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Topical tranexamic acid for melasma
By addressing the vascular component of melasma, off-label use of oral tranexamic acid has been a beneficial adjunct for this difficult-to-treat condition. For on-label use treating menorrhagia (the oral form) and short-term prophylaxis of bleeding in hemophilia patients undergoing dental procedures – (the injectable form), tranexamic acid acts as an antifibrinolytic.
By inhibiting plasminogen activation, according to a 2018 review article “tranexamic acid mitigates UV radiation–induced melanogenesis and neovascularization,” both exhibited in the clinical manifestations of melasma.1 In addition to inhibiting fibrinolysis, tranexamic acid has direct effects on UV-induced pigmentation, “via its inhibitory effects on UV light–induced plasminogen activator on keratinocytes and [subsequent] plasmin activity,” the article states. “Plasminogen activator induces tyrosinase activity, resulting in increased melanin synthesis. The presence of plasmin [which dissolves clots by degrading fibrin] results in increased production of both arachidonic acid and fibroblast growth factor, which stimulate melanogenesis and neovascularization, respectively.”
With oral use, the risk of clot formation, especially in those who have a history of blood clots, clotting disorders (such as factor V Leiden), smoking, or other hypercoagulability risks should be weighed.
Topical tranexamic acid used locally mitigates systemic risk, and according to published studies, has been found to be efficacious for hemostasis in knee and hip arthroplasty surgery and for epistaxis. However, clinical outcomes with the topical treatment have largely not been on par with regards to efficacy for melasma when compared with oral tranexamic acid.
. Topical tranexamic acid, in my experience, when applied immediately after fractional 1927-nm diode laser treatment, not only has been noted by patients to feel soothing, but anecdotally has been found to improve pigmentation.
Moreover, there are now several peer-reviewed studies showing some benefit for treating pigmentation from photodamage or melasma with laser-assisted delivery of topical tranexamic acid. Treatment of these conditions may also benefit from nonablative 1927-nm laser alone.
In one recently published study, 10 female melasma patients, Fitzpatrick skin types II-IV, underwent five full-face low-energy, low-density (power 4-5 W, fluence 2-8 mJ, 2-8 passes) 1927-nm fractional thulium fiber laser treatment.2 Topical tranexamic acid was applied immediately after laser treatment and continued twice daily for 7 days. Seven patients completed the study. Based on the Global Aesthetics Improvement Scale (GAIS) ratings, all seven patients noted improvement at day 180, at which time six of the patients were considered to have improved from baseline, according to the investigator GAIS ratings. Using the Melasma Area Severity Index (MASI) score, the greatest degree of improvement was seen at day 90; there were three recurrences of melasma with worsening of the MASI score between day 90 and day 180.
In a split-face, double-blind, randomized controlled study, 46 patients with Fitzpatrick skin types III-V, with recalcitrant melasma received four weekly treatments of full-face fractional 1927-nm thulium laser; topical tranexamic acid was applied to one side of the face and normal saline applied to the other side under occlusion, immediately after treatment.3 At 3 months, significant improvements from baseline were seen with Melanin Index (MI) and modified MASI (mMASI) scores for the sides treated with tranexamic acid and the control side, with no statistically significant differences between the two. However, at month 6, among the 29 patients available for follow-up, significant differences in MI and mMASI scores from baseline were still evident, with the exception of MI scores on the control sides.
No adverse events from using topical tranexamic acid with laser were noted in either study. Split-face randomized control studies with use of topical tranexamic acid after fractional 1927-nm diode laser in comparison to fractional 1927-nm thulium laser would be notable in this vascular and heat-sensitive condition as well.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
References
1. Sheu SL. Cutis. 2018 Feb;101(2):E7-E8.
2. Wang, JV et al. J Cosmet Dermatol. 2021 Jan;20(1):105-9.
3. Wanitphakdeedecha R. et al. Lasers Med Sci. 2020 Dec;35(9):2015-21.
By addressing the vascular component of melasma, off-label use of oral tranexamic acid has been a beneficial adjunct for this difficult-to-treat condition. For on-label use treating menorrhagia (the oral form) and short-term prophylaxis of bleeding in hemophilia patients undergoing dental procedures – (the injectable form), tranexamic acid acts as an antifibrinolytic.
By inhibiting plasminogen activation, according to a 2018 review article “tranexamic acid mitigates UV radiation–induced melanogenesis and neovascularization,” both exhibited in the clinical manifestations of melasma.1 In addition to inhibiting fibrinolysis, tranexamic acid has direct effects on UV-induced pigmentation, “via its inhibitory effects on UV light–induced plasminogen activator on keratinocytes and [subsequent] plasmin activity,” the article states. “Plasminogen activator induces tyrosinase activity, resulting in increased melanin synthesis. The presence of plasmin [which dissolves clots by degrading fibrin] results in increased production of both arachidonic acid and fibroblast growth factor, which stimulate melanogenesis and neovascularization, respectively.”
With oral use, the risk of clot formation, especially in those who have a history of blood clots, clotting disorders (such as factor V Leiden), smoking, or other hypercoagulability risks should be weighed.
Topical tranexamic acid used locally mitigates systemic risk, and according to published studies, has been found to be efficacious for hemostasis in knee and hip arthroplasty surgery and for epistaxis. However, clinical outcomes with the topical treatment have largely not been on par with regards to efficacy for melasma when compared with oral tranexamic acid.
