use for acne treatment and discuss recent clinical trials and practical strategies for patient selection, dosing, adverse effect management, and monitoring (Table).

History and Mechanism of Action

Because sebaceous gland activity is an important component of acne pathogenesis and is regulated by androgens,³ there has long been interest in identifying treatment strategies that can target the role of hormones in activating the sebaceous gland. In the 1980s, it became apparent that spironolactone, originally developed as a potassium-sparing diuretic, also might possess antiandrogenic properties that could be useful in the treatment of acne.⁴ Spironolactone has been found to decrease testosterone production, inhibit testosterone and dihydrotestosterone binding to androgen receptors,^5-8 and block 5α-reductase receptors of the sebaceous glands of skin.⁹

In 1984, Goodfellow et al¹⁰ conducted a trial in which 36 male and female patients with severe acne were randomized to placebo or spironolactone doses ranging from 50 to 200 mg/d. They found that spironolactone resulted in dose-dependent reductions of sebum production as well as improvement in patient- and clinician-reported assessments of acne. In 1986, another placebo-controlled crossover trial by Muhlemann et al¹¹ provided further support for the effectiveness of spironolactone for acne. This trial randomized 21 women to placebo or spironolactone 200 mg/d and found that spironolactone was associated with statistically significant (P<.001) improvements in acne lesion counts.

Recent Observational Studies and Trials

Following these early trials, several large case series have been published describing the successful use of spironolactone for acne, including a 2020 retrospective case series from the Mayo Clinic describing 395 patients.¹² The investigators found that almost 66% of patients had a complete response and almost 85% had a complete response or a partial response greater than 50%. They also found that the median time to initial response and maximal response were 3 and 5 months, respectively, and that efficacy was observed across acne subtypes, including for nodulocystic acne.¹² In addition, a 2021 case series describing 403 patients treated with spironolactone found that approximately 80% had reduction or complete clearance of acne, with improvements observed for both facial and truncal acne. In this cohort, doses of 100 to 150 mg/d typically were the most successful.¹³ A case series of 80 adolescent females also highlighted the efficacy of spironolactone in younger populations.¹⁴

Adding to these observational data, the multicenter, phase 3, double-blind Spironolactone for Adult Female Acne (SAFA) trial included 410 women (mean age, 29.2 years) who were randomized to receive either placebo or intervention (spironolactone 50 mg/d until week 6 and 100 mg/d until week 24).¹⁵ At 24 weeks, greater improvement in quality of life and participant self-assessed improvement were observed in the spironolactone group. In addition, at 12 weeks, rates of success were higher in the spironolactone group using the Investigator Global Assessment score (adjusted odds ratio 5.18 [95% CI, 2.18- 12.28]). Those randomized to receive spironolactone also had lower rates of oral antibiotic use at 52 weeks than the placebo group did (5.8% vs 13.5%, respectively).

In the SAFA trial, spironolactone was well tolerated; the most common adverse effects relative to placebo were lightheadedness (19% for spironolactone vs 12% for placebo) and headache (20% for spironolactone vs 12% for placebo). Notably, more than 95% of patients were able to increase from 50 mg/d to 100 mg/d at week 6, with greater than 90% tolerating 100 mg/d. As observational data suggest that spironolactone takes 3 to 5 months to reach peak efficacy, these findings provide further support that starting at a dose of at least 100 mg/d is likely optimal for most patients.¹⁶

A Potential Alternative to Oral Antibiotics

Oral antibiotics such as tetracyclines have long played a central role in the treatment of acne and remain a first-line treatment option.¹⁷ In addition, many of these antibiotic courses exceed 6 months in duration.¹ In fact, dermatologists prescribe more antibiotics per capita than any other specialty^1,18-20; however, this can be associated with the development of antibiotic resistance,^21,22 as well as other antibiotic-associated complications, including inflammatory bowel disease,²³ pharyngitis,²⁴Clostridium difficile infections, and cancer.^25-29

In addition to these concerns, many patients may prefer nonantibiotic alternatives to oral antibiotics, with more than 75% preferring a nonantibiotic option if available. For female patients with acne, antiandrogens such as spironolactone have been suggested as a potential alternative.³⁰ A 10-year retrospective study of female patients with acne found that those who had ever received hormonal therapy (ie, spironolactone or a combined oral contraceptive) received fewer cumulative days of oral antibiotics than those who did not (226 days vs 302 days, respectively).³¹ In addition, while oral antibiotics were the most common initial therapy prescribed for patients, as they progressed through their treatment course, more patients ended up on hormonal therapy than oral antibiotics. This study suggests that hormonal therapy such as spironolactone could represent an alternative to the use of systemic antibiotics.³¹

Further supporting the role of spironolactone as an alternative to oral antibiotics, a 2018 analysis of claims data found that spironolactone may have similar effectiveness to oral antibiotics for the treatment of acne.32 After adjusting for age and topical retinoid and oral contraceptive use, this study found that there was no significant difference in the odds of being prescribed a different systemic treatment within 1 year (ie, treatment failure) among those starting spironolactone vs those starting oral tetracycline-class antibiotics as their initial therapy for acne.

A multicenter, randomized, double-blind trial (Female Acne Spironolactone vs doxyCycline Efficacy [FASCE]) also evaluated the comparative effectiveness of doxycycline 100 mg/d for 3 months followed by an oral placebo for 3 months vs spironolactone 150 mg/d for 6 months among 133 adult women with acne. This study found that spironolactone had statistically significantly greater rates of Investigator Global Assessment treatment success after 6 months (odds ratio 2.87 [95% CI, 1.38-5.99; P=.007]).³³ Since spironolactone historically has been prescribed less often than oral antibiotics for women with acne, these findings support spironolactone as an underutilized treatment alternative. The ongoing Spironolactone versus Doxycycline for Acne: A Comparative Effectiveness, Noninferiority Evaluation trial—a 16-week, blinded trial comparing 100 mg/d doses of both drugs—should provide additional evidence regarding the relative role of spironolactone and oral antibiotics in the management of acne.³⁴

Ultimately, the decision to use spironolactone or other treatments such as oral antibiotics should be based on shared decision making between clinician and patient. Spironolactone has a relatively slow onset of efficacy, and other options such as oral antibiotics might be preferred by those looking for more immediate results; however, as women with acne often have activity that persists into adulthood, spironolactone might be preferable as a long-term maintenance therapy to avoid complications of prolonged antibiotic use.³⁵ Comorbidities also will influence the optimal choice of therapy (eg, spironolactone might be preferred in someone with inflammatory bowel disease, and oral antibiotics might be preferred in someone with orthostatic hypotension).

Patient Selection

Acne occurring along the lower face or jawline in adult women sometimes is referred to as hormonal acne, but this dogma is not particularly evidence based. An observational study of 374 patients found that almost 90% of adult women had acne involving multiple facial zones with a spectrum of facial acne severity similar to that in adolescents.³⁶ Only a small subset of these patients (11.2%) had acne localized solely to the mandibular area. In addition, acne along the lower face is not predictive of hyperandrogenism (eg, polycystic ovary syndrome).³⁷ Antiandrogen therapies such as spironolactone and clascoterone are effective in both men and women with acne^10,38 and in adolescents and adults, suggesting that hormones play a fundamental role in all acne and that addressing this mechanism can be useful broadly. Therefore, hormonal therapies such as spironolactone should not be restricted to only adult women with acne along the lower face.

While spironolactone can be effective for acne treatment in any age group, it may be most effective for adult women with acne. In the SAFA trial, prespecified subgroup analyses showed a statistically significant (P=.005) interaction term for age (categorized as <25 years and ≥25 years), which suggested that spironolactone might be a more effective treatment for women 25 years and older.¹⁵ In addition, subgroup analyses in the aforementioned 2018 analysis of claims data found that spironolactone was more effective relative to oral antibiotics in adults vs adolescents.³² Despite these limitations, several case series have highlighted that spironolactone is effective among adolescent populations with acne. A case series of spironolactone use in 73 patients aged 19 years or younger found that 68% of patients demonstrated resolution or improvement in their acne after spironolactone treatment.³⁹ Another case series among 80 adolescent females reported 80% of patients experiencing improvement of their acne.¹⁴

For those with more severe acne, spironolactone can be combined with other complementary treatment approaches such as topicals, oral antibiotics, or procedural modalities.⁴⁰

Dosing

We recommend starting spironolactone at a dose of 100 mg/d (the patient can take 50 mg/d for 1 week, then increase to 100 mg/d if there are no adverse effects at the lower dose). In the 1984 trial by Goodfellow et al,¹⁰ participants were randomized to doses of 50 mg/d, 100 mg/d, 150 mg/d, and 200 mg/d. In this trial, efficacy assessed by objective and subjective outcomes did not plateau until doses of 100 mg/d to 150 mg/d. In addition, a case series of 403 patients found that the most successful dosage of spironolactone generally was 100 mg/d or higher.¹³ Most of the patients who were started at this dosage either stayed at this level or escalated, whereas patients who started at lower dosages (25-75 mg/d) frequently increased their dosage over time. The SAFA trial also highlighted that most patients can tolerate a spironolactone dose of 100 mg/d.¹⁵ For specific populations, such as patients with polycystic ovary syndrome, a higher dose (mean dosage of 143 mg/d) may be required for efficacy.⁴¹ Given the slow onset of efficacy, typically taking 3 to 5 months, and the low rate of adverse effects, we believe the optimal starting dose is 100 mg/s to 150 mg/d. If adverse effects occur or lesions clear, then the dosage may be reduced.

Adverse Effects

Spironolactone generally is well tolerated; in the SAFA and FASCE trials, fewer than 1% of participants discontinued due to adverse effects.^15,33 Rates of discontinuation due to adverse effects typically have been less than 5% in case series of patients treated in routine clinical practice.^12-14

Because spironolactone is a diuretic and antihypertensive, the most common adverse effects are related to these characteristics. In the SAFA trial, dizziness, lightheadedness, and vertigo were reported more commonly in the spironolactone group than in the placebo group (19% vs 12%, respectively). Similarly, headaches also were reported more frequently in the spironolactone group than in the placebo group (20% vs 12%, respectively).¹⁵ One case series found that, among the 267 patients on spironolactone whose blood pressure was monitored, the mean reduction in systolic blood pressure was 3.5 mm Hg and the mean reduction in diastolic blood pressure was 0.9 mm Hg.¹³ For those with baseline orthostasis or in those who experience adverse effects related to hypotension, reducing the dose often can be helpful. Of note, while doses of 100 mg/d to 150 mg/d often are the most effective, randomized trials have found that spironolactone still can be effective for acne at doses as low as 25 mg/d to 50 mg/d.^10,38

Menstrual irregularities are another commonly cited adverse effect of spironolactone. While a systematic review found that 15% to 30% of patients treated with spironolactone experience menstrual irregularities, it has been difficult to evaluate whether this is due to the medication or other comorbidities, such as polycystic ovary syndrome.⁴² Notably, in the SAFA trial, rates of menstrual irregularities were equivalent between the spironolactone and placebo groups at a dose of 100 mg/d (32% vs 35%, respectively).¹⁵ In contrast, in the FASCE trial, menstrual irregularities were more commonly reported at a dose of 150 mg/d.³³ These findings are consistent with observational data suggesting that menstrual irregularities are much more common at spironolactone doses greater than 100 mg/d.⁴² Additionally, some evidence supports that for some patients these menstrual irregularities may resolve within 2 to 3 months of continued treatment.⁴³ It has been noted in several studies that menstrual irregularities are less likely to occur in patients who are using combined oral contraceptives; therefore, for patients who are amenable and have no contraindications, combined oral contraceptives can be considered to prevent or address menstrual irregularities.^13,42,44

More generally, combined oral contraceptives can be an excellent combination with spironolactone, as they have complementary characteristics. Spironolactone primarily blocks the effects of androgens, while combined oral contraceptives predominantly block the production of androgens. Whereas spironolactone typically causes hypotension and menstrual irregularities, combined oral contraceptives cause hypertension and help to regulate the menstrual cycle.

Spironolactone carries an official US Food and Drug Administration warning regarding possible tumorigenicity that is based on animal studies that used up to 150 times the normal dose of spironolactone used in humans⁴⁵; however, observational studies in humans have not identified such an association when spironolactone is used in normal clinical settings. A systematic review and metanalysis in 2022 reviewed data from a total population of more than 4 million individuals and found that there was no statistically significant association between spironolactone use and the risk for breast, ovarian, bladder, kidney, gastric, or esophageal cancers.⁴⁶ Additional studies also found no association between spironolactone use and cancers.⁴⁸ A more recent cohort study specifically among patients treated with spironolactone for acne also found no significant increased risk for breast cancer.⁴⁹

Combined oral contraceptives are associated with an increased risk for venous thromboembolisms, and there have been concerns that this risk may be greater in combined oral contraceptives that contain drospirenone.⁵⁰ Drospirenone is molecularly related to spironolactone, which has prompted the consideration of whether spironolactone use also conveys a risk for venous thromboembolism. Reassuringly, a retrospective study of claims data found that individuals on spironolactone were not more likely to develop a pulmonary embolism or a deep venous thrombosis than matched controls treated with tetracycline antibiotics, with a point estimate favoring decreased risk.⁵¹

Monitoring

Given that one of spironolactone’s mechanisms of action is aldosterone antagonism and thus the inhibition of potassium excretion, there have been concerns regarding risk for hyperkalemia. A retrospective study analyzing data from 2000 to 2014 found that, among 974 young women receiving spironolactone therapy, the rate of hyperkalemia was 0.72%, which is equivalent to the 0.76% baseline rate of hyperkalemia in the same population.⁵² Subsequent studies also have found that spironolactone does not appear to be associated with a meaningful risk for hyperkalemia among young healthy patients treated for acne.^38,53 These studies suggest that routine potassium monitoring is of low usefulness for healthy young women taking spironolactone for acne. The 2024 American Academy of Dermatology guidelines on the management of acne also state that potassium monitoring is not needed in healthy patients but that potassium testing should be considered for those with risk factors for hyperkalemia (eg, older age, medical comorbidities, medications).⁴⁰ Clinicians should still engage in shared decision making with patients to determine whether to check potassium. If potassium is to be monitored, it should be checked 1 to 2 weeks after spironolactone is started.^45,54

Since drospirenone also has aldosterone antagonistic properties,⁵⁵ there have been concerns about whether concomitant use of spironolactone and drospirenone-containing combined oral contraceptives might increase the risk for hyperkalemia.⁵⁶ However, a retrospective cohort study analyzing data from more than 1 million women found that drospirenone is not any more likely than levonorgestrel to cause hyperkalemia and that there is no interaction between drospirenone and spironolactone for hyperkalemia.⁵⁷ A subsequent prospective study of 27 women treated with combined oral contraceptives containing ethinyl estradiol/drospirenone and spironolactone also did not find any significant elevations in potassium.⁵⁸ Data from these studies suggest that spironolactone can safely be co-administered with drospirenone-containing combined oral contraceptives.

Reproductive Risks

Despite its utility in treating acne, spironolactone should not be used during pregnancy, and appropriate pregnancy prevention is recommended. Spironolactone crosses the placenta, and some animal studies have shown feminization of male fetuses.⁵⁹ While human data are limited to a few case reports that did not demonstrate an association of major malformations,⁶⁰ it generally is recommended to avoid spironolactone during pregnancy. Small studies have found that spironolactone has minimal transfer to breastmilk and is not associated with adverse effects in breastfed infants.^61-63 Accordingly, the World Health Organization considers spironolactone to be compatible with breastfeeding.⁶⁴ Notably, spironolactone may be associated with lactation suppression^65,66; therefore, it may be best if lactating patients ensure that their milk production is established prior to starting spironolactone and to increase their water intake to offset the diuretic effects.

Spironolactone also can result in gynecomastia in men and therefore typically is not prescribed for the treatment of acne in this population in oral form¹⁰; however, topical antiandrogens such as clascoterone can be used in both women and men with acne.⁶⁷

Conclusion

Spironolactone is a well-tolerated and effective treatment for women with acne, both in adult and adolescent populations. It is a potentially underutilized alternative to oral antibiotics. Spironolactone also is affordable, fully covered without any requirements in almost 90% of states under Medicaid and with a monthly cost of only $4.00 when obtained through major retailers in the United States, making it an optimal long-term treatment option for many patients.^52,68 We recommend a starting dose of 100 mg/d, which can be increased to 150 mg/d to 200 mg/d if needed for better acne control or decreased if adverse effects occur or acne clears. Potassium monitoring is of low usefulness in young healthy women, and studies have not identified an association between spironolactone use and increased risk for cancer.

Spironolactone is increasingly used off label for acne treatment and is now being prescribed for women with acne at a frequency similar to oral antibiotics.^1,2 In this article, we provide an overview of spironolactone use for acne treatment and discuss recent clinical trials and practical strategies for patient selection, dosing, adverse effect management, and monitoring (Table).

History and Mechanism of Action

Because sebaceous gland activity is an important component of acne pathogenesis and is regulated by androgens,³ there has long been interest in identifying treatment strategies that can target the role of hormones in activating the sebaceous gland. In the 1980s, it became apparent that spironolactone, originally developed as a potassium-sparing diuretic, also might possess antiandrogenic properties that could be useful in the treatment of acne.⁴ Spironolactone has been found to decrease testosterone production, inhibit testosterone and dihydrotestosterone binding to androgen receptors,^5-8 and block 5α-reductase receptors of the sebaceous glands of skin.⁹

In 1984, Goodfellow et al¹⁰ conducted a trial in which 36 male and female patients with severe acne were randomized to placebo or spironolactone doses ranging from 50 to 200 mg/d. They found that spironolactone resulted in dose-dependent reductions of sebum production as well as improvement in patient- and clinician-reported assessments of acne. In 1986, another placebo-controlled crossover trial by Muhlemann et al¹¹ provided further support for the effectiveness of spironolactone for acne. This trial randomized 21 women to placebo or spironolactone 200 mg/d and found that spironolactone was associated with statistically significant (P<.001) improvements in acne lesion counts.

Recent Observational Studies and Trials

Following these early trials, several large case series have been published describing the successful use of spironolactone for acne, including a 2020 retrospective case series from the Mayo Clinic describing 395 patients.¹² The investigators found that almost 66% of patients had a complete response and almost 85% had a complete response or a partial response greater than 50%. They also found that the median time to initial response and maximal response were 3 and 5 months, respectively, and that efficacy was observed across acne subtypes, including for nodulocystic acne.¹² In addition, a 2021 case series describing 403 patients treated with spironolactone found that approximately 80% had reduction or complete clearance of acne, with improvements observed for both facial and truncal acne. In this cohort, doses of 100 to 150 mg/d typically were the most successful.¹³ A case series of 80 adolescent females also highlighted the efficacy of spironolactone in younger populations.¹⁴

Adding to these observational data, the multicenter, phase 3, double-blind Spironolactone for Adult Female Acne (SAFA) trial included 410 women (mean age, 29.2 years) who were randomized to receive either placebo or intervention (spironolactone 50 mg/d until week 6 and 100 mg/d until week 24).¹⁵ At 24 weeks, greater improvement in quality of life and participant self-assessed improvement were observed in the spironolactone group. In addition, at 12 weeks, rates of success were higher in the spironolactone group using the Investigator Global Assessment score (adjusted odds ratio 5.18 [95% CI, 2.18- 12.28]). Those randomized to receive spironolactone also had lower rates of oral antibiotic use at 52 weeks than the placebo group did (5.8% vs 13.5%, respectively).