. Topical tranexamic acid, in my experience, when applied immediately after fractional 1927-nm diode laser treatment, not only has been noted by patients to feel soothing, but anecdotally has been found to improve pigmentation.
Moreover, there are now several peer-reviewed studies showing some benefit for treating pigmentation from photodamage or melasma with laser-assisted delivery of topical tranexamic acid. Treatment of these conditions may also benefit from nonablative 1927-nm laser alone.
In one recently published study, 10 female melasma patients, Fitzpatrick skin types II-IV, underwent five full-face low-energy, low-density (power 4-5 W, fluence 2-8 mJ, 2-8 passes) 1927-nm fractional thulium fiber laser treatment.2 Topical tranexamic acid was applied immediately after laser treatment and continued twice daily for 7 days. Seven patients completed the study. Based on the Global Aesthetics Improvement Scale (GAIS) ratings, all seven patients noted improvement at day 180, at which time six of the patients were considered to have improved from baseline, according to the investigator GAIS ratings. Using the Melasma Area Severity Index (MASI) score, the greatest degree of improvement was seen at day 90; there were three recurrences of melasma with worsening of the MASI score between day 90 and day 180.
In a split-face, double-blind, randomized controlled study, 46 patients with Fitzpatrick skin types III-V, with recalcitrant melasma received four weekly treatments of full-face fractional 1927-nm thulium laser; topical tranexamic acid was applied to one side of the face and normal saline applied to the other side under occlusion, immediately after treatment.3 At 3 months, significant improvements from baseline were seen with Melanin Index (MI) and modified MASI (mMASI) scores for the sides treated with tranexamic acid and the control side, with no statistically significant differences between the two. However, at month 6, among the 29 patients available for follow-up, significant differences in MI and mMASI scores from baseline were still evident, with the exception of MI scores on the control sides.
No adverse events from using topical tranexamic acid with laser were noted in either study. Split-face randomized control studies with use of topical tranexamic acid after fractional 1927-nm diode laser in comparison to fractional 1927-nm thulium laser would be notable in this vascular and heat-sensitive condition as well.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
References
1. Sheu SL. Cutis. 2018 Feb;101(2):E7-E8.
2. Wang, JV et al. J Cosmet Dermatol. 2021 Jan;20(1):105-9.
3. Wanitphakdeedecha R. et al. Lasers Med Sci. 2020 Dec;35(9):2015-21.
By addressing the vascular component of melasma, off-label use of oral tranexamic acid has been a beneficial adjunct for this difficult-to-treat condition. For on-label use treating menorrhagia (the oral form) and short-term prophylaxis of bleeding in hemophilia patients undergoing dental procedures – (the injectable form), tranexamic acid acts as an antifibrinolytic.
By inhibiting plasminogen activation, according to a 2018 review article “tranexamic acid mitigates UV radiation–induced melanogenesis and neovascularization,” both exhibited in the clinical manifestations of melasma.1 In addition to inhibiting fibrinolysis, tranexamic acid has direct effects on UV-induced pigmentation, “via its inhibitory effects on UV light–induced plasminogen activator on keratinocytes and [subsequent] plasmin activity,” the article states. “Plasminogen activator induces tyrosinase activity, resulting in increased melanin synthesis. The presence of plasmin [which dissolves clots by degrading fibrin] results in increased production of both arachidonic acid and fibroblast growth factor, which stimulate melanogenesis and neovascularization, respectively.”
With oral use, the risk of clot formation, especially in those who have a history of blood clots, clotting disorders (such as factor V Leiden), smoking, or other hypercoagulability risks should be weighed.
Topical tranexamic acid used locally mitigates systemic risk, and according to published studies, has been found to be efficacious for hemostasis in knee and hip arthroplasty surgery and for epistaxis. However, clinical outcomes with the topical treatment have largely not been on par with regards to efficacy for melasma when compared with oral tranexamic acid.
. Topical tranexamic acid, in my experience, when applied immediately after fractional 1927-nm diode laser treatment, not only has been noted by patients to feel soothing, but anecdotally has been found to improve pigmentation.
Moreover, there are now several peer-reviewed studies showing some benefit for treating pigmentation from photodamage or melasma with laser-assisted delivery of topical tranexamic acid. Treatment of these conditions may also benefit from nonablative 1927-nm laser alone.
In one recently published study, 10 female melasma patients, Fitzpatrick skin types II-IV, underwent five full-face low-energy, low-density (power 4-5 W, fluence 2-8 mJ, 2-8 passes) 1927-nm fractional thulium fiber laser treatment.2 Topical tranexamic acid was applied immediately after laser treatment and continued twice daily for 7 days. Seven patients completed the study. Based on the Global Aesthetics Improvement Scale (GAIS) ratings, all seven patients noted improvement at day 180, at which time six of the patients were considered to have improved from baseline, according to the investigator GAIS ratings. Using the Melasma Area Severity Index (MASI) score, the greatest degree of improvement was seen at day 90; there were three recurrences of melasma with worsening of the MASI score between day 90 and day 180.
In a split-face, double-blind, randomized controlled study, 46 patients with Fitzpatrick skin types III-V, with recalcitrant melasma received four weekly treatments of full-face fractional 1927-nm thulium laser; topical tranexamic acid was applied to one side of the face and normal saline applied to the other side under occlusion, immediately after treatment.3 At 3 months, significant improvements from baseline were seen with Melanin Index (MI) and modified MASI (mMASI) scores for the sides treated with tranexamic acid and the control side, with no statistically significant differences between the two. However, at month 6, among the 29 patients available for follow-up, significant differences in MI and mMASI scores from baseline were still evident, with the exception of MI scores on the control sides.
No adverse events from using topical tranexamic acid with laser were noted in either study. Split-face randomized control studies with use of topical tranexamic acid after fractional 1927-nm diode laser in comparison to fractional 1927-nm thulium laser would be notable in this vascular and heat-sensitive condition as well.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
References
1. Sheu SL. Cutis. 2018 Feb;101(2):E7-E8.
2. Wang, JV et al. J Cosmet Dermatol. 2021 Jan;20(1):105-9.
3. Wanitphakdeedecha R. et al. Lasers Med Sci. 2020 Dec;35(9):2015-21.
Vitiligo treatment options abound but consider patient goals
, according to Seemal Desai, MD, of the University of Texas, Dallas.
“We have topical steroids. We have vitamin D analogs, calcineurin inhibitors, and depigmentation therapy. We also have systemic therapy, phototherapy, surgical treatment, and even psychological therapy, Dr. Desai said in a presentation at MedscapeLive’s virtual Women’s & Pediatric Dermatology Seminar.
Head and neck vitiligo, which “tends to respond very nicely to treatment,” is one of the affected areas “where we have an important obligation to make sure our patients are effectively and aggressively treated,” he said.
According to Dr. Desai, there are three kinds of vitiligo. Active/unstable vitiligo is marked by depigmentation spreading across 1%-2% of body surface area per month, the size of about one to two palms. Refractory vitiligo responds poorly to therapy with less than 25% of affected areas experiencing repigmentation. And the third type is chronic vitiligo. “The majority of patients we see are in this phase, where depigmentation is present for at least 1 year with no history of spontaneous repigmentation.”
Before turning to therapy, he said, make sure to understand what the patient wants. “Are they even interested in being treated? I’ve had some patients with vitiligo, it’s only on their chest, and they’re always covered. They don’t even want anything. Then I have other patients who only want their face and hands treated because those are the only parts of their body that are exposed.”
To stabilize vitiligo, Dr. Desai recommends treating patients with “mini-pulse” oral therapy with systemic steroids. “I prescribe 4 milligrams of dexamethasone to be taken 2 consecutive days per week, such as Saturdays and Sundays. I usually halve the dose in children aged less than 16 years of age, so they’d be taking 2 milligrams.” Make sure, he said, to counsel patients on side effects.
He also recommends antioxidants, particularly polypodium leucotomos, “which has been shown in studies to increase the rates of head and neck repigmentation when combined with narrowband UVB.” He recommends 240 milligrams or higher, 2 or 3 times a day. He adds that alpha lipoic acid – in combination with vitamin C, vitamin E, and phototherapy – has also been shown to be effective in inducing repigmentation, especially on the head and neck.
As for newer drugs, Dr. Desai said afamelanotide, an analogue of alpha melanocyte-stimulating hormone combined with phototherapy, has shown promise. (It was approved in 2019 to increase pain free light exposure in adults with a history of phototoxic reactions related to erythropoietic protoporphyria.) Like other medications he mentioned, it isn’t FDA approved for treating vitiligo.
On another front, “Janus kinase inhibitors are our new frontier in treating vitiligo,” he said. “Tofacitinib can be dosed as an off-label usage in vitiligo in doses of 5 milligrams every other day, up to 5 milligrams daily. It’s half of the dose of rheumatoid arthritis, which is 5 milligrams b.i.d. You can actually start to see repigmentation as soon as 2 months, and then improvement up to 5 months.”
The drug requires laboratory monitoring and is expensive, he said, and JAK inhibitor side effects must be discussed with all patients.
Topical JAK inhibitors – tofacitinib 2% cream and ruxolitinib 1.5% cream – are also being evaluated as treatment for vitiligo. “I find that ruxolitinib works a little bit better, and the early bit of vitiligo data has shown that it tends to have more of a robust pigmentation response compared to tofacitinib,” said Dr. Desai, who gets these drugs compounded for topical use.
Dr. Desai added that he prefers to combine JAK inhibitors with phototherapy when possible.
For resistant vitiligo, he said, “lasers can help, especially Q-switched ruby and Q-switched Alexandrite laser. Q-switched Nd:Yag is very popular in Asia.”
In the big picture, he said, patients can benefit greatly from treatment. “Just think about the psychological improvement a patient would get by not having to get stares when walking in a mall and not having to deal with vitiligo lesions all over their cheek and neck.”
Dr. Desai disclosed performing clinical trials and/or consulting for numerous companies, including Pfizer, Allergan, AbbVie, and Dr. Reddy’s, among others. MedscapeLive and this news organization are owned by the same parent company.
, according to Seemal Desai, MD, of the University of Texas, Dallas.
“We have topical steroids. We have vitamin D analogs, calcineurin inhibitors, and depigmentation therapy. We also have systemic therapy, phototherapy, surgical treatment, and even psychological therapy, Dr. Desai said in a presentation at MedscapeLive’s virtual Women’s & Pediatric Dermatology Seminar.
Head and neck vitiligo, which “tends to respond very nicely to treatment,” is one of the affected areas “where we have an important obligation to make sure our patients are effectively and aggressively treated,” he said.