In the SAFA trial, spironolactone was well tolerated; the most common adverse effects relative to placebo were lightheadedness (19% for spironolactone vs 12% for placebo) and headache (20% for spironolactone vs 12% for placebo). Notably, more than 95% of patients were able to increase from 50 mg/d to 100 mg/d at week 6, with greater than 90% tolerating 100 mg/d. As observational data suggest that spironolactone takes 3 to 5 months to reach peak efficacy, these findings provide further support that starting at a dose of at least 100 mg/d is likely optimal for most patients.¹⁶

A Potential Alternative to Oral Antibiotics

Oral antibiotics such as tetracyclines have long played a central role in the treatment of acne and remain a first-line treatment option.¹⁷ In addition, many of these antibiotic courses exceed 6 months in duration.¹ In fact, dermatologists prescribe more antibiotics per capita than any other specialty^1,18-20; however, this can be associated with the development of antibiotic resistance,^21,22 as well as other antibiotic-associated complications, including inflammatory bowel disease,²³ pharyngitis,²⁴Clostridium difficile infections, and cancer.^25-29

In addition to these concerns, many patients may prefer nonantibiotic alternatives to oral antibiotics, with more than 75% preferring a nonantibiotic option if available. For female patients with acne, antiandrogens such as spironolactone have been suggested as a potential alternative.³⁰ A 10-year retrospective study of female patients with acne found that those who had ever received hormonal therapy (ie, spironolactone or a combined oral contraceptive) received fewer cumulative days of oral antibiotics than those who did not (226 days vs 302 days, respectively).³¹ In addition, while oral antibiotics were the most common initial therapy prescribed for patients, as they progressed through their treatment course, more patients ended up on hormonal therapy than oral antibiotics. This study suggests that hormonal therapy such as spironolactone could represent an alternative to the use of systemic antibiotics.³¹

Further supporting the role of spironolactone as an alternative to oral antibiotics, a 2018 analysis of claims data found that spironolactone may have similar effectiveness to oral antibiotics for the treatment of acne.32 After adjusting for age and topical retinoid and oral contraceptive use, this study found that there was no significant difference in the odds of being prescribed a different systemic treatment within 1 year (ie, treatment failure) among those starting spironolactone vs those starting oral tetracycline-class antibiotics as their initial therapy for acne.

A multicenter, randomized, double-blind trial (Female Acne Spironolactone vs doxyCycline Efficacy [FASCE]) also evaluated the comparative effectiveness of doxycycline 100 mg/d for 3 months followed by an oral placebo for 3 months vs spironolactone 150 mg/d for 6 months among 133 adult women with acne. This study found that spironolactone had statistically significantly greater rates of Investigator Global Assessment treatment success after 6 months (odds ratio 2.87 [95% CI, 1.38-5.99; P=.007]).³³ Since spironolactone historically has been prescribed less often than oral antibiotics for women with acne, these findings support spironolactone as an underutilized treatment alternative. The ongoing Spironolactone versus Doxycycline for Acne: A Comparative Effectiveness, Noninferiority Evaluation trial—a 16-week, blinded trial comparing 100 mg/d doses of both drugs—should provide additional evidence regarding the relative role of spironolactone and oral antibiotics in the management of acne.³⁴

Ultimately, the decision to use spironolactone or other treatments such as oral antibiotics should be based on shared decision making between clinician and patient. Spironolactone has a relatively slow onset of efficacy, and other options such as oral antibiotics might be preferred by those looking for more immediate results; however, as women with acne often have activity that persists into adulthood, spironolactone might be preferable as a long-term maintenance therapy to avoid complications of prolonged antibiotic use.³⁵ Comorbidities also will influence the optimal choice of therapy (eg, spironolactone might be preferred in someone with inflammatory bowel disease, and oral antibiotics might be preferred in someone with orthostatic hypotension).

Patient Selection

Acne occurring along the lower face or jawline in adult women sometimes is referred to as hormonal acne, but this dogma is not particularly evidence based. An observational study of 374 patients found that almost 90% of adult women had acne involving multiple facial zones with a spectrum of facial acne severity similar to that in adolescents.³⁶ Only a small subset of these patients (11.2%) had acne localized solely to the mandibular area. In addition, acne along the lower face is not predictive of hyperandrogenism (eg, polycystic ovary syndrome).³⁷ Antiandrogen therapies such as spironolactone and clascoterone are effective in both men and women with acne^10,38 and in adolescents and adults, suggesting that hormones play a fundamental role in all acne and that addressing this mechanism can be useful broadly. Therefore, hormonal therapies such as spironolactone should not be restricted to only adult women with acne along the lower face.

While spironolactone can be effective for acne treatment in any age group, it may be most effective for adult women with acne. In the SAFA trial, prespecified subgroup analyses showed a statistically significant (P=.005) interaction term for age (categorized as <25 years and ≥25 years), which suggested that spironolactone might be a more effective treatment for women 25 years and older.¹⁵ In addition, subgroup analyses in the aforementioned 2018 analysis of claims data found that spironolactone was more effective relative to oral antibiotics in adults vs adolescents.³² Despite these limitations, several case series have highlighted that spironolactone is effective among adolescent populations with acne. A case series of spironolactone use in 73 patients aged 19 years or younger found that 68% of patients demonstrated resolution or improvement in their acne after spironolactone treatment.³⁹ Another case series among 80 adolescent females reported 80% of patients experiencing improvement of their acne.¹⁴

For those with more severe acne, spironolactone can be combined with other complementary treatment approaches such as topicals, oral antibiotics, or procedural modalities.⁴⁰

Dosing

We recommend starting spironolactone at a dose of 100 mg/d (the patient can take 50 mg/d for 1 week, then increase to 100 mg/d if there are no adverse effects at the lower dose). In the 1984 trial by Goodfellow et al,¹⁰ participants were randomized to doses of 50 mg/d, 100 mg/d, 150 mg/d, and 200 mg/d. In this trial, efficacy assessed by objective and subjective outcomes did not plateau until doses of 100 mg/d to 150 mg/d. In addition, a case series of 403 patients found that the most successful dosage of spironolactone generally was 100 mg/d or higher.¹³ Most of the patients who were started at this dosage either stayed at this level or escalated, whereas patients who started at lower dosages (25-75 mg/d) frequently increased their dosage over time. The SAFA trial also highlighted that most patients can tolerate a spironolactone dose of 100 mg/d.¹⁵ For specific populations, such as patients with polycystic ovary syndrome, a higher dose (mean dosage of 143 mg/d) may be required for efficacy.⁴¹ Given the slow onset of efficacy, typically taking 3 to 5 months, and the low rate of adverse effects, we believe the optimal starting dose is 100 mg/s to 150 mg/d. If adverse effects occur or lesions clear, then the dosage may be reduced.

Adverse Effects

Spironolactone generally is well tolerated; in the SAFA and FASCE trials, fewer than 1% of participants discontinued due to adverse effects.^15,33 Rates of discontinuation due to adverse effects typically have been less than 5% in case series of patients treated in routine clinical practice.^12-14

Because spironolactone is a diuretic and antihypertensive, the most common adverse effects are related to these characteristics. In the SAFA trial, dizziness, lightheadedness, and vertigo were reported more commonly in the spironolactone group than in the placebo group (19% vs 12%, respectively). Similarly, headaches also were reported more frequently in the spironolactone group than in the placebo group (20% vs 12%, respectively).¹⁵ One case series found that, among the 267 patients on spironolactone whose blood pressure was monitored, the mean reduction in systolic blood pressure was 3.5 mm Hg and the mean reduction in diastolic blood pressure was 0.9 mm Hg.¹³ For those with baseline orthostasis or in those who experience adverse effects related to hypotension, reducing the dose often can be helpful. Of note, while doses of 100 mg/d to 150 mg/d often are the most effective, randomized trials have found that spironolactone still can be effective for acne at doses as low as 25 mg/d to 50 mg/d.^10,38

Menstrual irregularities are another commonly cited adverse effect of spironolactone. While a systematic review found that 15% to 30% of patients treated with spironolactone experience menstrual irregularities, it has been difficult to evaluate whether this is due to the medication or other comorbidities, such as polycystic ovary syndrome.⁴² Notably, in the SAFA trial, rates of menstrual irregularities were equivalent between the spironolactone and placebo groups at a dose of 100 mg/d (32% vs 35%, respectively).¹⁵ In contrast, in the FASCE trial, menstrual irregularities were more commonly reported at a dose of 150 mg/d.³³ These findings are consistent with observational data suggesting that menstrual irregularities are much more common at spironolactone doses greater than 100 mg/d.⁴² Additionally, some evidence supports that for some patients these menstrual irregularities may resolve within 2 to 3 months of continued treatment.⁴³ It has been noted in several studies that menstrual irregularities are less likely to occur in patients who are using combined oral contraceptives; therefore, for patients who are amenable and have no contraindications, combined oral contraceptives can be considered to prevent or address menstrual irregularities.^13,42,44

More generally, combined oral contraceptives can be an excellent combination with spironolactone, as they have complementary characteristics. Spironolactone primarily blocks the effects of androgens, while combined oral contraceptives predominantly block the production of androgens. Whereas spironolactone typically causes hypotension and menstrual irregularities, combined oral contraceptives cause hypertension and help to regulate the menstrual cycle.

Spironolactone carries an official US Food and Drug Administration warning regarding possible tumorigenicity that is based on animal studies that used up to 150 times the normal dose of spironolactone used in humans⁴⁵; however, observational studies in humans have not identified such an association when spironolactone is used in normal clinical settings. A systematic review and metanalysis in 2022 reviewed data from a total population of more than 4 million individuals and found that there was no statistically significant association between spironolactone use and the risk for breast, ovarian, bladder, kidney, gastric, or esophageal cancers.⁴⁶ Additional studies also found no association between spironolactone use and cancers.⁴⁸ A more recent cohort study specifically among patients treated with spironolactone for acne also found no significant increased risk for breast cancer.⁴⁹

Combined oral contraceptives are associated with an increased risk for venous thromboembolisms, and there have been concerns that this risk may be greater in combined oral contraceptives that contain drospirenone.⁵⁰ Drospirenone is molecularly related to spironolactone, which has prompted the consideration of whether spironolactone use also conveys a risk for venous thromboembolism. Reassuringly, a retrospective study of claims data found that individuals on spironolactone were not more likely to develop a pulmonary embolism or a deep venous thrombosis than matched controls treated with tetracycline antibiotics, with a point estimate favoring decreased risk.⁵¹

Monitoring

Given that one of spironolactone’s mechanisms of action is aldosterone antagonism and thus the inhibition of potassium excretion, there have been concerns regarding risk for hyperkalemia. A retrospective study analyzing data from 2000 to 2014 found that, among 974 young women receiving spironolactone therapy, the rate of hyperkalemia was 0.72%, which is equivalent to the 0.76% baseline rate of hyperkalemia in the same population.⁵² Subsequent studies also have found that spironolactone does not appear to be associated with a meaningful risk for hyperkalemia among young healthy patients treated for acne.^38,53 These studies suggest that routine potassium monitoring is of low usefulness for healthy young women taking spironolactone for acne. The 2024 American Academy of Dermatology guidelines on the management of acne also state that potassium monitoring is not needed in healthy patients but that potassium testing should be considered for those with risk factors for hyperkalemia (eg, older age, medical comorbidities, medications).⁴⁰ Clinicians should still engage in shared decision making with patients to determine whether to check potassium. If potassium is to be monitored, it should be checked 1 to 2 weeks after spironolactone is started.^45,54

Since drospirenone also has aldosterone antagonistic properties,⁵⁵ there have been concerns about whether concomitant use of spironolactone and drospirenone-containing combined oral contraceptives might increase the risk for hyperkalemia.⁵⁶ However, a retrospective cohort study analyzing data from more than 1 million women found that drospirenone is not any more likely than levonorgestrel to cause hyperkalemia and that there is no interaction between drospirenone and spironolactone for hyperkalemia.⁵⁷ A subsequent prospective study of 27 women treated with combined oral contraceptives containing ethinyl estradiol/drospirenone and spironolactone also did not find any significant elevations in potassium.⁵⁸ Data from these studies suggest that spironolactone can safely be co-administered with drospirenone-containing combined oral contraceptives.

Reproductive Risks

Despite its utility in treating acne, spironolactone should not be used during pregnancy, and appropriate pregnancy prevention is recommended. Spironolactone crosses the placenta, and some animal studies have shown feminization of male fetuses.⁵⁹ While human data are limited to a few case reports that did not demonstrate an association of major malformations,⁶⁰ it generally is recommended to avoid spironolactone during pregnancy. Small studies have found that spironolactone has minimal transfer to breastmilk and is not associated with adverse effects in breastfed infants.^61-63 Accordingly, the World Health Organization considers spironolactone to be compatible with breastfeeding.⁶⁴ Notably, spironolactone may be associated with lactation suppression^65,66; therefore, it may be best if lactating patients ensure that their milk production is established prior to starting spironolactone and to increase their water intake to offset the diuretic effects.

Spironolactone also can result in gynecomastia in men and therefore typically is not prescribed for the treatment of acne in this population in oral form¹⁰; however, topical antiandrogens such as clascoterone can be used in both women and men with acne.⁶⁷

Conclusion

Spironolactone is a well-tolerated and effective treatment for women with acne, both in adult and adolescent populations. It is a potentially underutilized alternative to oral antibiotics. Spironolactone also is affordable, fully covered without any requirements in almost 90% of states under Medicaid and with a monthly cost of only $4.00 when obtained through major retailers in the United States, making it an optimal long-term treatment option for many patients.^52,68 We recommend a starting dose of 100 mg/d, which can be increased to 150 mg/d to 200 mg/d if needed for better acne control or decreased if adverse effects occur or acne clears. Potassium monitoring is of low usefulness in young healthy women, and studies have not identified an association between spironolactone use and increased risk for cancer.

Rosacea is a chronic inflammatory skin condition affecting the central face—including the cheeks, nose, chin, and forehead—that causes considerable discomfort.¹ Its pathogenesis involves immune dysregulation, genetic predisposition, and microbial dysbiosis.² While immune and environmental factors are known triggers of rosacea, recent research highlights the roles of the gut and skin microbiomes in disease progression. While the skin microbiome interacts directly with the immune system to regulate inflammation and skin homeostasis, the gut microbiome also influences cutaneous inflammation, emphasizing the need to address both topical and internal microbiome imbalances.³ In this article, we review gut and skin microbial alterations in rosacea, focusing on the skin microbiome and including the gut-skin axis implications as well as therapeutic strategies aimed at microbiome balance to enhance patient outcomes.

Skin Microbiome Alterations in Rosacea

The human skin microbiome interacts with the immune system, and microbial imbalances have been shown to contribute to immune dysregulation. Several key microbial species have been identified as playing a large role in rosacea, including Demodex folliculorum, Staphylococcus epidermidis, Bacillus oleronius, and Cutibacterium acnes (Figure).

Demodex folliculorum is a microscopic mite is found in hair follicles and sebaceous glands. Patients with rosacea have higher densities of D folliculorum, which trigger follicular occlusion and immune activation.¹Bacillus oleronius be isolated from D folliculorum and can further activate toll-like receptor 2, leading to cytokine production and immune cell infiltration.^3,4 Increased propagation of this mite correlates with shifts in skin microbiome composition, demonstrating increased inflammatory microbial populations.³

Staphylococcus epidermidis normally is commensal but can become pathogenic (pathobiont) in rosacea due to disruptions in the skin microenvironment, where it can form biofilms and produce virulence factors, particularly in papulopustular rosacea.⁵

Bacillus oleronius has been isolated from D folliculorum mites and provokes inflammatory responses in patients with rosacea by triggering toll-like receptor 2 activation and cytokine secretion.⁶

Cutibacterium acnes commonly is associated with acne vulgaris. Its role in rosacea is unclear, but recent research suggests it may have a protective effect. A single-arm trial investigated the effects of minocycline on rosacea and found that treatment significantly reduced C acnes but increased microbial species diversity, improving inflammation.⁷ One longitudinal cohort study of 12 patients with rosacea found that C acnes levels were lower in those older than 60 years. Rosacea severity increased with age and correlated with a decline in C acnes, suggesting that it may confer some protective effect in rosacea.⁸ This finding is supported by studies that have shown a reduction in C acnes levels in patients with rosacea compared to controls.^4,8

Important mechanisms in rosacea include epidermal barrier dysfunction, transepidermal water loss, and decreased stratum corneum hydration, particularly in erythematotelangiectatic and papulopustular subtypes. The resulting alkaline skin pH contributes to barrier instability and heightened inflammation, permitting pathogenic bacteria to proliferate and disrupt skin microbial homeostasis.⁹ A recent study identified metabolic changes in the skin microbiome of patients with rosacea, showing that increased heme and hydrogen sulfide in rosacea skin microbiomes likely drive inflammation, while healthy skin microbiomes produce more anti-inflammatory adenosylcobalamin, thiazole, and L-isoleucine.¹ These findings highlight the link between microbial imbalances and inflammation in rosacea.

The Gut-Skin Axis in Rosacea

Gut microbiota play a critical role in managing systemic inflammation, and microbial dysbiosis in the intestine can influence the skin microbiome in rosacea. Patients with rosacea who have gastrointestinal conditions such as small intestinal bacterial overgrowth and Helicobacter pylori infection experience more severe rosacea symptoms.^3,10

Patients with rosacea have distinctive gut microbiota compositions, with an increased prevalence of proinflammatory bacterial species, potentially affecting the skin microbiome.^8,11 Systemic antibiotics have been shown to modulate the gut microbiome, indirectly influencing the skin microbiome.¹¹ A recent study demonstrated that doxycycline treatment in patients with rosacea altered skin microbial diversity, reducing C acnes while increasing Weissella confusa—highlighting the complicated relationship between systemic antibiotics and the gut-skin axis.⁸

Specific probiotics, such as Escherichia coli Nissle, when given orally shifted gut microbial balance to protective microbiota with increased Lactobacillus and Bifidobacteria species and decreased pathogenic bacteria. This improved rosacea symptoms, normalized immunoglobulin A levels, and suppressed cytokine interleukin 8 levels.¹⁰ Recent studies also suggest oral sarecycline, a narrow-spectrum antibiotic, may improve papulopustular rosacea symptoms through its anti-inflammatory effects while having minimal impact on gut microbiota diversity.^11,12

Gut-derived short-chain fatty acids, which are known to regulate immune function, also have been shown to influence the composition of skin microbiota, suggesting a direct link between gut dysbiosis and skin microbial imbalances. Notably, antibiotic and probiotic treatments targeting the gut microbiome (eg, rifaximin for small intestinal bacterial overgrowth) have been associated with improvements in rosacea symptoms, further underscoring the interconnectedness of the gut-skin axis.¹³ Understanding how gut-derived inflammation alters the skin microbiome may provide new therapeutic avenues for restoring microbial balance and reducing rosacea severity.

Immune Dysregulation and Inflammatory Pathways

Mechanisms of microbiome-driven inflammation via the innate immune system contribute to rosacea pathogenesis. Toll-like receptor 2 is upregulated in rosacea, producing increased peptides including cathelicidins.¹³ When abnormally processed, cathelicidins produce proinflammatory peptides and worsen rosacea symptoms such as erythema, telangiectasias, and neutrophilic infiltration by dysregulating the immune system and the skin barrier.⁶

Heightened levels of cytokines interleukin 8 and interferon α have been identified in patients with rosacea. These cytokines are involved in rosacea pathogenesis, including leukocyte recruitment, angiogenesis, and tissue remodeling and further activate the inflammatory cascade.^8,14

Mendelian randomization studies have provided confirmation of a causal link between skin microbiota alterations and inflammatory skin diseases including rosacea.² Specific alterations in bacteria such as Cutibacterium and Staphylococcus microbial species have been associated with shifts in host immune gene expression, potentially predisposing individuals to abnormal immune activation and inflammation.^2,8 These studies show the potential of leveraging precision medicine to design therapies that target pathways that improve microbial imbalances seen in rosacea.

Environmental and Lifestyle Factors Affecting the Skin Microbiome

Individuals with rosacea often have increased sensitivity to environmental and lifestyle stressors such as high temperatures, UV exposure, and sugar and alcohol consumption. These factors influence the composition of the skin microbiome and potentially contribute to rosacea development and disease exacerbation; therefore, trigger avoidance is an important way to manage rosacea.

High temperatures and UV exposure—Demodex activity increases in response to heat exposure and subsequently worsens rosacea symptoms, while exposure to UV radiation can change the composition of the skin microbiome by encouraging inflammatory responses such as oxidative stress reactions.⁴ This effect on the skin microbiome is driven partly by the increased presence of certain skin microbial species, such as S epidermidis, which secrete virulence factors at higher temperatures and further contribute to inflammation.^1,4

High-glycemic diet and alcohol consumption—High-glycemic diets and alcohol intake have been associated with gut dysbiosis and increased disease severity in rosacea. Processed foods and high sugar consumption can promote proinflammatory reactions that cause skin dysbiosis and exacerbate symptoms.¹⁵ Increased consumption of anti-inflammatory foods or consumption of probiotics and prebiotics can improve microbial balance.