According to Dr. Desai, there are three kinds of vitiligo. Active/unstable vitiligo is marked by depigmentation spreading across 1%-2% of body surface area per month, the size of about one to two palms. Refractory vitiligo responds poorly to therapy with less than 25% of affected areas experiencing repigmentation. And the third type is chronic vitiligo. “The majority of patients we see are in this phase, where depigmentation is present for at least 1 year with no history of spontaneous repigmentation.”
Before turning to therapy, he said, make sure to understand what the patient wants. “Are they even interested in being treated? I’ve had some patients with vitiligo, it’s only on their chest, and they’re always covered. They don’t even want anything. Then I have other patients who only want their face and hands treated because those are the only parts of their body that are exposed.”
To stabilize vitiligo, Dr. Desai recommends treating patients with “mini-pulse” oral therapy with systemic steroids. “I prescribe 4 milligrams of dexamethasone to be taken 2 consecutive days per week, such as Saturdays and Sundays. I usually halve the dose in children aged less than 16 years of age, so they’d be taking 2 milligrams.” Make sure, he said, to counsel patients on side effects.
He also recommends antioxidants, particularly polypodium leucotomos, “which has been shown in studies to increase the rates of head and neck repigmentation when combined with narrowband UVB.” He recommends 240 milligrams or higher, 2 or 3 times a day. He adds that alpha lipoic acid – in combination with vitamin C, vitamin E, and phototherapy – has also been shown to be effective in inducing repigmentation, especially on the head and neck.
As for newer drugs, Dr. Desai said afamelanotide, an analogue of alpha melanocyte-stimulating hormone combined with phototherapy, has shown promise. (It was approved in 2019 to increase pain free light exposure in adults with a history of phototoxic reactions related to erythropoietic protoporphyria.) Like other medications he mentioned, it isn’t FDA approved for treating vitiligo.
On another front, “Janus kinase inhibitors are our new frontier in treating vitiligo,” he said. “Tofacitinib can be dosed as an off-label usage in vitiligo in doses of 5 milligrams every other day, up to 5 milligrams daily. It’s half of the dose of rheumatoid arthritis, which is 5 milligrams b.i.d. You can actually start to see repigmentation as soon as 2 months, and then improvement up to 5 months.”
The drug requires laboratory monitoring and is expensive, he said, and JAK inhibitor side effects must be discussed with all patients.
Topical JAK inhibitors – tofacitinib 2% cream and ruxolitinib 1.5% cream – are also being evaluated as treatment for vitiligo. “I find that ruxolitinib works a little bit better, and the early bit of vitiligo data has shown that it tends to have more of a robust pigmentation response compared to tofacitinib,” said Dr. Desai, who gets these drugs compounded for topical use.
Dr. Desai added that he prefers to combine JAK inhibitors with phototherapy when possible.
For resistant vitiligo, he said, “lasers can help, especially Q-switched ruby and Q-switched Alexandrite laser. Q-switched Nd:Yag is very popular in Asia.”
In the big picture, he said, patients can benefit greatly from treatment. “Just think about the psychological improvement a patient would get by not having to get stares when walking in a mall and not having to deal with vitiligo lesions all over their cheek and neck.”
Dr. Desai disclosed performing clinical trials and/or consulting for numerous companies, including Pfizer, Allergan, AbbVie, and Dr. Reddy’s, among others. MedscapeLive and this news organization are owned by the same parent company.
, according to Seemal Desai, MD, of the University of Texas, Dallas.
“We have topical steroids. We have vitamin D analogs, calcineurin inhibitors, and depigmentation therapy. We also have systemic therapy, phototherapy, surgical treatment, and even psychological therapy, Dr. Desai said in a presentation at MedscapeLive’s virtual Women’s & Pediatric Dermatology Seminar.
Head and neck vitiligo, which “tends to respond very nicely to treatment,” is one of the affected areas “where we have an important obligation to make sure our patients are effectively and aggressively treated,” he said.
According to Dr. Desai, there are three kinds of vitiligo. Active/unstable vitiligo is marked by depigmentation spreading across 1%-2% of body surface area per month, the size of about one to two palms. Refractory vitiligo responds poorly to therapy with less than 25% of affected areas experiencing repigmentation. And the third type is chronic vitiligo. “The majority of patients we see are in this phase, where depigmentation is present for at least 1 year with no history of spontaneous repigmentation.”
Before turning to therapy, he said, make sure to understand what the patient wants. “Are they even interested in being treated? I’ve had some patients with vitiligo, it’s only on their chest, and they’re always covered. They don’t even want anything. Then I have other patients who only want their face and hands treated because those are the only parts of their body that are exposed.”
To stabilize vitiligo, Dr. Desai recommends treating patients with “mini-pulse” oral therapy with systemic steroids. “I prescribe 4 milligrams of dexamethasone to be taken 2 consecutive days per week, such as Saturdays and Sundays. I usually halve the dose in children aged less than 16 years of age, so they’d be taking 2 milligrams.” Make sure, he said, to counsel patients on side effects.
He also recommends antioxidants, particularly polypodium leucotomos, “which has been shown in studies to increase the rates of head and neck repigmentation when combined with narrowband UVB.” He recommends 240 milligrams or higher, 2 or 3 times a day. He adds that alpha lipoic acid – in combination with vitamin C, vitamin E, and phototherapy – has also been shown to be effective in inducing repigmentation, especially on the head and neck.