Therapeutic Implications

The influence of the skin and gut microbiome on rosacea have been well described in the medical literature; therefore, many therapeutic strategies aim to address microbiome dysbiosis, including the use of antibiotics, anthelmintics, and a range of topical agents as well as probiotics, microbiome-friendly skin care products, and dietary modifications.

Antibiotics and Anthelmintics—Topical and oral antibiotics such as metronidazole and doxycycline reduce microbial load and inflammation.^5,7,8 Ivermectin, an anthelmintic, has demonstrated efficacy in decreasing Demodex colonization and associated inflammation by interfering with mite survival and reducing bacterial interactions on the skin.⁵ Recent literature also has explored next-generation antibiotics that disrupt biofilm production by bacteria, which could positively affect outcomes while safeguarding antibiotic stewardship.¹⁵ Given its targeted antimicrobial activity and low propensity for microbial resistance, sarecycline represents a promising therapeutic option for managing rosacea symptoms with reduced risk for microbiome-related adverse events.^12,16

Probiotics and Skin Care Interventions—Probiotics, prebiotics, and postbiotics have emerged as promising approaches to improve rosacea outcomes. Topical probiotics have been shown to maintain skin microbiome homeostasis, reduce inflammation, and enhance epidermal barrier function, making them a promising adjunctive therapy for rosacea.^17,18 Physiological pH cleansers and moisturizers formulated with microbiome-friendly ingredients may reduce transepidermal water loss and improve skin hydration, which are critical in microbial equilibrium.⁹ Oral administration of E coli Nissle, Lactobacillus, and Bifidobacterium have shown potential in improving microbial balance and reducing disease severity.¹⁰

Other Topical Therapies—Azelaic acid and benzoyl peroxide can improve rosacea symptoms by decreasing inflammation and also may shift the skin microbiome.^19,20 Formulations of topical therapies, including microencapsulated benzoyl peroxide, show improved efficacy in targeting pathogenic bacteria while maintaining tolerability.¹⁹

Dietary Modifications—Avoiding triggers such as alcohol and high-glycemic foods can help reduce gut and skin dysbiosis.¹³ Polyphenol-rich foods and prebiotic fiber may promote beneficial gut and skin microbial composition and currently are being studied.¹³

Emerging Therapies—Long-pulsed alexandrite laser therapy has been shown to reduce facial erythema and modulate skin microbiota.²¹ Patients with treatment-resistant rosacea may benefit from advanced precision targeted antimicrobials.

The future of rosacea treatment may involve integrating established and emerging microbiome-targeted treatment strategies to improve short- and long-term patient outcomes in rosacea.

Conclusion

As our understanding of rosacea, its pathogenesis, and the role of the skin microbiome continues to grow, so does our ability to develop increasingly effective and well-tolerated treatments. Future research should focus on how changes to the skin microbiome can influence disease progression and treatment responses as well as potential therapies targeting the skin microbiome. Integrating precision treatments that restore microbial balance alongside more traditional therapies may improve outcomes by addressing both inflammation and epidermal barrier dysfunction. Additionally, strategies that support a healthy skin microbiome, such as microbiome-friendly skin care and topical probiotics, should be further explored to enhance long-term disease management. There remains a dearth of literature addressing how the skin microbiome of patients with rosacea can be optimized to maximize treatment, highlighting the need for more research into these interventions.

Rosacea is a chronic inflammatory skin condition affecting the central face—including the cheeks, nose, chin, and forehead—that causes considerable discomfort.¹ Its pathogenesis involves immune dysregulation, genetic predisposition, and microbial dysbiosis.² While immune and environmental factors are known triggers of rosacea, recent research highlights the roles of the gut and skin microbiomes in disease progression. While the skin microbiome interacts directly with the immune system to regulate inflammation and skin homeostasis, the gut microbiome also influences cutaneous inflammation, emphasizing the need to address both topical and internal microbiome imbalances.³ In this article, we review gut and skin microbial alterations in rosacea, focusing on the skin microbiome and including the gut-skin axis implications as well as therapeutic strategies aimed at microbiome balance to enhance patient outcomes.

Skin Microbiome Alterations in Rosacea

The human skin microbiome interacts with the immune system, and microbial imbalances have been shown to contribute to immune dysregulation. Several key microbial species have been identified as playing a large role in rosacea, including Demodex folliculorum, Staphylococcus epidermidis, Bacillus oleronius, and Cutibacterium acnes (Figure).

Demodex folliculorum is a microscopic mite is found in hair follicles and sebaceous glands. Patients with rosacea have higher densities of D folliculorum, which trigger follicular occlusion and immune activation.¹Bacillus oleronius be isolated from D folliculorum and can further activate toll-like receptor 2, leading to cytokine production and immune cell infiltration.^3,4 Increased propagation of this mite correlates with shifts in skin microbiome composition, demonstrating increased inflammatory microbial populations.³

Staphylococcus epidermidis normally is commensal but can become pathogenic (pathobiont) in rosacea due to disruptions in the skin microenvironment, where it can form biofilms and produce virulence factors, particularly in papulopustular rosacea.⁵

Bacillus oleronius has been isolated from D folliculorum mites and provokes inflammatory responses in patients with rosacea by triggering toll-like receptor 2 activation and cytokine secretion.⁶

Cutibacterium acnes commonly is associated with acne vulgaris. Its role in rosacea is unclear, but recent research suggests it may have a protective effect. A single-arm trial investigated the effects of minocycline on rosacea and found that treatment significantly reduced C acnes but increased microbial species diversity, improving inflammation.⁷ One longitudinal cohort study of 12 patients with rosacea found that C acnes levels were lower in those older than 60 years. Rosacea severity increased with age and correlated with a decline in C acnes, suggesting that it may confer some protective effect in rosacea.⁸ This finding is supported by studies that have shown a reduction in C acnes levels in patients with rosacea compared to controls.^4,8

Important mechanisms in rosacea include epidermal barrier dysfunction, transepidermal water loss, and decreased stratum corneum hydration, particularly in erythematotelangiectatic and papulopustular subtypes. The resulting alkaline skin pH contributes to barrier instability and heightened inflammation, permitting pathogenic bacteria to proliferate and disrupt skin microbial homeostasis.⁹ A recent study identified metabolic changes in the skin microbiome of patients with rosacea, showing that increased heme and hydrogen sulfide in rosacea skin microbiomes likely drive inflammation, while healthy skin microbiomes produce more anti-inflammatory adenosylcobalamin, thiazole, and L-isoleucine.¹ These findings highlight the link between microbial imbalances and inflammation in rosacea.

The Gut-Skin Axis in Rosacea

Gut microbiota play a critical role in managing systemic inflammation, and microbial dysbiosis in the intestine can influence the skin microbiome in rosacea. Patients with rosacea who have gastrointestinal conditions such as small intestinal bacterial overgrowth and Helicobacter pylori infection experience more severe rosacea symptoms.^3,10

Patients with rosacea have distinctive gut microbiota compositions, with an increased prevalence of proinflammatory bacterial species, potentially affecting the skin microbiome.^8,11 Systemic antibiotics have been shown to modulate the gut microbiome, indirectly influencing the skin microbiome.¹¹ A recent study demonstrated that doxycycline treatment in patients with rosacea altered skin microbial diversity, reducing C acnes while increasing Weissella confusa—highlighting the complicated relationship between systemic antibiotics and the gut-skin axis.⁸

Specific probiotics, such as Escherichia coli Nissle, when given orally shifted gut microbial balance to protective microbiota with increased Lactobacillus and Bifidobacteria species and decreased pathogenic bacteria. This improved rosacea symptoms, normalized immunoglobulin A levels, and suppressed cytokine interleukin 8 levels.¹⁰ Recent studies also suggest oral sarecycline, a narrow-spectrum antibiotic, may improve papulopustular rosacea symptoms through its anti-inflammatory effects while having minimal impact on gut microbiota diversity.^11,12

Gut-derived short-chain fatty acids, which are known to regulate immune function, also have been shown to influence the composition of skin microbiota, suggesting a direct link between gut dysbiosis and skin microbial imbalances. Notably, antibiotic and probiotic treatments targeting the gut microbiome (eg, rifaximin for small intestinal bacterial overgrowth) have been associated with improvements in rosacea symptoms, further underscoring the interconnectedness of the gut-skin axis.¹³ Understanding how gut-derived inflammation alters the skin microbiome may provide new therapeutic avenues for restoring microbial balance and reducing rosacea severity.

Immune Dysregulation and Inflammatory Pathways

Mechanisms of microbiome-driven inflammation via the innate immune system contribute to rosacea pathogenesis. Toll-like receptor 2 is upregulated in rosacea, producing increased peptides including cathelicidins.¹³ When abnormally processed, cathelicidins produce proinflammatory peptides and worsen rosacea symptoms such as erythema, telangiectasias, and neutrophilic infiltration by dysregulating the immune system and the skin barrier.⁶

Heightened levels of cytokines interleukin 8 and interferon α have been identified in patients with rosacea. These cytokines are involved in rosacea pathogenesis, including leukocyte recruitment, angiogenesis, and tissue remodeling and further activate the inflammatory cascade.^8,14

Mendelian randomization studies have provided confirmation of a causal link between skin microbiota alterations and inflammatory skin diseases including rosacea.² Specific alterations in bacteria such as Cutibacterium and Staphylococcus microbial species have been associated with shifts in host immune gene expression, potentially predisposing individuals to abnormal immune activation and inflammation.^2,8 These studies show the potential of leveraging precision medicine to design therapies that target pathways that improve microbial imbalances seen in rosacea.

Environmental and Lifestyle Factors Affecting the Skin Microbiome

Individuals with rosacea often have increased sensitivity to environmental and lifestyle stressors such as high temperatures, UV exposure, and sugar and alcohol consumption. These factors influence the composition of the skin microbiome and potentially contribute to rosacea development and disease exacerbation; therefore, trigger avoidance is an important way to manage rosacea.

High temperatures and UV exposure—Demodex activity increases in response to heat exposure and subsequently worsens rosacea symptoms, while exposure to UV radiation can change the composition of the skin microbiome by encouraging inflammatory responses such as oxidative stress reactions.⁴ This effect on the skin microbiome is driven partly by the increased presence of certain skin microbial species, such as S epidermidis, which secrete virulence factors at higher temperatures and further contribute to inflammation.^1,4

High-glycemic diet and alcohol consumption—High-glycemic diets and alcohol intake have been associated with gut dysbiosis and increased disease severity in rosacea. Processed foods and high sugar consumption can promote proinflammatory reactions that cause skin dysbiosis and exacerbate symptoms.¹⁵ Increased consumption of anti-inflammatory foods or consumption of probiotics and prebiotics can improve microbial balance.

Therapeutic Implications

The influence of the skin and gut microbiome on rosacea have been well described in the medical literature; therefore, many therapeutic strategies aim to address microbiome dysbiosis, including the use of antibiotics, anthelmintics, and a range of topical agents as well as probiotics, microbiome-friendly skin care products, and dietary modifications.

Antibiotics and Anthelmintics—Topical and oral antibiotics such as metronidazole and doxycycline reduce microbial load and inflammation.^5,7,8 Ivermectin, an anthelmintic, has demonstrated efficacy in decreasing Demodex colonization and associated inflammation by interfering with mite survival and reducing bacterial interactions on the skin.⁵ Recent literature also has explored next-generation antibiotics that disrupt biofilm production by bacteria, which could positively affect outcomes while safeguarding antibiotic stewardship.¹⁵ Given its targeted antimicrobial activity and low propensity for microbial resistance, sarecycline represents a promising therapeutic option for managing rosacea symptoms with reduced risk for microbiome-related adverse events.^12,16

Probiotics and Skin Care Interventions—Probiotics, prebiotics, and postbiotics have emerged as promising approaches to improve rosacea outcomes. Topical probiotics have been shown to maintain skin microbiome homeostasis, reduce inflammation, and enhance epidermal barrier function, making them a promising adjunctive therapy for rosacea.^17,18 Physiological pH cleansers and moisturizers formulated with microbiome-friendly ingredients may reduce transepidermal water loss and improve skin hydration, which are critical in microbial equilibrium.⁹ Oral administration of E coli Nissle, Lactobacillus, and Bifidobacterium have shown potential in improving microbial balance and reducing disease severity.¹⁰

Other Topical Therapies—Azelaic acid and benzoyl peroxide can improve rosacea symptoms by decreasing inflammation and also may shift the skin microbiome.^19,20 Formulations of topical therapies, including microencapsulated benzoyl peroxide, show improved efficacy in targeting pathogenic bacteria while maintaining tolerability.¹⁹

Dietary Modifications—Avoiding triggers such as alcohol and high-glycemic foods can help reduce gut and skin dysbiosis.¹³ Polyphenol-rich foods and prebiotic fiber may promote beneficial gut and skin microbial composition and currently are being studied.¹³

Emerging Therapies—Long-pulsed alexandrite laser therapy has been shown to reduce facial erythema and modulate skin microbiota.²¹ Patients with treatment-resistant rosacea may benefit from advanced precision targeted antimicrobials.

The future of rosacea treatment may involve integrating established and emerging microbiome-targeted treatment strategies to improve short- and long-term patient outcomes in rosacea.

Conclusion

As our understanding of rosacea, its pathogenesis, and the role of the skin microbiome continues to grow, so does our ability to develop increasingly effective and well-tolerated treatments. Future research should focus on how changes to the skin microbiome can influence disease progression and treatment responses as well as potential therapies targeting the skin microbiome. Integrating precision treatments that restore microbial balance alongside more traditional therapies may improve outcomes by addressing both inflammation and epidermal barrier dysfunction. Additionally, strategies that support a healthy skin microbiome, such as microbiome-friendly skin care and topical probiotics, should be further explored to enhance long-term disease management. There remains a dearth of literature addressing how the skin microbiome of patients with rosacea can be optimized to maximize treatment, highlighting the need for more research into these interventions.

Rosacea is a chronic inflammatory skin condition affecting the central face—including the cheeks, nose, chin, and forehead—that causes considerable discomfort.¹ Its pathogenesis involves immune dysregulation, genetic predisposition, and microbial dysbiosis.² While immune and environmental factors are known triggers of rosacea, recent research highlights the roles of the gut and skin microbiomes in disease progression. While the skin microbiome interacts directly with the immune system to regulate inflammation and skin homeostasis, the gut microbiome also influences cutaneous inflammation, emphasizing the need to address both topical and internal microbiome imbalances.³ In this article, we review gut and skin microbial alterations in rosacea, focusing on the skin microbiome and including the gut-skin axis implications as well as therapeutic strategies aimed at microbiome balance to enhance patient outcomes.

Skin Microbiome Alterations in Rosacea

The human skin microbiome interacts with the immune system, and microbial imbalances have been shown to contribute to immune dysregulation. Several key microbial species have been identified as playing a large role in rosacea, including Demodex folliculorum, Staphylococcus epidermidis, Bacillus oleronius, and Cutibacterium acnes (Figure).

Demodex folliculorum is a microscopic mite is found in hair follicles and sebaceous glands. Patients with rosacea have higher densities of D folliculorum, which trigger follicular occlusion and immune activation.¹Bacillus oleronius be isolated from D folliculorum and can further activate toll-like receptor 2, leading to cytokine production and immune cell infiltration.^3,4 Increased propagation of this mite correlates with shifts in skin microbiome composition, demonstrating increased inflammatory microbial populations.³

Staphylococcus epidermidis normally is commensal but can become pathogenic (pathobiont) in rosacea due to disruptions in the skin microenvironment, where it can form biofilms and produce virulence factors, particularly in papulopustular rosacea.⁵

Bacillus oleronius has been isolated from D folliculorum mites and provokes inflammatory responses in patients with rosacea by triggering toll-like receptor 2 activation and cytokine secretion.⁶

Cutibacterium acnes commonly is associated with acne vulgaris. Its role in rosacea is unclear, but recent research suggests it may have a protective effect. A single-arm trial investigated the effects of minocycline on rosacea and found that treatment significantly reduced C acnes but increased microbial species diversity, improving inflammation.⁷ One longitudinal cohort study of 12 patients with rosacea found that C acnes levels were lower in those older than 60 years. Rosacea severity increased with age and correlated with a decline in C acnes, suggesting that it may confer some protective effect in rosacea.⁸ This finding is supported by studies that have shown a reduction in C acnes levels in patients with rosacea compared to controls.^4,8

Important mechanisms in rosacea include epidermal barrier dysfunction, transepidermal water loss, and decreased stratum corneum hydration, particularly in erythematotelangiectatic and papulopustular subtypes. The resulting alkaline skin pH contributes to barrier instability and heightened inflammation, permitting pathogenic bacteria to proliferate and disrupt skin microbial homeostasis.⁹ A recent study identified metabolic changes in the skin microbiome of patients with rosacea, showing that increased heme and hydrogen sulfide in rosacea skin microbiomes likely drive inflammation, while healthy skin microbiomes produce more anti-inflammatory adenosylcobalamin, thiazole, and L-isoleucine.¹ These findings highlight the link between microbial imbalances and inflammation in rosacea.

The Gut-Skin Axis in Rosacea

Gut microbiota play a critical role in managing systemic inflammation, and microbial dysbiosis in the intestine can influence the skin microbiome in rosacea. Patients with rosacea who have gastrointestinal conditions such as small intestinal bacterial overgrowth and Helicobacter pylori infection experience more severe rosacea symptoms.^3,10

Patients with rosacea have distinctive gut microbiota compositions, with an increased prevalence of proinflammatory bacterial species, potentially affecting the skin microbiome.^8,11 Systemic antibiotics have been shown to modulate the gut microbiome, indirectly influencing the skin microbiome.¹¹ A recent study demonstrated that doxycycline treatment in patients with rosacea altered skin microbial diversity, reducing C acnes while increasing Weissella confusa—highlighting the complicated relationship between systemic antibiotics and the gut-skin axis.⁸

Specific probiotics, such as Escherichia coli Nissle, when given orally shifted gut microbial balance to protective microbiota with increased Lactobacillus and Bifidobacteria species and decreased pathogenic bacteria. This improved rosacea symptoms, normalized immunoglobulin A levels, and suppressed cytokine interleukin 8 levels.¹⁰ Recent studies also suggest oral sarecycline, a narrow-spectrum antibiotic, may improve papulopustular rosacea symptoms through its anti-inflammatory effects while having minimal impact on gut microbiota diversity.^11,12

Gut-derived short-chain fatty acids, which are known to regulate immune function, also have been shown to influence the composition of skin microbiota, suggesting a direct link between gut dysbiosis and skin microbial imbalances. Notably, antibiotic and probiotic treatments targeting the gut microbiome (eg, rifaximin for small intestinal bacterial overgrowth) have been associated with improvements in rosacea symptoms, further underscoring the interconnectedness of the gut-skin axis.¹³ Understanding how gut-derived inflammation alters the skin microbiome may provide new therapeutic avenues for restoring microbial balance and reducing rosacea severity.

Immune Dysregulation and Inflammatory Pathways

Mechanisms of microbiome-driven inflammation via the innate immune system contribute to rosacea pathogenesis. Toll-like receptor 2 is upregulated in rosacea, producing increased peptides including cathelicidins.¹³ When abnormally processed, cathelicidins produce proinflammatory peptides and worsen rosacea symptoms such as erythema, telangiectasias, and neutrophilic infiltration by dysregulating the immune system and the skin barrier.⁶

Heightened levels of cytokines interleukin 8 and interferon α have been identified in patients with rosacea. These cytokines are involved in rosacea pathogenesis, including leukocyte recruitment, angiogenesis, and tissue remodeling and further activate the inflammatory cascade.^8,14

Mendelian randomization studies have provided confirmation of a causal link between skin microbiota alterations and inflammatory skin diseases including rosacea.² Specific alterations in bacteria such as Cutibacterium and Staphylococcus microbial species have been associated with shifts in host immune gene expression, potentially predisposing individuals to abnormal immune activation and inflammation.^2,8 These studies show the potential of leveraging precision medicine to design therapies that target pathways that improve microbial imbalances seen in rosacea.

Environmental and Lifestyle Factors Affecting the Skin Microbiome

Individuals with rosacea often have increased sensitivity to environmental and lifestyle stressors such as high temperatures, UV exposure, and sugar and alcohol consumption. These factors influence the composition of the skin microbiome and potentially contribute to rosacea development and disease exacerbation; therefore, trigger avoidance is an important way to manage rosacea.

High temperatures and UV exposure—Demodex activity increases in response to heat exposure and subsequently worsens rosacea symptoms, while exposure to UV radiation can change the composition of the skin microbiome by encouraging inflammatory responses such as oxidative stress reactions.⁴ This effect on the skin microbiome is driven partly by the increased presence of certain skin microbial species, such as S epidermidis, which secrete virulence factors at higher temperatures and further contribute to inflammation.^1,4

High-glycemic diet and alcohol consumption—High-glycemic diets and alcohol intake have been associated with gut dysbiosis and increased disease severity in rosacea. Processed foods and high sugar consumption can promote proinflammatory reactions that cause skin dysbiosis and exacerbate symptoms.¹⁵ Increased consumption of anti-inflammatory foods or consumption of probiotics and prebiotics can improve microbial balance.

Therapeutic Implications

The influence of the skin and gut microbiome on rosacea have been well described in the medical literature; therefore, many therapeutic strategies aim to address microbiome dysbiosis, including the use of antibiotics, anthelmintics, and a range of topical agents as well as probiotics, microbiome-friendly skin care products, and dietary modifications.

Antibiotics and Anthelmintics—Topical and oral antibiotics such as metronidazole and doxycycline reduce microbial load and inflammation.^5,7,8 Ivermectin, an anthelmintic, has demonstrated efficacy in decreasing Demodex colonization and associated inflammation by interfering with mite survival and reducing bacterial interactions on the skin.⁵ Recent literature also has explored next-generation antibiotics that disrupt biofilm production by bacteria, which could positively affect outcomes while safeguarding antibiotic stewardship.¹⁵ Given its targeted antimicrobial activity and low propensity for microbial resistance, sarecycline represents a promising therapeutic option for managing rosacea symptoms with reduced risk for microbiome-related adverse events.^12,16

Probiotics and Skin Care Interventions—Probiotics, prebiotics, and postbiotics have emerged as promising approaches to improve rosacea outcomes. Topical probiotics have been shown to maintain skin microbiome homeostasis, reduce inflammation, and enhance epidermal barrier function, making them a promising adjunctive therapy for rosacea.^17,18 Physiological pH cleansers and moisturizers formulated with microbiome-friendly ingredients may reduce transepidermal water loss and improve skin hydration, which are critical in microbial equilibrium.⁹ Oral administration of E coli Nissle, Lactobacillus, and Bifidobacterium have shown potential in improving microbial balance and reducing disease severity.¹⁰

Other Topical Therapies—Azelaic acid and benzoyl peroxide can improve rosacea symptoms by decreasing inflammation and also may shift the skin microbiome.^19,20 Formulations of topical therapies, including microencapsulated benzoyl peroxide, show improved efficacy in targeting pathogenic bacteria while maintaining tolerability.¹⁹

Dietary Modifications—Avoiding triggers such as alcohol and high-glycemic foods can help reduce gut and skin dysbiosis.¹³ Polyphenol-rich foods and prebiotic fiber may promote beneficial gut and skin microbial composition and currently are being studied.¹³

Emerging Therapies—Long-pulsed alexandrite laser therapy has been shown to reduce facial erythema and modulate skin microbiota.²¹ Patients with treatment-resistant rosacea may benefit from advanced precision targeted antimicrobials.

The future of rosacea treatment may involve integrating established and emerging microbiome-targeted treatment strategies to improve short- and long-term patient outcomes in rosacea.

Conclusion

As our understanding of rosacea, its pathogenesis, and the role of the skin microbiome continues to grow, so does our ability to develop increasingly effective and well-tolerated treatments. Future research should focus on how changes to the skin microbiome can influence disease progression and treatment responses as well as potential therapies targeting the skin microbiome. Integrating precision treatments that restore microbial balance alongside more traditional therapies may improve outcomes by addressing both inflammation and epidermal barrier dysfunction. Additionally, strategies that support a healthy skin microbiome, such as microbiome-friendly skin care and topical probiotics, should be further explored to enhance long-term disease management. There remains a dearth of literature addressing how the skin microbiome of patients with rosacea can be optimized to maximize treatment, highlighting the need for more research into these interventions.

Patients often ask dermatologists how to best care for their specific hair type; however, there are no formal recommendations that apply to the many different hair care practices utilized by Black patients, as hair types in this community can range from wavy to tightly coiled.¹ Understanding the the history of hair care in those of African ancestry and various styling practices in this population is necessary to adequately counsel patients and gain trust in the doctor-patient relationship. In this article, we provide an overview of hair care recommendations based on common styling practices in Black women.

A PubMed search of articles indexed for MEDLINE using the terms Black hair care, African American hair management, hair loss prevention, hair care practices, natural hair, natural-hair styles, alopecia, hairdressing, hair breakage, hair fragility, heat-stressed hair, traction alopecia, and natural hair care yielded 305 results; 107 duplicates were identified and removed, leaving 198 articles to be screened for eligibility (ie, English-language studies created in the past 15 years). Sixty-eight full-text articles were screened against the exclusion criteria, which included case reports and case series, articles not focused on Afro-textured hair, and cancer-related hair loss. Three additional fulltext articles were identified via resources from Wayne State University library (Detroit, Michigan) that were not available on PubMed. A total of 29 full-text articles were included in our review.

Background on Hair Care and Styling in African Populations

It is difficult to understand the history of hair in those of African ancestry in the United States.² Prior to slavery, hair styling was considered a way of identification, classification, and communication as well as a medium through which to connect with the spiritual world in many parts of Africa. Hair-styling practices in Africa included elaborate cornrows, threading, and braiding with many accessories. Notable hair-styling products included natural butters, herbs, and powders to assist with moisture retention. Scarves also were used during this time for ceremonies or protection.³ During the mass enslavement of African populations and their transportation to the Americas by Europeans, slaveholders routinely cut off all the hair of both men and women in order to objectify and erase the culture of African hair styling passed down through generations.^4,5 Hair texture then was weaponized to create a caste system in plantation life, in which Black slaves with straight hair textures were granted the “privilege” of domestic work, while those with kinky hair were relegated to arduous manual labor in the fields.⁴ Years later, during the 1800s, laws were enacted in the United States to prohibit Black women from wearing tightly coiled natural hair in public places.⁵ Over the next few centuries from the 1800s to the early 2000s, various hair-styling trends such as the use of hot combs, perms, afros, and Jheri curls developed as a means for Black individuals to conform to societal pressure to adopt more European features; however, as time progressed, afros, braids, locs, and natural hair would become more dominant as statements against these same societal pressures.⁵

The natural hair movement, which emerged in the United States in the 2000s, encouraged Black women to abandon the use of toxic chemical hair straighteners, cultivate healthier hair care practices, disrupt Eurocentric standards of wearing straightened hair, and facilitate self-definition of beauty ideals from the Civil Rights Movement of the 1960s.^4,5 It is estimated that between 30% and 70% of all Black women in the United States wear natural hair, including 79% of millennial Black women younger than 30 years⁶; however, several new trends such as wigs and weaves have grown in popularity since the early 2000s due to mainstream pop culture and improvements in creating natural hairlines.^7,8

Key Features of Afro-Textured Hair

Individuals of African descent have the most diverse hair texture phenotypes, ranging from straight to tightly coiled.⁹ Although hair is chemically similar across various racial groups, differences are noted mainly in the shape of the hair shaft, with elliptical and curved shapes seen in Afrotextured hair. These differences yield more tightly curled strands than in other hair types; however, these features also contribute to fragility, as it creates points of weakness and decreases the tensile strength of the hair shaft.¹⁰ This inherent fragility leads to higher rates of hair breakage as well as lower moisture content and slower growth rates, which is why Afro-textured hair requires special care.⁹

Afro-textured hair generally falls into 2 main categories of the Andre Walker hair typing system: 4A-4C and 3A-3C.¹¹ In the 4A-4C category, hair is described as coily or kinky. Common concerns related to this hair type include dryness and brittleness with increased susceptibility to breakage. The 3A-3C category is described as loose to corkscrew curls, with a common concern of dryness.^11,12 Additionally, Loussouarn et al¹³ established a method to further define natural hair curliness using curve diameter and curl meters on glass plates to measure the curvature of hair strands. This method allows for assessing diversity and range of curliness within various races without relying on ethnic origin.¹³

Common Hair Care Practices

A description of each hair type and recommended styling practices with their levels of evidence can be found in the eTable.

Natural Hair—Natural hair is classified as hair that has not been chemically changed by perms, heat, or other straightening treatments.^12,14 For natural hair, retaining the moisture of the hair shaft should be the main focus, as moisture loss leads to considerable dryness.¹⁴ Generally, it is recommended to wash natural hair once per week or every other week; however, this can change based on hair length and oil production on the scalp. Washing daily may be ideal for shorter hair and monthly for longer hair to help prevent product build-up that can have a drying effect.¹⁵ Avoid shampoos that are drying (eg, sulfate and silicone products). The co-washing method also can be utilized, which entails washing the hair with a conditioning cleanser instead of shampoo and conditioner. However, this technique is not meant to completely replace shampoo.¹⁶ In fact, a clarifying shampoo is recommended after co-washing 3 or 4 times.¹⁶ The use of a hot oil treatment twice per month can promote moisture retention and reduce split-end formation.¹⁷ For maintenance between washes, many utilize the liquid, oil, cream (LOC) or liquid, cream, oil (LCO) methods, which describe regimens that utilize water, an oil of choice, and cream such as shea butter to lock in moisture.¹⁸ This method can be used as often as needed for dry hair.

Due to the susceptibility of Afro-textured hair to tangle and knot, using a wide-tooth comb, detangling brush, or detangling conditioners is a grade B recommendation for care (eTable). Though not widely documented in the literature, many of our patients have had anecdotal success detangling their hair simply by pulling hair strands apart by hand or “finger detangling” as well as using wide-tooth combs. Although both hair types are healthier in their natural states, kinky hair (type 4A-4C) is extremely fragile and more difficult to manage than less kinky hair (type 3A-3C).¹⁸

Special care is needed when detangling due to strands being weaker when wet.¹⁹ Detangling should be performed in a retrograde fashion. Deep conditioning can aid in moisture retention and should be performed weekly or biweekly.^17-20 Depending on the health of the hair, protein treatments can be considered on a monthly basis to help preserve the cuticle. Styling with braids, twists, or other protective styles can then be completed on an individual basis.

Thermal Straightening—A blowout involves straightening the hair after a wash with the use of a hair dryer.²¹ This common hair-styling method does not employ the use of chemicals beyond light hair oils and heat-protectant creams or sprays, typically resulting in a less kinky afro or semi-straight hair. Thermal straightening utilizes heat to temporarily straighten hair strands. Flat irons with heated metal plates then can be used after blow-drying the hair to fully straighten and smooth the strands. These processes combined commonly are known as a silk press.^21-22

For thermally straightened hair, it is recommended to either wrap the hair around the scalp to keep it flat or pin curl the hair and cover with a bonnet to sleep. Safe straightening techniques with the use of a flat iron include setting the temperature no higher than 175 °F or a low/medium setting while also limiting use to once per week if possible.²³ The number of passes of the flat iron also should be limited to 1 to 2 to reduce breakage. A heat-protectant cream or spray also can be applied to the hair before flat ironing to minimize damage. Applying heat protectant to the hair prior to styling will help minimize heat damage by distributing the heat along the hair fiber surface, avoiding water boiling in the hair shaft and the development of bubble hair leading to damage.²⁴

Chemical Straightening—Similar to how relaxers, perms, and Jheri curl treatments chemically modify hair texture using distinct chemicals yielding different curl patterns, the Brazilian blowout similarly straightens hair using a hair dryer and chemicals applied to hair strands after washing.^21-24 Relaxers utilize sodium or guanidine hydroxide for straightening, perms use ammonium thioglycolate for curling, and Jheri curl treatments employ thioglycolates or mercaptans for defined curls. However, these treatments generally are cautioned against due to potential hair damage and recent associations with uterine and breast cancer in Black women. Research has suggested that endocrine disrupters in these products, especially those marketed to Black women, contribute to hormone-related disease processes.^25,26 One study found higher concentrations of alkylphenols, the fragrance marker diethyl phthalate, and parabens in relaxers²⁷; however, more research is needed to determine specific chemicals associated with these cancers.

Braids and Locs—Braiding is a technique that involves interlocking 3 or more sections of hair that may or may not be fixated to the scalp like a cornrow,¹¹ and one can utilize extensions or natural hair depending on the desired outcome. Intended for long-term wear (ie, weeks to months), braids minimize breakage and reduce daily styling needs. Two popular styles—cornrows and individual braids—differ in preparation and weaving techniques. Cornrows are an Afro-centric style involving uniform, tightly woven braids that are close to the scalp, creating distinct patterns. Conversely, individual braids weave separate hair sections, offering diverse styling possibilities. Braiding practices should exclude hairline edges—often termed baby hairs—to prevent traction alopecia. Minimal use of edge gel, which helps to tame the vellus hairs at the frontotemporal scalp, as well as mindful weave volume, weight, and length are recommended to avert breakage. Braids that cause pain are too tight, can damage hair, and may cause traction alopecia.¹¹ Braids should not be worn for longer than 3 months at a time and require biweekly washing with diluted shampoo and conditioner. Proper drying by wringing the hair with a microfiber towel is essential to avoid frizz and mold formation.

Locs are a low-maintenance hairstyle considered permanent until cut.²⁸ This style involves twisting, palm rolling, or using tools such as crochet hooks to “lock” the hair. Regular maintenance with retwisting and cleaning is vital for loc health. Increased weight and tight twisting of locs can cause damage to the scalp and hair strands; however, locs are known to increase hair volume over time, often due to the accumulation of hairs that would otherwise have been shed in the telogen phase.²⁸

Wigs and Weaves—Wigs consist of synthetic or human hair that can be strapped to the head with an adjustable band or glued to the scalp depending on the desired style.²⁹ Wigs are removed daily, which allows for quick access to hair for cleansing and moisturizing. In contrast, weaves typically are sewn into the natural hair, which may make it difficult to reach the scalp for cleansing, leading to dryness and product build-up.²⁹ Notably, there is evidence of a relationship between long-term use of weaves and traction alopecia.³⁰

Wigs can have a fully synthetic hair line or lace hair line and can range from very affordable to expensive. When applied correctly, both styles offer an easy way to cover and protect the natural hair by reducing the amount of physical trauma related to daily hair styling. A lace-front wig contains a frontal thin mesh or lace that camouflages the natural frontal hairline.^29,30 A risk of lace-front wigs is that they can cause friction alopecia secondary to repeated use of adhesives and repeated friction against the hairline. Generally, wigs and weaves should be cared for as one would care for one’s own hair.

Hair Care in Black Children—Children’s hair care begins with washing the hair and scalp with shampoo, applying conditioner, and detangling as needed.³¹ After rinsing out the conditioner, a leave-in conditioner can assist with moisture retention and further detangling. The hair is then styled, either wet or dry. Recommendations for hair care practices in Black children include loose hairstyles that do not strain hair roots and nightly removal of root-securing accessories (eg, barrettes, elastic hairbeads). Frequent cornrow styling and friction on chemically straightened hair were identified by a survey as considerable traction alopecia risk factors.³² Thus, educating caregivers on appropriate hair-grooming practices for children is important.

Hair Protection—Proactive steps to reduce hair loss include wearing satin bonnets and/or using satin pillowcases while sleeping regardless of hairstyle. Although evidence is limited, it is thought that satin and silk allow the hair to retain its moisture and natural oils, preventing breakage and friction.^33,34 Frequent hair trimming every 2 to 4 months can reduce breakage when doing thermal treatments.^35,36 When prolonged or repetitive styles are used, it is encouraged to give the hair a break between styles to recover from the repeated stress. Wearing an intermittent updo or high bun—a hairstyle in which the hair is pulled upward—can prevent breakage by reducing heavy strain on the hair; however, it is important to avoid the use of rubber bands due to friction and risk for tangling of hair strands. Instead, the use of covered elastic ties and/or those without metal is preferred.¹¹ Alternatively, if a polished and neat appearance with slicked-back hair is desired, the practice of tautly pulling the hair is not recommended. Instead, use of an alcohol-free gel is suggested along with a satin scarf wrapped around the hairline to facilitate the setting of the hair in place.¹¹

A common practice to preserve curly hairstyles while sleeping is known as the pineapple method, which protects the hair and aids in preserving the freshness and style of the curls.³⁷ It consists of a loosely tied high ponytail at the top of the head allowing the curls to fall forward. This minimizes frizz and prevents the curls from forming knots.

Conclusion

Hair care recommendations in Black women can be complex due to a wide range of personal care preferences and styling techniques in this population. While evidence in the literature is limited, it still is important for dermatologists to be familiar with the different hair care practices utilized by Black women so they can effectively counsel patients and improve hair health. Knowledge of optimal hair care practices can aid in the prevention of common hair disorders that disproportionately affect this patient population, such as traction alopecia and trichorrhexis nodosa or breakage.

Patients often ask dermatologists how to best care for their specific hair type; however, there are no formal recommendations that apply to the many different hair care practices utilized by Black patients, as hair types in this community can range from wavy to tightly coiled.¹ Understanding the the history of hair care in those of African ancestry and various styling practices in this population is necessary to adequately counsel patients and gain trust in the doctor-patient relationship. In this article, we provide an overview of hair care recommendations based on common styling practices in Black women.

A PubMed search of articles indexed for MEDLINE using the terms Black hair care, African American hair management, hair loss prevention, hair care practices, natural hair, natural-hair styles, alopecia, hairdressing, hair breakage, hair fragility, heat-stressed hair, traction alopecia, and natural hair care yielded 305 results; 107 duplicates were identified and removed, leaving 198 articles to be screened for eligibility (ie, English-language studies created in the past 15 years). Sixty-eight full-text articles were screened against the exclusion criteria, which included case reports and case series, articles not focused on Afro-textured hair, and cancer-related hair loss. Three additional fulltext articles were identified via resources from Wayne State University library (Detroit, Michigan) that were not available on PubMed. A total of 29 full-text articles were included in our review.

Background on Hair Care and Styling in African Populations

It is difficult to understand the history of hair in those of African ancestry in the United States.² Prior to slavery, hair styling was considered a way of identification, classification, and communication as well as a medium through which to connect with the spiritual world in many parts of Africa. Hair-styling practices in Africa included elaborate cornrows, threading, and braiding with many accessories. Notable hair-styling products included natural butters, herbs, and powders to assist with moisture retention. Scarves also were used during this time for ceremonies or protection.³ During the mass enslavement of African populations and their transportation to the Americas by Europeans, slaveholders routinely cut off all the hair of both men and women in order to objectify and erase the culture of African hair styling passed down through generations.^4,5 Hair texture then was weaponized to create a caste system in plantation life, in which Black slaves with straight hair textures were granted the “privilege” of domestic work, while those with kinky hair were relegated to arduous manual labor in the fields.⁴ Years later, during the 1800s, laws were enacted in the United States to prohibit Black women from wearing tightly coiled natural hair in public places.⁵ Over the next few centuries from the 1800s to the early 2000s, various hair-styling trends such as the use of hot combs, perms, afros, and Jheri curls developed as a means for Black individuals to conform to societal pressure to adopt more European features; however, as time progressed, afros, braids, locs, and natural hair would become more dominant as statements against these same societal pressures.⁵

The natural hair movement, which emerged in the United States in the 2000s, encouraged Black women to abandon the use of toxic chemical hair straighteners, cultivate healthier hair care practices, disrupt Eurocentric standards of wearing straightened hair, and facilitate self-definition of beauty ideals from the Civil Rights Movement of the 1960s.^4,5 It is estimated that between 30% and 70% of all Black women in the United States wear natural hair, including 79% of millennial Black women younger than 30 years⁶; however, several new trends such as wigs and weaves have grown in popularity since the early 2000s due to mainstream pop culture and improvements in creating natural hairlines.^7,8

Key Features of Afro-Textured Hair

Individuals of African descent have the most diverse hair texture phenotypes, ranging from straight to tightly coiled.⁹ Although hair is chemically similar across various racial groups, differences are noted mainly in the shape of the hair shaft, with elliptical and curved shapes seen in Afrotextured hair. These differences yield more tightly curled strands than in other hair types; however, these features also contribute to fragility, as it creates points of weakness and decreases the tensile strength of the hair shaft.¹⁰ This inherent fragility leads to higher rates of hair breakage as well as lower moisture content and slower growth rates, which is why Afro-textured hair requires special care.⁹

Afro-textured hair generally falls into 2 main categories of the Andre Walker hair typing system: 4A-4C and 3A-3C.¹¹ In the 4A-4C category, hair is described as coily or kinky. Common concerns related to this hair type include dryness and brittleness with increased susceptibility to breakage. The 3A-3C category is described as loose to corkscrew curls, with a common concern of dryness.^11,12 Additionally, Loussouarn et al¹³ established a method to further define natural hair curliness using curve diameter and curl meters on glass plates to measure the curvature of hair strands. This method allows for assessing diversity and range of curliness within various races without relying on ethnic origin.¹³

Common Hair Care Practices

A description of each hair type and recommended styling practices with their levels of evidence can be found in the eTable.