As for newer drugs, Dr. Desai said afamelanotide, an analogue of alpha melanocyte-stimulating hormone combined with phototherapy, has shown promise. (It was approved in 2019 to increase pain free light exposure in adults with a history of phototoxic reactions related to erythropoietic protoporphyria.) Like other medications he mentioned, it isn’t FDA approved for treating vitiligo.
On another front, “Janus kinase inhibitors are our new frontier in treating vitiligo,” he said. “Tofacitinib can be dosed as an off-label usage in vitiligo in doses of 5 milligrams every other day, up to 5 milligrams daily. It’s half of the dose of rheumatoid arthritis, which is 5 milligrams b.i.d. You can actually start to see repigmentation as soon as 2 months, and then improvement up to 5 months.”
The drug requires laboratory monitoring and is expensive, he said, and JAK inhibitor side effects must be discussed with all patients.
Topical JAK inhibitors – tofacitinib 2% cream and ruxolitinib 1.5% cream – are also being evaluated as treatment for vitiligo. “I find that ruxolitinib works a little bit better, and the early bit of vitiligo data has shown that it tends to have more of a robust pigmentation response compared to tofacitinib,” said Dr. Desai, who gets these drugs compounded for topical use.
Dr. Desai added that he prefers to combine JAK inhibitors with phototherapy when possible.
For resistant vitiligo, he said, “lasers can help, especially Q-switched ruby and Q-switched Alexandrite laser. Q-switched Nd:Yag is very popular in Asia.”
In the big picture, he said, patients can benefit greatly from treatment. “Just think about the psychological improvement a patient would get by not having to get stares when walking in a mall and not having to deal with vitiligo lesions all over their cheek and neck.”
Dr. Desai disclosed performing clinical trials and/or consulting for numerous companies, including Pfizer, Allergan, AbbVie, and Dr. Reddy’s, among others. MedscapeLive and this news organization are owned by the same parent company.
FROM MEDSCAPELIVE WOMEN’S & PEDIATRIC DERMATOLOGY SEMINAR
Combination approach to melasma treatment yields best results
When establishing a treatment plan for patients with melasma, counseling them about realistic expectations is key.
“It’s important that they understand that this is a chronic condition, so it does require long-term maintenance therapy,” Arisa E. Ortiz, MD, said at the virtual annual Masters of Aesthetics Symposium. “We can improve melasma, but it’s difficult to cure melasma.”
While hydroquinone and other bleaching agents are typical treatment mainstays, chemical peels with glycolic acid, trichloroacetic acid, and salicylic acid can benefit some individuals. “For chemical peels, I really like glycolic acid peels because there is no downtime; it peels at the microscopic level,” said Dr. Ortiz, who is director of laser and cosmetic dermatology at the University of California, San Diego. “This is something they may need to repeat monthly, and having a week of peeling may be difficult to go through every month.”
Other common melasma treatments include lasers, intense pulsed light (IPL), and oral medications. “I personally am not impressed with microdermabrasion for melasma, so I don’t use that very much,” she said. “With laser treatment, you want to make sure you’re using low-energy lasers so that it doesn’t exacerbate or make them relapse or rebound.”
While hydroquinone is a mainstay of therapy, “you can’t use it chronically because of the risk of ochronosis (permanent darkening), so you do need to take drug holidays,” Dr. Ortiz said. “During those drug holidays, you want to make sure patients have a nonhydroquinone bleaching agent so that they don’t flare.” Options include lignin peroxidase, oligopeptide, Lytera, Melaplex, 4-n-butylresorcinol, Cysteamine cream, tranexamic acid, and oral antioxidants.
In a study sponsored by SkinMedica, investigators conducted a randomized, double-blind, half-face study in females with moderate to severe facial hyperpigmentation to assess the efficacy and tolerability of three new skin brightener formulations containing SMA-432, a prostaglandin E2 inhibitor, compared with topical 4% hydroquinone (J Drugs Dermatol 2012 Dec;11[12]:1478-82). They found that the nonhydroquinone skin formulations were better tolerated and were just as effective as 4% hydroquinone.
In a separate unpublished study of 22 females, investigators assessed the efficacy of the U.SK Advanced Defense Booster, which contains ferulic acid, maslinic acid, peptides, and olive leaf extract. They observed that 98% of patients saw improvement after 28 days of treatment.
When it comes to using lasers for melasma treatment, low-energy devices provide the best outcomes. “I prefer using something like the 1927-nm fractional diode lasers at 3.75% density, really low densities because there’s less risk for rebound,” Dr. Ortiz said. “They also enhance skin permeability for the use of topicals.”
In an observational study of 27 female patients with refractory melasma, Arielle Kauvar, MD, director of New York Laser & Skin Care, combined microdermabrasion with the Q-switched Nd:YAG (Lasers in Surgery and Medicine 2012; 44:117-24). “The settings she used were very low fluence, so there was no clinical endpoint or no whitening,” Dr. Ortiz said. Specifically, she used a laser at 1.6-2 J/cm2 with a 5- or 6-mm spot size immediately following microdermabrasion for 4 weeks. “She got a good improvement using a skin care regimen of sunscreen, hydroquinone, and tretinoin or vitamin C,” she said. “Remission lasted at least 6 months.”
In a study presented at the 2019 annual meeting of the America Society for Laser Medicine and Surgery, Dr. Ortiz and Tanya Greywal, MD, of the University of California, San Diego, used three passes of the 10764-nm Nd:YAG laser to treat 10 subjects with melasma skin types 2-5. The device has a 650-microsecond pulse duration, a 6-mm spot size, and an energy mode of 11-14 J/cm3. “There was no downtime with these patients, and they saw a mean improvement of 26%-50% as early as 3 weeks,” she said. “Patients did require multiple treatments to see adequate resolution, but no anesthesia or numbing cream was required. This is a good option for patients who need chronic maintenance treatment.”
Topicals also play a key role following the laser treatment of melasma. Dr. Ortiz characterized clobetasol as “kind of like the magic ointment.” She uses one application immediately post procedure “whenever I’m worried about a patient having postinflammatory hyperpigmentation or if I don’t want melasma patients to rebound. It can help reduce swelling and inflammation to decrease the risk of postinflammatory hyperpigmentation.”
Researchers have discovered that there is a vascular component to melasma. Paul M. Friedman, MD, of the Dermatology and Laser Surgery Center, Houston, and his colleagues used spectrocolorimetry to detect an underlying prominent vascular component in 11 patients with melasma (Lasers Surg Med 2017 Jan;49[1]:20-6). They determined that melasma lesions exhibiting subtle or subclinical telangiectatic erythema may be improved by combined vascular-targeted laser therapy together with fractional low-powered diode laser therapy. “A parallel improvement in telangiectatic erythema suggests a relationship between the underlying vasculature and hyperpigmentation,” said Dr. Ortiz, who was not affiliated with the study. “So, patients who have a vascular component to their melasma actually can get improved efficacy.”
Another strategy for melasma patients involves oral treatment with Polypodium leucotomos extract (PLE), a fern from the Polypodiaceae family with antioxidant properties that has been shown to be photoprotective against UVA and UVB radiation. “I like to think of it as an internal sunscreen,” Dr. Ortiz said. “It does not replace your external sunscreen, but it adds extra protection. It has been shown to significantly reduce the severity of sunburn and decrease the risk of UV radiation–induced skin cancer, as well as prevent skin aging.” The purported mechanism of action includes decreasing UV-mediated oxidative damage to DNA, enhancing the activity of endogenous antioxidant systems, increasing the minimal erythema dose, blocking UV radiation–induced cyclooxygenase-2 expression, reducing UV-induced immune suppression, and promoting p53 suppressor gene expression.
In a pilot placebo-controlled study of melasma patients on their normal regimen of hydroquinone and sunscreen, 40 Asian patients with melasma were randomized to receive either oral PLE supplementation or placebo for 12 weeks (J Clin Aesthet Dermatol 2018 Mar;11[3]:14-9). They found that PLE significantly improved and accelerated the outcome reached with hydroquinone and sunscreen from the first month of treatment, compared with placebo.
Dr. Ortiz next discussed the role of oral tranexamic acid, an antifibrinolytic, procoagulant agent that is approved by the Food and Drug Administration for the treatment of menorrhagia and for prevention of hemorrhage in patients with hemophilia undergoing tooth extractions. “It is a synthetic lysine derivative that inhibits plasminogen activation by blocking lysine-binding sites on the plasminogen molecule, and it’s a game changer for melasma treatment,” she said. “One of the side effects is that it inhibits melanogenesis and neovascularization. It’s been effective for melasma, but its use is limited by the risk for thromboembolism. It’s a slight increased risk, something patients should be aware of, but not something that should scare us away from prescribing it.”
In a study of 561 patients with melasma, 90% improved after a median treatment duration of 4 months, and only 7% had side effects (J Am Acad Dermatol 2016;75:385-92). The most common side effects were abdominal bloating and pain. One patient developed a DVT during treatment, but that person was found to have a protein S deficiency.
The daily dosing of tranexamic acid for menorrhagia is 3,900 mg daily, while the dose for melasma has ranged from 500 mg-1,500 mg per day, Dr. Ortiz said. It’s available as a 650-mg pill in the United States. “I prescribe 325 mg twice a day, but studies have shown that 650 mg once a day is just as effective,” she said.
Prior to prescribing tranexamic acid, Dr. Ortiz does not order labs, but she performs an extensive history of present illness. She does not prescribe it in patients with an increased risk of clotting, including people who smoke and those who take oral contraceptives or are on hormone supplementation. Use is also contraindicated in people with a current malignancy, those with a history of stroke or DVT, and those who have any clotting disorder.
She concluded her presentation by noting that she favors a combination approach to treating melasma patients that starts with a broad spectrum sunscreen and PLE. “For bleaching, I like to use 12% hydroquinone with 6% kojic acid in VersaBase,” she said. “Once I get them in better control, then I switch them to 4% hydroquinone for maintenance. I use glycolic peels, low-energy lasers, and tranexamic acid if the melasma is severe, and they have no contraindications. A combination approach really achieves the best results, and counseling is key.”
Dr. Ortiz disclosed having financial relationships with numerous pharmaceutical and device companies. She is also cochair of MOA.
When establishing a treatment plan for patients with melasma, counseling them about realistic expectations is key.
“It’s important that they understand that this is a chronic condition, so it does require long-term maintenance therapy,” Arisa E. Ortiz, MD, said at the virtual annual Masters of Aesthetics Symposium. “We can improve melasma, but it’s difficult to cure melasma.”