Natural Hair—Natural hair is classified as hair that has not been chemically changed by perms, heat, or other straightening treatments.^12,14 For natural hair, retaining the moisture of the hair shaft should be the main focus, as moisture loss leads to considerable dryness.¹⁴ Generally, it is recommended to wash natural hair once per week or every other week; however, this can change based on hair length and oil production on the scalp. Washing daily may be ideal for shorter hair and monthly for longer hair to help prevent product build-up that can have a drying effect.¹⁵ Avoid shampoos that are drying (eg, sulfate and silicone products). The co-washing method also can be utilized, which entails washing the hair with a conditioning cleanser instead of shampoo and conditioner. However, this technique is not meant to completely replace shampoo.¹⁶ In fact, a clarifying shampoo is recommended after co-washing 3 or 4 times.¹⁶ The use of a hot oil treatment twice per month can promote moisture retention and reduce split-end formation.¹⁷ For maintenance between washes, many utilize the liquid, oil, cream (LOC) or liquid, cream, oil (LCO) methods, which describe regimens that utilize water, an oil of choice, and cream such as shea butter to lock in moisture.¹⁸ This method can be used as often as needed for dry hair.

Due to the susceptibility of Afro-textured hair to tangle and knot, using a wide-tooth comb, detangling brush, or detangling conditioners is a grade B recommendation for care (eTable). Though not widely documented in the literature, many of our patients have had anecdotal success detangling their hair simply by pulling hair strands apart by hand or “finger detangling” as well as using wide-tooth combs. Although both hair types are healthier in their natural states, kinky hair (type 4A-4C) is extremely fragile and more difficult to manage than less kinky hair (type 3A-3C).¹⁸

Special care is needed when detangling due to strands being weaker when wet.¹⁹ Detangling should be performed in a retrograde fashion. Deep conditioning can aid in moisture retention and should be performed weekly or biweekly.^17-20 Depending on the health of the hair, protein treatments can be considered on a monthly basis to help preserve the cuticle. Styling with braids, twists, or other protective styles can then be completed on an individual basis.

Thermal Straightening—A blowout involves straightening the hair after a wash with the use of a hair dryer.²¹ This common hair-styling method does not employ the use of chemicals beyond light hair oils and heat-protectant creams or sprays, typically resulting in a less kinky afro or semi-straight hair. Thermal straightening utilizes heat to temporarily straighten hair strands. Flat irons with heated metal plates then can be used after blow-drying the hair to fully straighten and smooth the strands. These processes combined commonly are known as a silk press.^21-22

For thermally straightened hair, it is recommended to either wrap the hair around the scalp to keep it flat or pin curl the hair and cover with a bonnet to sleep. Safe straightening techniques with the use of a flat iron include setting the temperature no higher than 175 °F or a low/medium setting while also limiting use to once per week if possible.²³ The number of passes of the flat iron also should be limited to 1 to 2 to reduce breakage. A heat-protectant cream or spray also can be applied to the hair before flat ironing to minimize damage. Applying heat protectant to the hair prior to styling will help minimize heat damage by distributing the heat along the hair fiber surface, avoiding water boiling in the hair shaft and the development of bubble hair leading to damage.²⁴

Chemical Straightening—Similar to how relaxers, perms, and Jheri curl treatments chemically modify hair texture using distinct chemicals yielding different curl patterns, the Brazilian blowout similarly straightens hair using a hair dryer and chemicals applied to hair strands after washing.^21-24 Relaxers utilize sodium or guanidine hydroxide for straightening, perms use ammonium thioglycolate for curling, and Jheri curl treatments employ thioglycolates or mercaptans for defined curls. However, these treatments generally are cautioned against due to potential hair damage and recent associations with uterine and breast cancer in Black women. Research has suggested that endocrine disrupters in these products, especially those marketed to Black women, contribute to hormone-related disease processes.^25,26 One study found higher concentrations of alkylphenols, the fragrance marker diethyl phthalate, and parabens in relaxers²⁷; however, more research is needed to determine specific chemicals associated with these cancers.

Braids and Locs—Braiding is a technique that involves interlocking 3 or more sections of hair that may or may not be fixated to the scalp like a cornrow,¹¹ and one can utilize extensions or natural hair depending on the desired outcome. Intended for long-term wear (ie, weeks to months), braids minimize breakage and reduce daily styling needs. Two popular styles—cornrows and individual braids—differ in preparation and weaving techniques. Cornrows are an Afro-centric style involving uniform, tightly woven braids that are close to the scalp, creating distinct patterns. Conversely, individual braids weave separate hair sections, offering diverse styling possibilities. Braiding practices should exclude hairline edges—often termed baby hairs—to prevent traction alopecia. Minimal use of edge gel, which helps to tame the vellus hairs at the frontotemporal scalp, as well as mindful weave volume, weight, and length are recommended to avert breakage. Braids that cause pain are too tight, can damage hair, and may cause traction alopecia.¹¹ Braids should not be worn for longer than 3 months at a time and require biweekly washing with diluted shampoo and conditioner. Proper drying by wringing the hair with a microfiber towel is essential to avoid frizz and mold formation.

Locs are a low-maintenance hairstyle considered permanent until cut.²⁸ This style involves twisting, palm rolling, or using tools such as crochet hooks to “lock” the hair. Regular maintenance with retwisting and cleaning is vital for loc health. Increased weight and tight twisting of locs can cause damage to the scalp and hair strands; however, locs are known to increase hair volume over time, often due to the accumulation of hairs that would otherwise have been shed in the telogen phase.²⁸

Wigs and Weaves—Wigs consist of synthetic or human hair that can be strapped to the head with an adjustable band or glued to the scalp depending on the desired style.²⁹ Wigs are removed daily, which allows for quick access to hair for cleansing and moisturizing. In contrast, weaves typically are sewn into the natural hair, which may make it difficult to reach the scalp for cleansing, leading to dryness and product build-up.²⁹ Notably, there is evidence of a relationship between long-term use of weaves and traction alopecia.³⁰

Wigs can have a fully synthetic hair line or lace hair line and can range from very affordable to expensive. When applied correctly, both styles offer an easy way to cover and protect the natural hair by reducing the amount of physical trauma related to daily hair styling. A lace-front wig contains a frontal thin mesh or lace that camouflages the natural frontal hairline.^29,30 A risk of lace-front wigs is that they can cause friction alopecia secondary to repeated use of adhesives and repeated friction against the hairline. Generally, wigs and weaves should be cared for as one would care for one’s own hair.

Hair Care in Black Children—Children’s hair care begins with washing the hair and scalp with shampoo, applying conditioner, and detangling as needed.³¹ After rinsing out the conditioner, a leave-in conditioner can assist with moisture retention and further detangling. The hair is then styled, either wet or dry. Recommendations for hair care practices in Black children include loose hairstyles that do not strain hair roots and nightly removal of root-securing accessories (eg, barrettes, elastic hairbeads). Frequent cornrow styling and friction on chemically straightened hair were identified by a survey as considerable traction alopecia risk factors.³² Thus, educating caregivers on appropriate hair-grooming practices for children is important.

Hair Protection—Proactive steps to reduce hair loss include wearing satin bonnets and/or using satin pillowcases while sleeping regardless of hairstyle. Although evidence is limited, it is thought that satin and silk allow the hair to retain its moisture and natural oils, preventing breakage and friction.^33,34 Frequent hair trimming every 2 to 4 months can reduce breakage when doing thermal treatments.^35,36 When prolonged or repetitive styles are used, it is encouraged to give the hair a break between styles to recover from the repeated stress. Wearing an intermittent updo or high bun—a hairstyle in which the hair is pulled upward—can prevent breakage by reducing heavy strain on the hair; however, it is important to avoid the use of rubber bands due to friction and risk for tangling of hair strands. Instead, the use of covered elastic ties and/or those without metal is preferred.¹¹ Alternatively, if a polished and neat appearance with slicked-back hair is desired, the practice of tautly pulling the hair is not recommended. Instead, use of an alcohol-free gel is suggested along with a satin scarf wrapped around the hairline to facilitate the setting of the hair in place.¹¹

A common practice to preserve curly hairstyles while sleeping is known as the pineapple method, which protects the hair and aids in preserving the freshness and style of the curls.³⁷ It consists of a loosely tied high ponytail at the top of the head allowing the curls to fall forward. This minimizes frizz and prevents the curls from forming knots.

Conclusion

Hair care recommendations in Black women can be complex due to a wide range of personal care preferences and styling techniques in this population. While evidence in the literature is limited, it still is important for dermatologists to be familiar with the different hair care practices utilized by Black women so they can effectively counsel patients and improve hair health. Knowledge of optimal hair care practices can aid in the prevention of common hair disorders that disproportionately affect this patient population, such as traction alopecia and trichorrhexis nodosa or breakage.

Patients often ask dermatologists how to best care for their specific hair type; however, there are no formal recommendations that apply to the many different hair care practices utilized by Black patients, as hair types in this community can range from wavy to tightly coiled.¹ Understanding the the history of hair care in those of African ancestry and various styling practices in this population is necessary to adequately counsel patients and gain trust in the doctor-patient relationship. In this article, we provide an overview of hair care recommendations based on common styling practices in Black women.

A PubMed search of articles indexed for MEDLINE using the terms Black hair care, African American hair management, hair loss prevention, hair care practices, natural hair, natural-hair styles, alopecia, hairdressing, hair breakage, hair fragility, heat-stressed hair, traction alopecia, and natural hair care yielded 305 results; 107 duplicates were identified and removed, leaving 198 articles to be screened for eligibility (ie, English-language studies created in the past 15 years). Sixty-eight full-text articles were screened against the exclusion criteria, which included case reports and case series, articles not focused on Afro-textured hair, and cancer-related hair loss. Three additional fulltext articles were identified via resources from Wayne State University library (Detroit, Michigan) that were not available on PubMed. A total of 29 full-text articles were included in our review.

Background on Hair Care and Styling in African Populations

It is difficult to understand the history of hair in those of African ancestry in the United States.² Prior to slavery, hair styling was considered a way of identification, classification, and communication as well as a medium through which to connect with the spiritual world in many parts of Africa. Hair-styling practices in Africa included elaborate cornrows, threading, and braiding with many accessories. Notable hair-styling products included natural butters, herbs, and powders to assist with moisture retention. Scarves also were used during this time for ceremonies or protection.³ During the mass enslavement of African populations and their transportation to the Americas by Europeans, slaveholders routinely cut off all the hair of both men and women in order to objectify and erase the culture of African hair styling passed down through generations.^4,5 Hair texture then was weaponized to create a caste system in plantation life, in which Black slaves with straight hair textures were granted the “privilege” of domestic work, while those with kinky hair were relegated to arduous manual labor in the fields.⁴ Years later, during the 1800s, laws were enacted in the United States to prohibit Black women from wearing tightly coiled natural hair in public places.⁵ Over the next few centuries from the 1800s to the early 2000s, various hair-styling trends such as the use of hot combs, perms, afros, and Jheri curls developed as a means for Black individuals to conform to societal pressure to adopt more European features; however, as time progressed, afros, braids, locs, and natural hair would become more dominant as statements against these same societal pressures.⁵

The natural hair movement, which emerged in the United States in the 2000s, encouraged Black women to abandon the use of toxic chemical hair straighteners, cultivate healthier hair care practices, disrupt Eurocentric standards of wearing straightened hair, and facilitate self-definition of beauty ideals from the Civil Rights Movement of the 1960s.^4,5 It is estimated that between 30% and 70% of all Black women in the United States wear natural hair, including 79% of millennial Black women younger than 30 years⁶; however, several new trends such as wigs and weaves have grown in popularity since the early 2000s due to mainstream pop culture and improvements in creating natural hairlines.^7,8

Key Features of Afro-Textured Hair

Individuals of African descent have the most diverse hair texture phenotypes, ranging from straight to tightly coiled.⁹ Although hair is chemically similar across various racial groups, differences are noted mainly in the shape of the hair shaft, with elliptical and curved shapes seen in Afrotextured hair. These differences yield more tightly curled strands than in other hair types; however, these features also contribute to fragility, as it creates points of weakness and decreases the tensile strength of the hair shaft.¹⁰ This inherent fragility leads to higher rates of hair breakage as well as lower moisture content and slower growth rates, which is why Afro-textured hair requires special care.⁹

Afro-textured hair generally falls into 2 main categories of the Andre Walker hair typing system: 4A-4C and 3A-3C.¹¹ In the 4A-4C category, hair is described as coily or kinky. Common concerns related to this hair type include dryness and brittleness with increased susceptibility to breakage. The 3A-3C category is described as loose to corkscrew curls, with a common concern of dryness.^11,12 Additionally, Loussouarn et al¹³ established a method to further define natural hair curliness using curve diameter and curl meters on glass plates to measure the curvature of hair strands. This method allows for assessing diversity and range of curliness within various races without relying on ethnic origin.¹³

Common Hair Care Practices

A description of each hair type and recommended styling practices with their levels of evidence can be found in the eTable.

Natural Hair—Natural hair is classified as hair that has not been chemically changed by perms, heat, or other straightening treatments.^12,14 For natural hair, retaining the moisture of the hair shaft should be the main focus, as moisture loss leads to considerable dryness.¹⁴ Generally, it is recommended to wash natural hair once per week or every other week; however, this can change based on hair length and oil production on the scalp. Washing daily may be ideal for shorter hair and monthly for longer hair to help prevent product build-up that can have a drying effect.¹⁵ Avoid shampoos that are drying (eg, sulfate and silicone products). The co-washing method also can be utilized, which entails washing the hair with a conditioning cleanser instead of shampoo and conditioner. However, this technique is not meant to completely replace shampoo.¹⁶ In fact, a clarifying shampoo is recommended after co-washing 3 or 4 times.¹⁶ The use of a hot oil treatment twice per month can promote moisture retention and reduce split-end formation.¹⁷ For maintenance between washes, many utilize the liquid, oil, cream (LOC) or liquid, cream, oil (LCO) methods, which describe regimens that utilize water, an oil of choice, and cream such as shea butter to lock in moisture.¹⁸ This method can be used as often as needed for dry hair.

Due to the susceptibility of Afro-textured hair to tangle and knot, using a wide-tooth comb, detangling brush, or detangling conditioners is a grade B recommendation for care (eTable). Though not widely documented in the literature, many of our patients have had anecdotal success detangling their hair simply by pulling hair strands apart by hand or “finger detangling” as well as using wide-tooth combs. Although both hair types are healthier in their natural states, kinky hair (type 4A-4C) is extremely fragile and more difficult to manage than less kinky hair (type 3A-3C).¹⁸

Special care is needed when detangling due to strands being weaker when wet.¹⁹ Detangling should be performed in a retrograde fashion. Deep conditioning can aid in moisture retention and should be performed weekly or biweekly.^17-20 Depending on the health of the hair, protein treatments can be considered on a monthly basis to help preserve the cuticle. Styling with braids, twists, or other protective styles can then be completed on an individual basis.

Thermal Straightening—A blowout involves straightening the hair after a wash with the use of a hair dryer.²¹ This common hair-styling method does not employ the use of chemicals beyond light hair oils and heat-protectant creams or sprays, typically resulting in a less kinky afro or semi-straight hair. Thermal straightening utilizes heat to temporarily straighten hair strands. Flat irons with heated metal plates then can be used after blow-drying the hair to fully straighten and smooth the strands. These processes combined commonly are known as a silk press.^21-22

For thermally straightened hair, it is recommended to either wrap the hair around the scalp to keep it flat or pin curl the hair and cover with a bonnet to sleep. Safe straightening techniques with the use of a flat iron include setting the temperature no higher than 175 °F or a low/medium setting while also limiting use to once per week if possible.²³ The number of passes of the flat iron also should be limited to 1 to 2 to reduce breakage. A heat-protectant cream or spray also can be applied to the hair before flat ironing to minimize damage. Applying heat protectant to the hair prior to styling will help minimize heat damage by distributing the heat along the hair fiber surface, avoiding water boiling in the hair shaft and the development of bubble hair leading to damage.²⁴

Chemical Straightening—Similar to how relaxers, perms, and Jheri curl treatments chemically modify hair texture using distinct chemicals yielding different curl patterns, the Brazilian blowout similarly straightens hair using a hair dryer and chemicals applied to hair strands after washing.^21-24 Relaxers utilize sodium or guanidine hydroxide for straightening, perms use ammonium thioglycolate for curling, and Jheri curl treatments employ thioglycolates or mercaptans for defined curls. However, these treatments generally are cautioned against due to potential hair damage and recent associations with uterine and breast cancer in Black women. Research has suggested that endocrine disrupters in these products, especially those marketed to Black women, contribute to hormone-related disease processes.^25,26 One study found higher concentrations of alkylphenols, the fragrance marker diethyl phthalate, and parabens in relaxers²⁷; however, more research is needed to determine specific chemicals associated with these cancers.

Braids and Locs—Braiding is a technique that involves interlocking 3 or more sections of hair that may or may not be fixated to the scalp like a cornrow,¹¹ and one can utilize extensions or natural hair depending on the desired outcome. Intended for long-term wear (ie, weeks to months), braids minimize breakage and reduce daily styling needs. Two popular styles—cornrows and individual braids—differ in preparation and weaving techniques. Cornrows are an Afro-centric style involving uniform, tightly woven braids that are close to the scalp, creating distinct patterns. Conversely, individual braids weave separate hair sections, offering diverse styling possibilities. Braiding practices should exclude hairline edges—often termed baby hairs—to prevent traction alopecia. Minimal use of edge gel, which helps to tame the vellus hairs at the frontotemporal scalp, as well as mindful weave volume, weight, and length are recommended to avert breakage. Braids that cause pain are too tight, can damage hair, and may cause traction alopecia.¹¹ Braids should not be worn for longer than 3 months at a time and require biweekly washing with diluted shampoo and conditioner. Proper drying by wringing the hair with a microfiber towel is essential to avoid frizz and mold formation.

Locs are a low-maintenance hairstyle considered permanent until cut.²⁸ This style involves twisting, palm rolling, or using tools such as crochet hooks to “lock” the hair. Regular maintenance with retwisting and cleaning is vital for loc health. Increased weight and tight twisting of locs can cause damage to the scalp and hair strands; however, locs are known to increase hair volume over time, often due to the accumulation of hairs that would otherwise have been shed in the telogen phase.²⁸

Wigs and Weaves—Wigs consist of synthetic or human hair that can be strapped to the head with an adjustable band or glued to the scalp depending on the desired style.²⁹ Wigs are removed daily, which allows for quick access to hair for cleansing and moisturizing. In contrast, weaves typically are sewn into the natural hair, which may make it difficult to reach the scalp for cleansing, leading to dryness and product build-up.²⁹ Notably, there is evidence of a relationship between long-term use of weaves and traction alopecia.³⁰

Wigs can have a fully synthetic hair line or lace hair line and can range from very affordable to expensive. When applied correctly, both styles offer an easy way to cover and protect the natural hair by reducing the amount of physical trauma related to daily hair styling. A lace-front wig contains a frontal thin mesh or lace that camouflages the natural frontal hairline.^29,30 A risk of lace-front wigs is that they can cause friction alopecia secondary to repeated use of adhesives and repeated friction against the hairline. Generally, wigs and weaves should be cared for as one would care for one’s own hair.