While hydroquinone and other bleaching agents are typical treatment mainstays, chemical peels with glycolic acid, trichloroacetic acid, and salicylic acid can benefit some individuals. “For chemical peels, I really like glycolic acid peels because there is no downtime; it peels at the microscopic level,” said Dr. Ortiz, who is director of laser and cosmetic dermatology at the University of California, San Diego. “This is something they may need to repeat monthly, and having a week of peeling may be difficult to go through every month.”
Other common melasma treatments include lasers, intense pulsed light (IPL), and oral medications. “I personally am not impressed with microdermabrasion for melasma, so I don’t use that very much,” she said. “With laser treatment, you want to make sure you’re using low-energy lasers so that it doesn’t exacerbate or make them relapse or rebound.”
While hydroquinone is a mainstay of therapy, “you can’t use it chronically because of the risk of ochronosis (permanent darkening), so you do need to take drug holidays,” Dr. Ortiz said. “During those drug holidays, you want to make sure patients have a nonhydroquinone bleaching agent so that they don’t flare.” Options include lignin peroxidase, oligopeptide, Lytera, Melaplex, 4-n-butylresorcinol, Cysteamine cream, tranexamic acid, and oral antioxidants.
In a study sponsored by SkinMedica, investigators conducted a randomized, double-blind, half-face study in females with moderate to severe facial hyperpigmentation to assess the efficacy and tolerability of three new skin brightener formulations containing SMA-432, a prostaglandin E2 inhibitor, compared with topical 4% hydroquinone (J Drugs Dermatol 2012 Dec;11[12]:1478-82). They found that the nonhydroquinone skin formulations were better tolerated and were just as effective as 4% hydroquinone.
In a separate unpublished study of 22 females, investigators assessed the efficacy of the U.SK Advanced Defense Booster, which contains ferulic acid, maslinic acid, peptides, and olive leaf extract. They observed that 98% of patients saw improvement after 28 days of treatment.
When it comes to using lasers for melasma treatment, low-energy devices provide the best outcomes. “I prefer using something like the 1927-nm fractional diode lasers at 3.75% density, really low densities because there’s less risk for rebound,” Dr. Ortiz said. “They also enhance skin permeability for the use of topicals.”
In an observational study of 27 female patients with refractory melasma, Arielle Kauvar, MD, director of New York Laser & Skin Care, combined microdermabrasion with the Q-switched Nd:YAG (Lasers in Surgery and Medicine 2012; 44:117-24). “The settings she used were very low fluence, so there was no clinical endpoint or no whitening,” Dr. Ortiz said. Specifically, she used a laser at 1.6-2 J/cm2 with a 5- or 6-mm spot size immediately following microdermabrasion for 4 weeks. “She got a good improvement using a skin care regimen of sunscreen, hydroquinone, and tretinoin or vitamin C,” she said. “Remission lasted at least 6 months.”
In a study presented at the 2019 annual meeting of the America Society for Laser Medicine and Surgery, Dr. Ortiz and Tanya Greywal, MD, of the University of California, San Diego, used three passes of the 10764-nm Nd:YAG laser to treat 10 subjects with melasma skin types 2-5. The device has a 650-microsecond pulse duration, a 6-mm spot size, and an energy mode of 11-14 J/cm3. “There was no downtime with these patients, and they saw a mean improvement of 26%-50% as early as 3 weeks,” she said. “Patients did require multiple treatments to see adequate resolution, but no anesthesia or numbing cream was required. This is a good option for patients who need chronic maintenance treatment.”
Topicals also play a key role following the laser treatment of melasma. Dr. Ortiz characterized clobetasol as “kind of like the magic ointment.” She uses one application immediately post procedure “whenever I’m worried about a patient having postinflammatory hyperpigmentation or if I don’t want melasma patients to rebound. It can help reduce swelling and inflammation to decrease the risk of postinflammatory hyperpigmentation.”
Researchers have discovered that there is a vascular component to melasma. Paul M. Friedman, MD, of the Dermatology and Laser Surgery Center, Houston, and his colleagues used spectrocolorimetry to detect an underlying prominent vascular component in 11 patients with melasma (Lasers Surg Med 2017 Jan;49[1]:20-6). They determined that melasma lesions exhibiting subtle or subclinical telangiectatic erythema may be improved by combined vascular-targeted laser therapy together with fractional low-powered diode laser therapy. “A parallel improvement in telangiectatic erythema suggests a relationship between the underlying vasculature and hyperpigmentation,” said Dr. Ortiz, who was not affiliated with the study. “So, patients who have a vascular component to their melasma actually can get improved efficacy.”
Another strategy for melasma patients involves oral treatment with Polypodium leucotomos extract (PLE), a fern from the Polypodiaceae family with antioxidant properties that has been shown to be photoprotective against UVA and UVB radiation. “I like to think of it as an internal sunscreen,” Dr. Ortiz said. “It does not replace your external sunscreen, but it adds extra protection. It has been shown to significantly reduce the severity of sunburn and decrease the risk of UV radiation–induced skin cancer, as well as prevent skin aging.” The purported mechanism of action includes decreasing UV-mediated oxidative damage to DNA, enhancing the activity of endogenous antioxidant systems, increasing the minimal erythema dose, blocking UV radiation–induced cyclooxygenase-2 expression, reducing UV-induced immune suppression, and promoting p53 suppressor gene expression.