Hair Care in Black Children—Children’s hair care begins with washing the hair and scalp with shampoo, applying conditioner, and detangling as needed.³¹ After rinsing out the conditioner, a leave-in conditioner can assist with moisture retention and further detangling. The hair is then styled, either wet or dry. Recommendations for hair care practices in Black children include loose hairstyles that do not strain hair roots and nightly removal of root-securing accessories (eg, barrettes, elastic hairbeads). Frequent cornrow styling and friction on chemically straightened hair were identified by a survey as considerable traction alopecia risk factors.³² Thus, educating caregivers on appropriate hair-grooming practices for children is important.

Hair Protection—Proactive steps to reduce hair loss include wearing satin bonnets and/or using satin pillowcases while sleeping regardless of hairstyle. Although evidence is limited, it is thought that satin and silk allow the hair to retain its moisture and natural oils, preventing breakage and friction.^33,34 Frequent hair trimming every 2 to 4 months can reduce breakage when doing thermal treatments.^35,36 When prolonged or repetitive styles are used, it is encouraged to give the hair a break between styles to recover from the repeated stress. Wearing an intermittent updo or high bun—a hairstyle in which the hair is pulled upward—can prevent breakage by reducing heavy strain on the hair; however, it is important to avoid the use of rubber bands due to friction and risk for tangling of hair strands. Instead, the use of covered elastic ties and/or those without metal is preferred.¹¹ Alternatively, if a polished and neat appearance with slicked-back hair is desired, the practice of tautly pulling the hair is not recommended. Instead, use of an alcohol-free gel is suggested along with a satin scarf wrapped around the hairline to facilitate the setting of the hair in place.¹¹

A common practice to preserve curly hairstyles while sleeping is known as the pineapple method, which protects the hair and aids in preserving the freshness and style of the curls.³⁷ It consists of a loosely tied high ponytail at the top of the head allowing the curls to fall forward. This minimizes frizz and prevents the curls from forming knots.

Conclusion

Hair care recommendations in Black women can be complex due to a wide range of personal care preferences and styling techniques in this population. While evidence in the literature is limited, it still is important for dermatologists to be familiar with the different hair care practices utilized by Black women so they can effectively counsel patients and improve hair health. Knowledge of optimal hair care practices can aid in the prevention of common hair disorders that disproportionately affect this patient population, such as traction alopecia and trichorrhexis nodosa or breakage.

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones (Figure).^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided. 

EPIDEMIOLOGY 

The incidence of SKs increases with age.3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹ 

KEY CLINICAL FEATURES 

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules. 2 Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters. ^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4 

WORTH NOTING 

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸ 

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.4 The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶ 

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions. 4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰ 

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigatorblinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P =.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful. 

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹ 

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹² 

HEALTH DISPARITY HIGHLIGHT 

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address— and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden. 

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones (Figure).^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided. 

EPIDEMIOLOGY 

The incidence of SKs increases with age.3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹ 

KEY CLINICAL FEATURES 

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules. 2 Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters. ^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4 

WORTH NOTING 

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸ 

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.4 The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶ 

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions. 4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰ 

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigatorblinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P =.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful. 

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹ 

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹² 

HEALTH DISPARITY HIGHLIGHT 

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address— and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden. 

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones (Figure).^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided. 

EPIDEMIOLOGY 

The incidence of SKs increases with age.3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹ 

KEY CLINICAL FEATURES 

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules. 2 Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters. ^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4 

WORTH NOTING 

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸ 

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.4 The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶ 

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions. 4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰ 

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigatorblinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P =.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful. 

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹ 

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹² 

HEALTH DISPARITY HIGHLIGHT 

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address— and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden. 

Prurigo nodularis (PN) is a chronic inflammatory skin condition characterized by firm hyperkeratotic nodules that develops when patients persistently scratch or rub intensely itchy areas of the skin. This potent itch-scratch cycle can be traced back to a dysfunctional interplay between cutaneous nerve fibers and the local immune environment.^1-3 Pruritis lasting at least 6 weeks is a hallmark symptom of PN and can be accompanied by pain and/or a burning sensation.⁴ The lesions are symmetrically distributed in areas that are easy to scratch (eg, arms, legs, trunk), typically sparing the face, palms, and soles; however, facial lesions have been reported in pediatric patients with PN, who also are more likely to have back, hand, and foot involvement.^5,6

PN can greatly affect patients’ quality of life, leading to increased rates of depression and anxiety.^7-9 Patients with severe symptoms also report increased sleep disturbance, distraction from work, selfconsciousness leading to social isolation, and missed days of work/school.⁹ In one study, patients with PN reported missing at least 1 day of work, school, training, or learning; giving up a leisure activity or sport; or refusing an invitation to dinner or a party in the past 3 months due to the disease.¹⁰

Epidemiology

PN has a prevalence of 72 per 100,000 individuals in the United States, most commonly affecting adults aged 51 to 65 years and disproportionately affecting African American and female patients.^11-13 Most patients with PN experience a 2-year delay in diagnosis after initial onset of symptoms. ¹⁰ Adults with PN have an increased likelihood of having other dermatologic conditions, including atopic dermatitis (AD) and psoriasis.¹¹ Nearly two-thirds of pediatric patients with PN present with AD, and those with AD showed more resistance to first-line treatment options.⁵

Key Clinical Features

Compared to White patients, who typically present with lesions that appear erythematous or pink, patients with darker skin tones may present with hyperpigmented nodules that are larger and darker.¹² The pruritic nodules often show signs of scratching or picking (eg, excoriations, lichenification, and angulated erosions).⁴

Worth Noting

Diagnosis of PN is made clinically, but skin biopsy may be helpful to rule out alternative diseases. Histologically, the hairy palm sign may be present in addition to other histologic features commonly associated with excessive scratching or rubbing of the skin.

Patients with PN have a high risk for HIV, which is not surprising considering HIV is a known systemic cause of generalized chronic pruritus. Other associations include type 2 diabetes mellitus and thyroid, kidney, and liver disease. ^11,13 Workup for patients with PN should include a complete blood count with differential; liver and renal function testing; and testing for C-reactive protein, thyroid-stimulating hormone, and lactate dehydrogenase.^4,14 Hemoglobin A1c and HIV testing as well as a hepatitis panel should be considered when appropriate. Because generalized pruritus may be a sign of malignancy, chest radiography and lymph node and abdominal ultrasonography should be performed in patients who have experienced itch for less than 1 year along with B symptoms (fever, night sweats, ≥ 10% weight loss over 6 months, fatigue).¹⁴ Frequent scratching can disrupt the skin barrier, contributing to the increased risk for skin infections.¹³ All patients with a suspected PN diagnosis also should undergo screening for depression and anxiety, as patients with PN are at an increased risk for these conditions.⁴

Treatment of PN starts with breaking the itch-scratch cycle by addressing the underlying cause of the pruritus. Therapies are focused on addressing the immunologic and neural components of the disease. Topical treatments include moderate to strong corticosteroids, calcineurin inhibitors (tacrolimus or pimecrolimus), capsaicin, and antipruritic emollients. Systemic agents include phototherapy (narrow-band UVB or excimer laser), gabapentin, pregabalin, paroxetine, and amitriptyline to address the neural component of itch. Methotrexate or cyclosporine can be used to address the immunologic component of PN and diminish the itch. That said, methotrexate and cyclosporine often are inadequate to control pruritus. ¹⁰ Of note, sedating antihistamines are not effective in treating itch in PN but can be used as an adjuvant therapy for sleep disturbances in these patients.¹⁵

The only drugs currently approved by the US Food and Drug Administration to treat PN are the biologics dupilumab (targeting the IL-4 receptor) approved in 2022 and nemolizumab (targeting the IL-31 receptor) approved in 2024.^16-18 The evidence that these injectable biologics work is heartening in a condition that has historically been very challenging to treat.^16,18 It should be noted that the high cost of these 2 medications can restrict access to care for patients who are uninsured or underinsured.

Resolution of a prurigo nodule may result in a hyperpigmented macule taking months to years to fade.

Health Disparity Highlight

Patients with PN have a considerable comorbidity burden, negative impact on quality of life, and increased health care utilization rates.¹² PN is 3.4 times more common in Black patients than White patients.¹³ Black patients with PN have increased mortality, higher health care utilization rates, and increased systemic inflammation compared to White patients.^12,19,20

Prurigo nodularis (PN) is a chronic inflammatory skin condition characterized by firm hyperkeratotic nodules that develops when patients persistently scratch or rub intensely itchy areas of the skin. This potent itch-scratch cycle can be traced back to a dysfunctional interplay between cutaneous nerve fibers and the local immune environment.^1-3 Pruritis lasting at least 6 weeks is a hallmark symptom of PN and can be accompanied by pain and/or a burning sensation.⁴ The lesions are symmetrically distributed in areas that are easy to scratch (eg, arms, legs, trunk), typically sparing the face, palms, and soles; however, facial lesions have been reported in pediatric patients with PN, who also are more likely to have back, hand, and foot involvement.^5,6

PN can greatly affect patients’ quality of life, leading to increased rates of depression and anxiety.^7-9 Patients with severe symptoms also report increased sleep disturbance, distraction from work, selfconsciousness leading to social isolation, and missed days of work/school.⁹ In one study, patients with PN reported missing at least 1 day of work, school, training, or learning; giving up a leisure activity or sport; or refusing an invitation to dinner or a party in the past 3 months due to the disease.¹⁰

Epidemiology

PN has a prevalence of 72 per 100,000 individuals in the United States, most commonly affecting adults aged 51 to 65 years and disproportionately affecting African American and female patients.^11-13 Most patients with PN experience a 2-year delay in diagnosis after initial onset of symptoms. ¹⁰ Adults with PN have an increased likelihood of having other dermatologic conditions, including atopic dermatitis (AD) and psoriasis.¹¹ Nearly two-thirds of pediatric patients with PN present with AD, and those with AD showed more resistance to first-line treatment options.⁵

Key Clinical Features

Compared to White patients, who typically present with lesions that appear erythematous or pink, patients with darker skin tones may present with hyperpigmented nodules that are larger and darker.¹² The pruritic nodules often show signs of scratching or picking (eg, excoriations, lichenification, and angulated erosions).⁴

Worth Noting

Diagnosis of PN is made clinically, but skin biopsy may be helpful to rule out alternative diseases. Histologically, the hairy palm sign may be present in addition to other histologic features commonly associated with excessive scratching or rubbing of the skin.

Patients with PN have a high risk for HIV, which is not surprising considering HIV is a known systemic cause of generalized chronic pruritus. Other associations include type 2 diabetes mellitus and thyroid, kidney, and liver disease. ^11,13 Workup for patients with PN should include a complete blood count with differential; liver and renal function testing; and testing for C-reactive protein, thyroid-stimulating hormone, and lactate dehydrogenase.^4,14 Hemoglobin A1c and HIV testing as well as a hepatitis panel should be considered when appropriate. Because generalized pruritus may be a sign of malignancy, chest radiography and lymph node and abdominal ultrasonography should be performed in patients who have experienced itch for less than 1 year along with B symptoms (fever, night sweats, ≥ 10% weight loss over 6 months, fatigue).¹⁴ Frequent scratching can disrupt the skin barrier, contributing to the increased risk for skin infections.¹³ All patients with a suspected PN diagnosis also should undergo screening for depression and anxiety, as patients with PN are at an increased risk for these conditions.⁴

Treatment of PN starts with breaking the itch-scratch cycle by addressing the underlying cause of the pruritus. Therapies are focused on addressing the immunologic and neural components of the disease. Topical treatments include moderate to strong corticosteroids, calcineurin inhibitors (tacrolimus or pimecrolimus), capsaicin, and antipruritic emollients. Systemic agents include phototherapy (narrow-band UVB or excimer laser), gabapentin, pregabalin, paroxetine, and amitriptyline to address the neural component of itch. Methotrexate or cyclosporine can be used to address the immunologic component of PN and diminish the itch. That said, methotrexate and cyclosporine often are inadequate to control pruritus. ¹⁰ Of note, sedating antihistamines are not effective in treating itch in PN but can be used as an adjuvant therapy for sleep disturbances in these patients.¹⁵

The only drugs currently approved by the US Food and Drug Administration to treat PN are the biologics dupilumab (targeting the IL-4 receptor) approved in 2022 and nemolizumab (targeting the IL-31 receptor) approved in 2024.^16-18 The evidence that these injectable biologics work is heartening in a condition that has historically been very challenging to treat.^16,18 It should be noted that the high cost of these 2 medications can restrict access to care for patients who are uninsured or underinsured.

Resolution of a prurigo nodule may result in a hyperpigmented macule taking months to years to fade.

Health Disparity Highlight

Patients with PN have a considerable comorbidity burden, negative impact on quality of life, and increased health care utilization rates.¹² PN is 3.4 times more common in Black patients than White patients.¹³ Black patients with PN have increased mortality, higher health care utilization rates, and increased systemic inflammation compared to White patients.^12,19,20

Prurigo nodularis (PN) is a chronic inflammatory skin condition characterized by firm hyperkeratotic nodules that develops when patients persistently scratch or rub intensely itchy areas of the skin. This potent itch-scratch cycle can be traced back to a dysfunctional interplay between cutaneous nerve fibers and the local immune environment.^1-3 Pruritis lasting at least 6 weeks is a hallmark symptom of PN and can be accompanied by pain and/or a burning sensation.⁴ The lesions are symmetrically distributed in areas that are easy to scratch (eg, arms, legs, trunk), typically sparing the face, palms, and soles; however, facial lesions have been reported in pediatric patients with PN, who also are more likely to have back, hand, and foot involvement.^5,6

PN can greatly affect patients’ quality of life, leading to increased rates of depression and anxiety.^7-9 Patients with severe symptoms also report increased sleep disturbance, distraction from work, selfconsciousness leading to social isolation, and missed days of work/school.⁹ In one study, patients with PN reported missing at least 1 day of work, school, training, or learning; giving up a leisure activity or sport; or refusing an invitation to dinner or a party in the past 3 months due to the disease.¹⁰

Epidemiology

PN has a prevalence of 72 per 100,000 individuals in the United States, most commonly affecting adults aged 51 to 65 years and disproportionately affecting African American and female patients.^11-13 Most patients with PN experience a 2-year delay in diagnosis after initial onset of symptoms. ¹⁰ Adults with PN have an increased likelihood of having other dermatologic conditions, including atopic dermatitis (AD) and psoriasis.¹¹ Nearly two-thirds of pediatric patients with PN present with AD, and those with AD showed more resistance to first-line treatment options.⁵

Key Clinical Features

Compared to White patients, who typically present with lesions that appear erythematous or pink, patients with darker skin tones may present with hyperpigmented nodules that are larger and darker.¹² The pruritic nodules often show signs of scratching or picking (eg, excoriations, lichenification, and angulated erosions).⁴

Worth Noting

Diagnosis of PN is made clinically, but skin biopsy may be helpful to rule out alternative diseases. Histologically, the hairy palm sign may be present in addition to other histologic features commonly associated with excessive scratching or rubbing of the skin.

Patients with PN have a high risk for HIV, which is not surprising considering HIV is a known systemic cause of generalized chronic pruritus. Other associations include type 2 diabetes mellitus and thyroid, kidney, and liver disease. ^11,13 Workup for patients with PN should include a complete blood count with differential; liver and renal function testing; and testing for C-reactive protein, thyroid-stimulating hormone, and lactate dehydrogenase.^4,14 Hemoglobin A1c and HIV testing as well as a hepatitis panel should be considered when appropriate. Because generalized pruritus may be a sign of malignancy, chest radiography and lymph node and abdominal ultrasonography should be performed in patients who have experienced itch for less than 1 year along with B symptoms (fever, night sweats, ≥ 10% weight loss over 6 months, fatigue).¹⁴ Frequent scratching can disrupt the skin barrier, contributing to the increased risk for skin infections.¹³ All patients with a suspected PN diagnosis also should undergo screening for depression and anxiety, as patients with PN are at an increased risk for these conditions.⁴

Treatment of PN starts with breaking the itch-scratch cycle by addressing the underlying cause of the pruritus. Therapies are focused on addressing the immunologic and neural components of the disease. Topical treatments include moderate to strong corticosteroids, calcineurin inhibitors (tacrolimus or pimecrolimus), capsaicin, and antipruritic emollients. Systemic agents include phototherapy (narrow-band UVB or excimer laser), gabapentin, pregabalin, paroxetine, and amitriptyline to address the neural component of itch. Methotrexate or cyclosporine can be used to address the immunologic component of PN and diminish the itch. That said, methotrexate and cyclosporine often are inadequate to control pruritus. ¹⁰ Of note, sedating antihistamines are not effective in treating itch in PN but can be used as an adjuvant therapy for sleep disturbances in these patients.¹⁵

The only drugs currently approved by the US Food and Drug Administration to treat PN are the biologics dupilumab (targeting the IL-4 receptor) approved in 2022 and nemolizumab (targeting the IL-31 receptor) approved in 2024.^16-18 The evidence that these injectable biologics work is heartening in a condition that has historically been very challenging to treat.^16,18 It should be noted that the high cost of these 2 medications can restrict access to care for patients who are uninsured or underinsured.

Resolution of a prurigo nodule may result in a hyperpigmented macule taking months to years to fade.

Health Disparity Highlight

Patients with PN have a considerable comorbidity burden, negative impact on quality of life, and increased health care utilization rates.¹² PN is 3.4 times more common in Black patients than White patients.¹³ Black patients with PN have increased mortality, higher health care utilization rates, and increased systemic inflammation compared to White patients.^12,19,20

Hidradenitis suppurativa (HS) is a debilitating dermatologic condition characterized by recurrent episodes of neutrophilic inflammation affecting the apocrine and pilosebaceous units that most commonly affects individuals aged 20 to 40 years. Originating from the hair follicles, inflammation initiates the formation of painful nodules and abscesses that can progress to sinus tracts or fistulas accompanied by the development of extensive scarring, exquisite pain, and malodorous drainage.¹ The lesions most commonly occur in intertriginous zones as well as areas rich in apocrine glands. The distinctive and sometimes irreversible clinical features of HS profoundly influence patients’ well-being and have lasting social, personal, and emotional impacts on their lives.²

Bimekizumab is a monoclonal antibody that specifically targets IL-17A and IL-17F, aiming to inhibit the downstream effects responsible for the chronic inflammation and tissue damage characteristic of HS.³ In HS lesions, IL-17 cytokines produced by T helper 17 (Th17) cells stimulate the production of chemokines (such as CC motif chemokine ligand 20) and neutrophil-attracting chemokines (including C-X-C motif chemokine ligands 1 and 8), cytokines (such as granulocyte colony-stimulating factor and IL-19), and epidermal antimicrobial proteins.^1,2 This cascade results in the chemotaxis of monocytes and neutrophils in the skin, recruiting additional Th17 and myeloid cells and further amplifying IL-17 production.¹

Bimekizumab’s mechanism of action strategically disrupts this feed-forward inflammatory loop, decreasing the transcription of neutrophil-attracting chemokines, IL-19, and epidermal antimicrobial proteins (Figure).^1,2 This leads to diminished recruitment of Th17 cells and inhibits the chemotaxis of monocytes and neutrophils in the skin, effectively addressing the chronic inflammation and tissue damage characteristic of HS.

We present a comprehensive review of the current standards of care, the underlying molecular pathophysiology of HS, and evaluation of the efficacy and safety of bimekizumab.

Evaluating HS Severity

The Hurley staging system provides a valuable framework for evaluating the severity of HS based on lesion characteristics. Stage I is characterized by abscess formation without tracts or scars. Stage II is characterized by recurrent abscesses with sinus tracts and scarring. Stage III is characterized by diffuse involvement, multiple interconnected sinus tracts, and abscesses across an entire area, leaving little to no uninvolved skin.⁴

Treatment strategies for HS vary based on Hurley staging (eTable).^5-11 For mild cases (stage I), topical and intralesional therapies are common, while moderate to severe cases (stages II and III) may require extensive surgical approaches or systemic drugs such as antibiotics, hormonal therapies, retinoids, or immunosuppressive/biologic agents.²

Adalimumab, an anti–tumor necrosis factor (TNF) α monoclonal antibody, was the first US Food and Drug Administration (FDA)–approved biologic for HS. Secukinumab, a monoclonal antibody against IL-17A, subsequently was approved by the FDA for moderate to severe HS.¹² Off-label use of biologics including infliximab and ustekinumab expands the available treatment options for HS. In one Phase II randomized clinical trial (RCT), infliximab showed efficacy in reducing Hidradenitis Suppurativa Severity Index scores, with 26.7% (4/15) of patients achieving a 50% or greater reduction compared to placebo, although this was not statistically significant. Similarly, ustekinumab demonstrated promising results, with 47.1% (8/17) of patients achieving Hidradenitis Suppurativa Clinical Response (HiSCR) at week 40.² This multifaceted approach aims to address the varying degrees of severity and optimize outcomes for individuals with HS.

Molecular Pathophysiology of HS

The pathogenesis of HS is multifactorial, involving a complex interplay of genetic, environmental, and behavioral factors.² Approximately 33% to 40% of patients with HS worldwide report a first-degree relative with the condition, indicating a hereditary element with an autosomal-dominant transmission pattern and highlighting the global relevance of genetic factors in HS.⁴ Hidradenitis suppurativa is highly prevalent in individuals with obesity, likely due to increased intertriginous surface area, skin friction, sweat production, and hormonal changes in these patients. Smoking also commonly is associated with HS, with nicotine potentially contributing to increased follicular plugging.¹ Hormonal influences also play a role, as evidenced by a greater prevalence of HS in females, disease onset typically occurring between puberty and menopause, and symptomatic fluctuations correlating with menstrual cycles and exogenous hormones.⁴

Altered infundibular keratinization with subsequent hyperkeratosis/occlusion and innate immune pathway activation are key events leading to development of HS.¹ These events are mediated by release of pathogen- and danger-associated molecular patterns, leading to inflammasome-mediated IL-1α release, followed by downstream cytokine release.² Elevated levels of TNF-α, IL-1Β, IL-10, IL-17, and particularly IL-17A have been detected in HS lesional skin. The IL-17 family comprises multiple members, namely IL-17A, IL-17C, IL-17E, and IL17F. IL-17A and IL-17F often are co-expressed and secreted predominantly by a subset of CD4+ T helper cells, namely Th17 cells.² IL-17 cytokines exert pro-inflammatory effects, influencing immune cell activity and contributing to skin inflammation, particularly in HS.

Given the pivotal role of IL-17 in the pathogenesis of HS, the exploration of IL-17–targeted agents has become a focal point in clinical research. Bimekizumab, a novel IL-17 inhibitor, has emerged as a promising candidate, offering a potential breakthrough in the treatment landscape for individuals affected by HS.

Bimekizumab for HS Management

A phase II, double-blind, placebo-controlled RCT included 90 patients with moderate to severe HS (age range, 18-70 years) who were randomly assigned in a 2:1:1 ratio to receive either bimekizumab 320 mg every 2 weeks (with a 640-mg loading dose at baseline)(n=46), placebo (n=21), or adalimumab 40 mg once weekly from week 4 onward (following an initial 160-mg loading dose at baseline and 80-mg dose at week 2)(n=21). The study included a 12-week treatment period followed by a 20-week safety follow-up period. The primary endpoint was the achievement of HiSCR₅₀—defined as a reduction of at least 50% nodules, coupled with no increase in the number of abscesses or draining fistulas relative to baseline—at week 12. Additionally, the study assessed the number of patients who achieved a modified HiSCR with 75% reduction (HiSCR₇₅) of combined abscess and inflammatory nodule count or a modified HiSCR with 90% reduction (HiSCR₉₀). At week 12, the modeled response rates were estimated using a Bayesian logistic regression model. For HiSCR₅₀, the modeled rate for bimekizumab was 57.3%, with an observed rate of 62.5% (25/40), compared to a modeled rate of 26.1% for placebo (observed rate, 27.8% [5/18]). The posterior probability of superiority for bimekizumab over placebo was 0.998. By week 12, bimekizumab-treated patients achieved modeled HiSCR₇₅ and HiSCR₉₀ rates of 46.0% and 32.0%, respectively, with observed rates of 50.0% (20/40) for HiSCR₇₅ and 35.0% (14/40) for HiSCR₉₀. In comparison, placebo-treated patients achieved modeled HiSCR75 and HiSCR₉₀ rates of 10.0% and 0%, respectively, with observed rates of 11.1% (2/18) for HiSCR₇₅ and 0% (0/18) for HiSCR₉₀. Adalimumab-treated participants demonstrated intermediate results, achieving modeled HiSCR₇₅ and HiSCR₉₀ rates of 35.0% and 15.0%, respectively, with observed rates of 38.88% (7/18) for HiSCR₇₅ and 16.66% (3/18) for HiSCR₉₀.⁷

Bimekizumab was effective in the treatment of moderate to severe HS with comparable results to adalimumab.⁷ The incidence of treatment-emergent adverse events was similar across treatment arms (bimekizumab, 69.6% [32/46]; placebo, 61.9% [13/21]; adalimumab, 71.4% [15/21]). The most common treatment-emergent adverse events in the biologic treatment arms were infections (43.5% [20/46] in the bimekizumab group and 42.9% [9/21] in the adalimumab group), skin and subcutaneous tissue disorders (28.3% [13/46] in the bimekizumab group and 42.9% [9/21] in the adalimumab group), and general disorders/administration site conditions (21.7% [10/46] in the bimekizumab group and 23.8% [5/21] in the adalimumab group). Serious adverse events occurred in 4.3% (2/46) of patients in the bimekizumab group, 9.5% (2/21) of patients in the placebo group, and 4.8% (1/21) of patients in the adalimumab group. Serious adverse events that required hospitalization were due to anemia and empyema in the bimekizumab group; worsening HS in the adalimumab group; and myocardial infarction, hypoesthesia, headache, and dizziness in the placebo group. No deaths occurred in this study. Overall, bimekizumab was well tolerated, and discontinuation rates were low across all arms. The primary reason for discontinuation was withdrawal of consent (not due to an adverse event) or loss to follow-up.⁷

Two completed 48-week phase III RCTs, BE HEARD I and BE HEARD II, evaluated the efficacy and safety of bimekizumab in patients with moderate to severe HS.¹³ In both trials, 2 bimekizumab dosing regimens (320 mg every 2 weeks and 320 mg every 4 weeks) were compared with placebo during the 16-week initial and 32-week maintenance treatment periods. The primary endpoint of week 16 was achieved by 47.8% (138/289) and 51.9% (151/291) of patients receiving bimekizumab every 2 weeks in BE HEARD I (n=505) and BE HEARD II (n=509), respectively, compared with 29.2% (21/72) and 32.4% (24/74) of the placebo group. The bimekizumab 320 mg every 4 weeks dosing regimen met the primary endpoint only in BE HEARD II, with 53.5% (77/144) of patients achieving HiSCR₅₀ compared to 32.4% (24/74) with placebo (P=0.0038).¹³ Both trials met the key secondary endpoint of HiSCR₇₅ at week 16 for bimekizumab 320 mg every 2 weeks vs placebo. In BE HEARD I, 33.6% (97/289) of patients receiving bimekizumab achieved HiSCR₇₅ versus 18.1% (13/72) taking placebo. In BE HEARD II, 35.7% (104/291) of patients receiving bimekizumab achieved HiSCR₇₅ vs 16.2% (12/74) taking placebo. Responses were maintained or increased through week 48 in both trials. The most common treatment-emergent adverse events through week 48 were worsening HS, COVID-19 infection, diarrhea, oral candidiasis, and headache.¹³

A smaller scale case series investigated the use of bimekizumab in 4 female patients aged 20 to 62 years with moderate to severe HS and concomitant plaque or inverse psoriasis.⁸ A monthly loading dose of 320 mg was given during weeks 0 to 12 followed by a maintenance dose of 320 mg administered every 8 weeks. The International Hidradenitis Suppurativa Score System, visual analogue scale, and Dermatology Life Quality Index were used to assess the effectiveness of therapy by comparing scores before and after 4 and 16 weeks of treatment. A reduction of pain and improvement of HS lesions was observed in 3 (75.0%) patients after the first dosage of bimekizumab, with completed remission of HS by week 16. The fourth patient (25.0%) experienced substantial improvement in all measures, although not complete remission. All 4 patients remained on bimekizumab, and no adverse effects were reported.⁸

A meta-analysis evaluated 16 RCTs of 9 biologics and 3 small-molecule inhibitors in 2076 patients with HS.¹⁰ Secukinumab was not included in this meta-analysis. Only adalimumab (risk ratio, 1.77; 95% CI, 1.44-2.17) and bimekizumab (risk ratio, 2.25; 95% CI, 1.03-4.92) were superior to placebo in achieving HiSCR response at weeks 12 to 16 in 5 RCTs and 1 RCT, respectively; however, no statistically significant differences were noted between adalimumab and bimekizumab (P=.56). This analysis concluded that adalimumab and bimekizumab are the only 2 biologics efficacious in reaching HiSCR and consistently improved both disease severity and quality of life in patients with HS with an acceptable safety profile.¹⁰ Furthermore, these biologics had no increase in serious adverse events when compared to placebo.¹⁰

A network meta-analysis of 10 clinical trials involving more than 900 total participants evaluated nonsurgical therapies for HS. The analysis used Surface Under the Cumulative Ranking curve (SUCRA) values to estimate the efficacy of treatments in achieving clinical response according to HiSCR criteria. These values range from 0% to 100%, with 100% representing the best possible ranking for efficacy. Bimekizumab showed the highest estimated efficacy with a SUCRA value of 67%, followed by adalimumab (64%), anakinra (49%), and placebo (19%). These SUCRA values indicate the relative ranking of treatments, with higher values suggesting greater likelihood of achieving clinical response, rather than representing the actual percentage of patients achieving HiSCR. Bimekizumab was found to be more efficacious than placebo (P<.05).¹⁴

Building on the initial evidence of bimekizumab’s efficacy, BE HEARD I and BE HEARD II addressed some limitations of prior studies, including small sample sizes and insufficient stratification.¹³ Notably, stratification by baseline Hurley stage severity (ie, the most severe stage of disease assigned at baseline) and baseline systemic antibiotic use helped mitigate bias and ensured a more robust assessment of treatment efficacy; however, certain limitations persist. While the trials demonstrated rapid and clinically meaningful responses maintained up to 48 weeks, longer-term data beyond this period are limited, leaving gaps in understanding the durability of treatment effects over years. Additionally, despite appropriate stratification, the generalizability of the findings to broader patient populations remains unclear, as trial participants may not fully represent the diversity of patients seen in clinical practice.¹³

Future research is needed to address these limitations. The use of validated HS biomarkers as endpoints could enhance the ability to evaluate biologic efficacy and identify predictors of response. Comparative studies with other biologics also are warranted to establish the relative efficacy of bimekizumab within the growing therapeutic landscape for HS. Finally, real-world evidence from larger and more diverse populations will be critical to confirm the trial findings and assess long-term safety and effectiveness in routine clinical practice.¹³

Conclusion

The existing literature and recent phase III RCTs, BE HEARD I and BE HEARD II, demonstrate that bimekizumab is an effective treatment for moderate to severe HS, with robust efficacy according to HiSCR scores and sustained responses through 48 weeks. These trials addressed some prior limitations, including small sample sizes and insufficient stratification, providing a more comprehensive evaluation of bimekizumab’s clinical impact. The safety profile of bimekizumab remains favorable, with low discontinuation rates and manageable adverse events, such as infection, gastrointestinal upset, headache, and injection-site reactions. Long-term efficacy and safety data beyond 48 weeks still are needed to fully establish its durability and impact in diverse populations. The recent FDA approval of bimekizumab for moderate to severe HS provides patients with a new treatment option, offering a more positive clinical outlook.

Hidradenitis suppurativa (HS) is a debilitating dermatologic condition characterized by recurrent episodes of neutrophilic inflammation affecting the apocrine and pilosebaceous units that most commonly affects individuals aged 20 to 40 years. Originating from the hair follicles, inflammation initiates the formation of painful nodules and abscesses that can progress to sinus tracts or fistulas accompanied by the development of extensive scarring, exquisite pain, and malodorous drainage.¹ The lesions most commonly occur in intertriginous zones as well as areas rich in apocrine glands. The distinctive and sometimes irreversible clinical features of HS profoundly influence patients’ well-being and have lasting social, personal, and emotional impacts on their lives.²

Bimekizumab is a monoclonal antibody that specifically targets IL-17A and IL-17F, aiming to inhibit the downstream effects responsible for the chronic inflammation and tissue damage characteristic of HS.³ In HS lesions, IL-17 cytokines produced by T helper 17 (Th17) cells stimulate the production of chemokines (such as CC motif chemokine ligand 20) and neutrophil-attracting chemokines (including C-X-C motif chemokine ligands 1 and 8), cytokines (such as granulocyte colony-stimulating factor and IL-19), and epidermal antimicrobial proteins.^1,2 This cascade results in the chemotaxis of monocytes and neutrophils in the skin, recruiting additional Th17 and myeloid cells and further amplifying IL-17 production.¹

Bimekizumab’s mechanism of action strategically disrupts this feed-forward inflammatory loop, decreasing the transcription of neutrophil-attracting chemokines, IL-19, and epidermal antimicrobial proteins (Figure).^1,2 This leads to diminished recruitment of Th17 cells and inhibits the chemotaxis of monocytes and neutrophils in the skin, effectively addressing the chronic inflammation and tissue damage characteristic of HS.

We present a comprehensive review of the current standards of care, the underlying molecular pathophysiology of HS, and evaluation of the efficacy and safety of bimekizumab.

Evaluating HS Severity

The Hurley staging system provides a valuable framework for evaluating the severity of HS based on lesion characteristics. Stage I is characterized by abscess formation without tracts or scars. Stage II is characterized by recurrent abscesses with sinus tracts and scarring. Stage III is characterized by diffuse involvement, multiple interconnected sinus tracts, and abscesses across an entire area, leaving little to no uninvolved skin.⁴

Treatment strategies for HS vary based on Hurley staging (eTable).^5-11 For mild cases (stage I), topical and intralesional therapies are common, while moderate to severe cases (stages II and III) may require extensive surgical approaches or systemic drugs such as antibiotics, hormonal therapies, retinoids, or immunosuppressive/biologic agents.²

Adalimumab, an anti–tumor necrosis factor (TNF) α monoclonal antibody, was the first US Food and Drug Administration (FDA)–approved biologic for HS. Secukinumab, a monoclonal antibody against IL-17A, subsequently was approved by the FDA for moderate to severe HS.¹² Off-label use of biologics including infliximab and ustekinumab expands the available treatment options for HS. In one Phase II randomized clinical trial (RCT), infliximab showed efficacy in reducing Hidradenitis Suppurativa Severity Index scores, with 26.7% (4/15) of patients achieving a 50% or greater reduction compared to placebo, although this was not statistically significant. Similarly, ustekinumab demonstrated promising results, with 47.1% (8/17) of patients achieving Hidradenitis Suppurativa Clinical Response (HiSCR) at week 40.² This multifaceted approach aims to address the varying degrees of severity and optimize outcomes for individuals with HS.

Molecular Pathophysiology of HS

The pathogenesis of HS is multifactorial, involving a complex interplay of genetic, environmental, and behavioral factors.² Approximately 33% to 40% of patients with HS worldwide report a first-degree relative with the condition, indicating a hereditary element with an autosomal-dominant transmission pattern and highlighting the global relevance of genetic factors in HS.⁴ Hidradenitis suppurativa is highly prevalent in individuals with obesity, likely due to increased intertriginous surface area, skin friction, sweat production, and hormonal changes in these patients. Smoking also commonly is associated with HS, with nicotine potentially contributing to increased follicular plugging.¹ Hormonal influences also play a role, as evidenced by a greater prevalence of HS in females, disease onset typically occurring between puberty and menopause, and symptomatic fluctuations correlating with menstrual cycles and exogenous hormones.⁴

Altered infundibular keratinization with subsequent hyperkeratosis/occlusion and innate immune pathway activation are key events leading to development of HS.¹ These events are mediated by release of pathogen- and danger-associated molecular patterns, leading to inflammasome-mediated IL-1α release, followed by downstream cytokine release.² Elevated levels of TNF-α, IL-1Β, IL-10, IL-17, and particularly IL-17A have been detected in HS lesional skin. The IL-17 family comprises multiple members, namely IL-17A, IL-17C, IL-17E, and IL17F. IL-17A and IL-17F often are co-expressed and secreted predominantly by a subset of CD4+ T helper cells, namely Th17 cells.² IL-17 cytokines exert pro-inflammatory effects, influencing immune cell activity and contributing to skin inflammation, particularly in HS.

Given the pivotal role of IL-17 in the pathogenesis of HS, the exploration of IL-17–targeted agents has become a focal point in clinical research. Bimekizumab, a novel IL-17 inhibitor, has emerged as a promising candidate, offering a potential breakthrough in the treatment landscape for individuals affected by HS.

Bimekizumab for HS Management

A phase II, double-blind, placebo-controlled RCT included 90 patients with moderate to severe HS (age range, 18-70 years) who were randomly assigned in a 2:1:1 ratio to receive either bimekizumab 320 mg every 2 weeks (with a 640-mg loading dose at baseline)(n=46), placebo (n=21), or adalimumab 40 mg once weekly from week 4 onward (following an initial 160-mg loading dose at baseline and 80-mg dose at week 2)(n=21). The study included a 12-week treatment period followed by a 20-week safety follow-up period. The primary endpoint was the achievement of HiSCR₅₀—defined as a reduction of at least 50% nodules, coupled with no increase in the number of abscesses or draining fistulas relative to baseline—at week 12. Additionally, the study assessed the number of patients who achieved a modified HiSCR with 75% reduction (HiSCR₇₅) of combined abscess and inflammatory nodule count or a modified HiSCR with 90% reduction (HiSCR₉₀). At week 12, the modeled response rates were estimated using a Bayesian logistic regression model. For HiSCR₅₀, the modeled rate for bimekizumab was 57.3%, with an observed rate of 62.5% (25/40), compared to a modeled rate of 26.1% for placebo (observed rate, 27.8% [5/18]). The posterior probability of superiority for bimekizumab over placebo was 0.998. By week 12, bimekizumab-treated patients achieved modeled HiSCR₇₅ and HiSCR₉₀ rates of 46.0% and 32.0%, respectively, with observed rates of 50.0% (20/40) for HiSCR₇₅ and 35.0% (14/40) for HiSCR₉₀. In comparison, placebo-treated patients achieved modeled HiSCR75 and HiSCR₉₀ rates of 10.0% and 0%, respectively, with observed rates of 11.1% (2/18) for HiSCR₇₅ and 0% (0/18) for HiSCR₉₀. Adalimumab-treated participants demonstrated intermediate results, achieving modeled HiSCR₇₅ and HiSCR₉₀ rates of 35.0% and 15.0%, respectively, with observed rates of 38.88% (7/18) for HiSCR₇₅ and 16.66% (3/18) for HiSCR₉₀.⁷

Bimekizumab was effective in the treatment of moderate to severe HS with comparable results to adalimumab.⁷ The incidence of treatment-emergent adverse events was similar across treatment arms (bimekizumab, 69.6% [32/46]; placebo, 61.9% [13/21]; adalimumab, 71.4% [15/21]). The most common treatment-emergent adverse events in the biologic treatment arms were infections (43.5% [20/46] in the bimekizumab group and 42.9% [9/21] in the adalimumab group), skin and subcutaneous tissue disorders (28.3% [13/46] in the bimekizumab group and 42.9% [9/21] in the adalimumab group), and general disorders/administration site conditions (21.7% [10/46] in the bimekizumab group and 23.8% [5/21] in the adalimumab group). Serious adverse events occurred in 4.3% (2/46) of patients in the bimekizumab group, 9.5% (2/21) of patients in the placebo group, and 4.8% (1/21) of patients in the adalimumab group. Serious adverse events that required hospitalization were due to anemia and empyema in the bimekizumab group; worsening HS in the adalimumab group; and myocardial infarction, hypoesthesia, headache, and dizziness in the placebo group. No deaths occurred in this study. Overall, bimekizumab was well tolerated, and discontinuation rates were low across all arms. The primary reason for discontinuation was withdrawal of consent (not due to an adverse event) or loss to follow-up.⁷

Two completed 48-week phase III RCTs, BE HEARD I and BE HEARD II, evaluated the efficacy and safety of bimekizumab in patients with moderate to severe HS.¹³ In both trials, 2 bimekizumab dosing regimens (320 mg every 2 weeks and 320 mg every 4 weeks) were compared with placebo during the 16-week initial and 32-week maintenance treatment periods. The primary endpoint of week 16 was achieved by 47.8% (138/289) and 51.9% (151/291) of patients receiving bimekizumab every 2 weeks in BE HEARD I (n=505) and BE HEARD II (n=509), respectively, compared with 29.2% (21/72) and 32.4% (24/74) of the placebo group. The bimekizumab 320 mg every 4 weeks dosing regimen met the primary endpoint only in BE HEARD II, with 53.5% (77/144) of patients achieving HiSCR₅₀ compared to 32.4% (24/74) with placebo (P=0.0038).¹³ Both trials met the key secondary endpoint of HiSCR₇₅ at week 16 for bimekizumab 320 mg every 2 weeks vs placebo. In BE HEARD I, 33.6% (97/289) of patients receiving bimekizumab achieved HiSCR₇₅ versus 18.1% (13/72) taking placebo. In BE HEARD II, 35.7% (104/291) of patients receiving bimekizumab achieved HiSCR₇₅ vs 16.2% (12/74) taking placebo. Responses were maintained or increased through week 48 in both trials. The most common treatment-emergent adverse events through week 48 were worsening HS, COVID-19 infection, diarrhea, oral candidiasis, and headache.¹³

A smaller scale case series investigated the use of bimekizumab in 4 female patients aged 20 to 62 years with moderate to severe HS and concomitant plaque or inverse psoriasis.⁸ A monthly loading dose of 320 mg was given during weeks 0 to 12 followed by a maintenance dose of 320 mg administered every 8 weeks. The International Hidradenitis Suppurativa Score System, visual analogue scale, and Dermatology Life Quality Index were used to assess the effectiveness of therapy by comparing scores before and after 4 and 16 weeks of treatment. A reduction of pain and improvement of HS lesions was observed in 3 (75.0%) patients after the first dosage of bimekizumab, with completed remission of HS by week 16. The fourth patient (25.0%) experienced substantial improvement in all measures, although not complete remission. All 4 patients remained on bimekizumab, and no adverse effects were reported.⁸

A meta-analysis evaluated 16 RCTs of 9 biologics and 3 small-molecule inhibitors in 2076 patients with HS.¹⁰ Secukinumab was not included in this meta-analysis. Only adalimumab (risk ratio, 1.77; 95% CI, 1.44-2.17) and bimekizumab (risk ratio, 2.25; 95% CI, 1.03-4.92) were superior to placebo in achieving HiSCR response at weeks 12 to 16 in 5 RCTs and 1 RCT, respectively; however, no statistically significant differences were noted between adalimumab and bimekizumab (P=.56). This analysis concluded that adalimumab and bimekizumab are the only 2 biologics efficacious in reaching HiSCR and consistently improved both disease severity and quality of life in patients with HS with an acceptable safety profile.¹⁰ Furthermore, these biologics had no increase in serious adverse events when compared to placebo.¹⁰

A network meta-analysis of 10 clinical trials involving more than 900 total participants evaluated nonsurgical therapies for HS. The analysis used Surface Under the Cumulative Ranking curve (SUCRA) values to estimate the efficacy of treatments in achieving clinical response according to HiSCR criteria. These values range from 0% to 100%, with 100% representing the best possible ranking for efficacy. Bimekizumab showed the highest estimated efficacy with a SUCRA value of 67%, followed by adalimumab (64%), anakinra (49%), and placebo (19%). These SUCRA values indicate the relative ranking of treatments, with higher values suggesting greater likelihood of achieving clinical response, rather than representing the actual percentage of patients achieving HiSCR. Bimekizumab was found to be more efficacious than placebo (P<.05).¹⁴

Building on the initial evidence of bimekizumab’s efficacy, BE HEARD I and BE HEARD II addressed some limitations of prior studies, including small sample sizes and insufficient stratification.¹³ Notably, stratification by baseline Hurley stage severity (ie, the most severe stage of disease assigned at baseline) and baseline systemic antibiotic use helped mitigate bias and ensured a more robust assessment of treatment efficacy; however, certain limitations persist. While the trials demonstrated rapid and clinically meaningful responses maintained up to 48 weeks, longer-term data beyond this period are limited, leaving gaps in understanding the durability of treatment effects over years. Additionally, despite appropriate stratification, the generalizability of the findings to broader patient populations remains unclear, as trial participants may not fully represent the diversity of patients seen in clinical practice.¹³

Future research is needed to address these limitations. The use of validated HS biomarkers as endpoints could enhance the ability to evaluate biologic efficacy and identify predictors of response. Comparative studies with other biologics also are warranted to establish the relative efficacy of bimekizumab within the growing therapeutic landscape for HS. Finally, real-world evidence from larger and more diverse populations will be critical to confirm the trial findings and assess long-term safety and effectiveness in routine clinical practice.¹³

Conclusion

The existing literature and recent phase III RCTs, BE HEARD I and BE HEARD II, demonstrate that bimekizumab is an effective treatment for moderate to severe HS, with robust efficacy according to HiSCR scores and sustained responses through 48 weeks. These trials addressed some prior limitations, including small sample sizes and insufficient stratification, providing a more comprehensive evaluation of bimekizumab’s clinical impact. The safety profile of bimekizumab remains favorable, with low discontinuation rates and manageable adverse events, such as infection, gastrointestinal upset, headache, and injection-site reactions. Long-term efficacy and safety data beyond 48 weeks still are needed to fully establish its durability and impact in diverse populations. The recent FDA approval of bimekizumab for moderate to severe HS provides patients with a new treatment option, offering a more positive clinical outlook.

Hidradenitis suppurativa (HS) is a debilitating dermatologic condition characterized by recurrent episodes of neutrophilic inflammation affecting the apocrine and pilosebaceous units that most commonly affects individuals aged 20 to 40 years. Originating from the hair follicles, inflammation initiates the formation of painful nodules and abscesses that can progress to sinus tracts or fistulas accompanied by the development of extensive scarring, exquisite pain, and malodorous drainage.¹ The lesions most commonly occur in intertriginous zones as well as areas rich in apocrine glands. The distinctive and sometimes irreversible clinical features of HS profoundly influence patients’ well-being and have lasting social, personal, and emotional impacts on their lives.²

Bimekizumab is a monoclonal antibody that specifically targets IL-17A and IL-17F, aiming to inhibit the downstream effects responsible for the chronic inflammation and tissue damage characteristic of HS.³ In HS lesions, IL-17 cytokines produced by T helper 17 (Th17) cells stimulate the production of chemokines (such as CC motif chemokine ligand 20) and neutrophil-attracting chemokines (including C-X-C motif chemokine ligands 1 and 8), cytokines (such as granulocyte colony-stimulating factor and IL-19), and epidermal antimicrobial proteins.^1,2 This cascade results in the chemotaxis of monocytes and neutrophils in the skin, recruiting additional Th17 and myeloid cells and further amplifying IL-17 production.¹

Bimekizumab’s mechanism of action strategically disrupts this feed-forward inflammatory loop, decreasing the transcription of neutrophil-attracting chemokines, IL-19, and epidermal antimicrobial proteins (Figure).^1,2 This leads to diminished recruitment of Th17 cells and inhibits the chemotaxis of monocytes and neutrophils in the skin, effectively addressing the chronic inflammation and tissue damage characteristic of HS.

We present a comprehensive review of the current standards of care, the underlying molecular pathophysiology of HS, and evaluation of the efficacy and safety of bimekizumab.

Evaluating HS Severity

The Hurley staging system provides a valuable framework for evaluating the severity of HS based on lesion characteristics. Stage I is characterized by abscess formation without tracts or scars. Stage II is characterized by recurrent abscesses with sinus tracts and scarring. Stage III is characterized by diffuse involvement, multiple interconnected sinus tracts, and abscesses across an entire area, leaving little to no uninvolved skin.⁴

Treatment strategies for HS vary based on Hurley staging (eTable).^5-11 For mild cases (stage I), topical and intralesional therapies are common, while moderate to severe cases (stages II and III) may require extensive surgical approaches or systemic drugs such as antibiotics, hormonal therapies, retinoids, or immunosuppressive/biologic agents.²

Adalimumab, an anti–tumor necrosis factor (TNF) α monoclonal antibody, was the first US Food and Drug Administration (FDA)–approved biologic for HS. Secukinumab, a monoclonal antibody against IL-17A, subsequently was approved by the FDA for moderate to severe HS.¹² Off-label use of biologics including infliximab and ustekinumab expands the available treatment options for HS. In one Phase II randomized clinical trial (RCT), infliximab showed efficacy in reducing Hidradenitis Suppurativa Severity Index scores, with 26.7% (4/15) of patients achieving a 50% or greater reduction compared to placebo, although this was not statistically significant. Similarly, ustekinumab demonstrated promising results, with 47.1% (8/17) of patients achieving Hidradenitis Suppurativa Clinical Response (HiSCR) at week 40.² This multifaceted approach aims to address the varying degrees of severity and optimize outcomes for individuals with HS.

Molecular Pathophysiology of HS

The pathogenesis of HS is multifactorial, involving a complex interplay of genetic, environmental, and behavioral factors.² Approximately 33% to 40% of patients with HS worldwide report a first-degree relative with the condition, indicating a hereditary element with an autosomal-dominant transmission pattern and highlighting the global relevance of genetic factors in HS.⁴ Hidradenitis suppurativa is highly prevalent in individuals with obesity, likely due to increased intertriginous surface area, skin friction, sweat production, and hormonal changes in these patients. Smoking also commonly is associated with HS, with nicotine potentially contributing to increased follicular plugging.¹ Hormonal influences also play a role, as evidenced by a greater prevalence of HS in females, disease onset typically occurring between puberty and menopause, and symptomatic fluctuations correlating with menstrual cycles and exogenous hormones.⁴

Altered infundibular keratinization with subsequent hyperkeratosis/occlusion and innate immune pathway activation are key events leading to development of HS.¹ These events are mediated by release of pathogen- and danger-associated molecular patterns, leading to inflammasome-mediated IL-1α release, followed by downstream cytokine release.² Elevated levels of TNF-α, IL-1Β, IL-10, IL-17, and particularly IL-17A have been detected in HS lesional skin. The IL-17 family comprises multiple members, namely IL-17A, IL-17C, IL-17E, and IL17F. IL-17A and IL-17F often are co-expressed and secreted predominantly by a subset of CD4+ T helper cells, namely Th17 cells.² IL-17 cytokines exert pro-inflammatory effects, influencing immune cell activity and contributing to skin inflammation, particularly in HS.

Given the pivotal role of IL-17 in the pathogenesis of HS, the exploration of IL-17–targeted agents has become a focal point in clinical research. Bimekizumab, a novel IL-17 inhibitor, has emerged as a promising candidate, offering a potential breakthrough in the treatment landscape for individuals affected by HS.

Bimekizumab for HS Management

A phase II, double-blind, placebo-controlled RCT included 90 patients with moderate to severe HS (age range, 18-70 years) who were randomly assigned in a 2:1:1 ratio to receive either bimekizumab 320 mg every 2 weeks (with a 640-mg loading dose at baseline)(n=46), placebo (n=21), or adalimumab 40 mg once weekly from week 4 onward (following an initial 160-mg loading dose at baseline and 80-mg dose at week 2)(n=21). The study included a 12-week treatment period followed by a 20-week safety follow-up period. The primary endpoint was the achievement of HiSCR₅₀—defined as a reduction of at least 50% nodules, coupled with no increase in the number of abscesses or draining fistulas relative to baseline—at week 12. Additionally, the study assessed the number of patients who achieved a modified HiSCR with 75% reduction (HiSCR₇₅) of combined abscess and inflammatory nodule count or a modified HiSCR with 90% reduction (HiSCR₉₀). At week 12, the modeled response rates were estimated using a Bayesian logistic regression model. For HiSCR₅₀, the modeled rate for bimekizumab was 57.3%, with an observed rate of 62.5% (25/40), compared to a modeled rate of 26.1% for placebo (observed rate, 27.8% [5/18]). The posterior probability of superiority for bimekizumab over placebo was 0.998. By week 12, bimekizumab-treated patients achieved modeled HiSCR₇₅ and HiSCR₉₀ rates of 46.0% and 32.0%, respectively, with observed rates of 50.0% (20/40) for HiSCR₇₅ and 35.0% (14/40) for HiSCR₉₀. In comparison, placebo-treated patients achieved modeled HiSCR75 and HiSCR₉₀ rates of 10.0% and 0%, respectively, with observed rates of 11.1% (2/18) for HiSCR₇₅ and 0% (0/18) for HiSCR₉₀. Adalimumab-treated participants demonstrated intermediate results, achieving modeled HiSCR₇₅ and HiSCR₉₀ rates of 35.0% and 15.0%, respectively, with observed rates of 38.88% (7/18) for HiSCR₇₅ and 16.66% (3/18) for HiSCR₉₀.⁷

Bimekizumab was effective in the treatment of moderate to severe HS with comparable results to adalimumab.⁷ The incidence of treatment-emergent adverse events was similar across treatment arms (bimekizumab, 69.6% [32/46]; placebo, 61.9% [13/21]; adalimumab, 71.4% [15/21]). The most common treatment-emergent adverse events in the biologic treatment arms were infections (43.5% [20/46] in the bimekizumab group and 42.9% [9/21] in the adalimumab group), skin and subcutaneous tissue disorders (28.3% [13/46] in the bimekizumab group and 42.9% [9/21] in the adalimumab group), and general disorders/administration site conditions (21.7% [10/46] in the bimekizumab group and 23.8% [5/21] in the adalimumab group). Serious adverse events occurred in 4.3% (2/46) of patients in the bimekizumab group, 9.5% (2/21) of patients in the placebo group, and 4.8% (1/21) of patients in the adalimumab group. Serious adverse events that required hospitalization were due to anemia and empyema in the bimekizumab group; worsening HS in the adalimumab group; and myocardial infarction, hypoesthesia, headache, and dizziness in the placebo group. No deaths occurred in this study. Overall, bimekizumab was well tolerated, and discontinuation rates were low across all arms. The primary reason for discontinuation was withdrawal of consent (not due to an adverse event) or loss to follow-up.⁷

Two completed 48-week phase III RCTs, BE HEARD I and BE HEARD II, evaluated the efficacy and safety of bimekizumab in patients with moderate to severe HS.¹³ In both trials, 2 bimekizumab dosing regimens (320 mg every 2 weeks and 320 mg every 4 weeks) were compared with placebo during the 16-week initial and 32-week maintenance treatment periods. The primary endpoint of week 16 was achieved by 47.8% (138/289) and 51.9% (151/291) of patients receiving bimekizumab every 2 weeks in BE HEARD I (n=505) and BE HEARD II (n=509), respectively, compared with 29.2% (21/72) and 32.4% (24/74) of the placebo group. The bimekizumab 320 mg every 4 weeks dosing regimen met the primary endpoint only in BE HEARD II, with 53.5% (77/144) of patients achieving HiSCR₅₀ compared to 32.4% (24/74) with placebo (P=0.0038).¹³ Both trials met the key secondary endpoint of HiSCR₇₅ at week 16 for bimekizumab 320 mg every 2 weeks vs placebo. In BE HEARD I, 33.6% (97/289) of patients receiving bimekizumab achieved HiSCR₇₅ versus 18.1% (13/72) taking placebo. In BE HEARD II, 35.7% (104/291) of patients receiving bimekizumab achieved HiSCR₇₅ vs 16.2% (12/74) taking placebo. Responses were maintained or increased through week 48 in both trials. The most common treatment-emergent adverse events through week 48 were worsening HS, COVID-19 infection, diarrhea, oral candidiasis, and headache.¹³

A smaller scale case series investigated the use of bimekizumab in 4 female patients aged 20 to 62 years with moderate to severe HS and concomitant plaque or inverse psoriasis.⁸ A monthly loading dose of 320 mg was given during weeks 0 to 12 followed by a maintenance dose of 320 mg administered every 8 weeks. The International Hidradenitis Suppurativa Score System, visual analogue scale, and Dermatology Life Quality Index were used to assess the effectiveness of therapy by comparing scores before and after 4 and 16 weeks of treatment. A reduction of pain and improvement of HS lesions was observed in 3 (75.0%) patients after the first dosage of bimekizumab, with completed remission of HS by week 16. The fourth patient (25.0%) experienced substantial improvement in all measures, although not complete remission. All 4 patients remained on bimekizumab, and no adverse effects were reported.⁸

A meta-analysis evaluated 16 RCTs of 9 biologics and 3 small-molecule inhibitors in 2076 patients with HS.¹⁰ Secukinumab was not included in this meta-analysis. Only adalimumab (risk ratio, 1.77; 95% CI, 1.44-2.17) and bimekizumab (risk ratio, 2.25; 95% CI, 1.03-4.92) were superior to placebo in achieving HiSCR response at weeks 12 to 16 in 5 RCTs and 1 RCT, respectively; however, no statistically significant differences were noted between adalimumab and bimekizumab (P=.56). This analysis concluded that adalimumab and bimekizumab are the only 2 biologics efficacious in reaching HiSCR and consistently improved both disease severity and quality of life in patients with HS with an acceptable safety profile.¹⁰ Furthermore, these biologics had no increase in serious adverse events when compared to placebo.¹⁰

A network meta-analysis of 10 clinical trials involving more than 900 total participants evaluated nonsurgical therapies for HS. The analysis used Surface Under the Cumulative Ranking curve (SUCRA) values to estimate the efficacy of treatments in achieving clinical response according to HiSCR criteria. These values range from 0% to 100%, with 100% representing the best possible ranking for efficacy. Bimekizumab showed the highest estimated efficacy with a SUCRA value of 67%, followed by adalimumab (64%), anakinra (49%), and placebo (19%). These SUCRA values indicate the relative ranking of treatments, with higher values suggesting greater likelihood of achieving clinical response, rather than representing the actual percentage of patients achieving HiSCR. Bimekizumab was found to be more efficacious than placebo (P<.05).¹⁴

Building on the initial evidence of bimekizumab’s efficacy, BE HEARD I and BE HEARD II addressed some limitations of prior studies, including small sample sizes and insufficient stratification.¹³ Notably, stratification by baseline Hurley stage severity (ie, the most severe stage of disease assigned at baseline) and baseline systemic antibiotic use helped mitigate bias and ensured a more robust assessment of treatment efficacy; however, certain limitations persist. While the trials demonstrated rapid and clinically meaningful responses maintained up to 48 weeks, longer-term data beyond this period are limited, leaving gaps in understanding the durability of treatment effects over years. Additionally, despite appropriate stratification, the generalizability of the findings to broader patient populations remains unclear, as trial participants may not fully represent the diversity of patients seen in clinical practice.¹³

Future research is needed to address these limitations. The use of validated HS biomarkers as endpoints could enhance the ability to evaluate biologic efficacy and identify predictors of response. Comparative studies with other biologics also are warranted to establish the relative efficacy of bimekizumab within the growing therapeutic landscape for HS. Finally, real-world evidence from larger and more diverse populations will be critical to confirm the trial findings and assess long-term safety and effectiveness in routine clinical practice.¹³

Conclusion

The existing literature and recent phase III RCTs, BE HEARD I and BE HEARD II, demonstrate that bimekizumab is an effective treatment for moderate to severe HS, with robust efficacy according to HiSCR scores and sustained responses through 48 weeks. These trials addressed some prior limitations, including small sample sizes and insufficient stratification, providing a more comprehensive evaluation of bimekizumab’s clinical impact. The safety profile of bimekizumab remains favorable, with low discontinuation rates and manageable adverse events, such as infection, gastrointestinal upset, headache, and injection-site reactions. Long-term efficacy and safety data beyond 48 weeks still are needed to fully establish its durability and impact in diverse populations. The recent FDA approval of bimekizumab for moderate to severe HS provides patients with a new treatment option, offering a more positive clinical outlook.