In a pilot placebo-controlled study of melasma patients on their normal regimen of hydroquinone and sunscreen, 40 Asian patients with melasma were randomized to receive either oral PLE supplementation or placebo for 12 weeks (J Clin Aesthet Dermatol 2018 Mar;11[3]:14-9). They found that PLE significantly improved and accelerated the outcome reached with hydroquinone and sunscreen from the first month of treatment, compared with placebo.
Dr. Ortiz next discussed the role of oral tranexamic acid, an antifibrinolytic, procoagulant agent that is approved by the Food and Drug Administration for the treatment of menorrhagia and for prevention of hemorrhage in patients with hemophilia undergoing tooth extractions. “It is a synthetic lysine derivative that inhibits plasminogen activation by blocking lysine-binding sites on the plasminogen molecule, and it’s a game changer for melasma treatment,” she said. “One of the side effects is that it inhibits melanogenesis and neovascularization. It’s been effective for melasma, but its use is limited by the risk for thromboembolism. It’s a slight increased risk, something patients should be aware of, but not something that should scare us away from prescribing it.”
In a study of 561 patients with melasma, 90% improved after a median treatment duration of 4 months, and only 7% had side effects (J Am Acad Dermatol 2016;75:385-92). The most common side effects were abdominal bloating and pain. One patient developed a DVT during treatment, but that person was found to have a protein S deficiency.
The daily dosing of tranexamic acid for menorrhagia is 3,900 mg daily, while the dose for melasma has ranged from 500 mg-1,500 mg per day, Dr. Ortiz said. It’s available as a 650-mg pill in the United States. “I prescribe 325 mg twice a day, but studies have shown that 650 mg once a day is just as effective,” she said.
Prior to prescribing tranexamic acid, Dr. Ortiz does not order labs, but she performs an extensive history of present illness. She does not prescribe it in patients with an increased risk of clotting, including people who smoke and those who take oral contraceptives or are on hormone supplementation. Use is also contraindicated in people with a current malignancy, those with a history of stroke or DVT, and those who have any clotting disorder.
She concluded her presentation by noting that she favors a combination approach to treating melasma patients that starts with a broad spectrum sunscreen and PLE. “For bleaching, I like to use 12% hydroquinone with 6% kojic acid in VersaBase,” she said. “Once I get them in better control, then I switch them to 4% hydroquinone for maintenance. I use glycolic peels, low-energy lasers, and tranexamic acid if the melasma is severe, and they have no contraindications. A combination approach really achieves the best results, and counseling is key.”
Dr. Ortiz disclosed having financial relationships with numerous pharmaceutical and device companies. She is also cochair of MOA.
When establishing a treatment plan for patients with melasma, counseling them about realistic expectations is key.
“It’s important that they understand that this is a chronic condition, so it does require long-term maintenance therapy,” Arisa E. Ortiz, MD, said at the virtual annual Masters of Aesthetics Symposium. “We can improve melasma, but it’s difficult to cure melasma.”
While hydroquinone and other bleaching agents are typical treatment mainstays, chemical peels with glycolic acid, trichloroacetic acid, and salicylic acid can benefit some individuals. “For chemical peels, I really like glycolic acid peels because there is no downtime; it peels at the microscopic level,” said Dr. Ortiz, who is director of laser and cosmetic dermatology at the University of California, San Diego. “This is something they may need to repeat monthly, and having a week of peeling may be difficult to go through every month.”
Other common melasma treatments include lasers, intense pulsed light (IPL), and oral medications. “I personally am not impressed with microdermabrasion for melasma, so I don’t use that very much,” she said. “With laser treatment, you want to make sure you’re using low-energy lasers so that it doesn’t exacerbate or make them relapse or rebound.”
While hydroquinone is a mainstay of therapy, “you can’t use it chronically because of the risk of ochronosis (permanent darkening), so you do need to take drug holidays,” Dr. Ortiz said. “During those drug holidays, you want to make sure patients have a nonhydroquinone bleaching agent so that they don’t flare.” Options include lignin peroxidase, oligopeptide, Lytera, Melaplex, 4-n-butylresorcinol, Cysteamine cream, tranexamic acid, and oral antioxidants.
In a study sponsored by SkinMedica, investigators conducted a randomized, double-blind, half-face study in females with moderate to severe facial hyperpigmentation to assess the efficacy and tolerability of three new skin brightener formulations containing SMA-432, a prostaglandin E2 inhibitor, compared with topical 4% hydroquinone (J Drugs Dermatol 2012 Dec;11[12]:1478-82). They found that the nonhydroquinone skin formulations were better tolerated and were just as effective as 4% hydroquinone.
In a separate unpublished study of 22 females, investigators assessed the efficacy of the U.SK Advanced Defense Booster, which contains ferulic acid, maslinic acid, peptides, and olive leaf extract. They observed that 98% of patients saw improvement after 28 days of treatment.
When it comes to using lasers for melasma treatment, low-energy devices provide the best outcomes. “I prefer using something like the 1927-nm fractional diode lasers at 3.75% density, really low densities because there’s less risk for rebound,” Dr. Ortiz said. “They also enhance skin permeability for the use of topicals.”
In an observational study of 27 female patients with refractory melasma, Arielle Kauvar, MD, director of New York Laser & Skin Care, combined microdermabrasion with the Q-switched Nd:YAG (Lasers in Surgery and Medicine 2012; 44:117-24). “The settings she used were very low fluence, so there was no clinical endpoint or no whitening,” Dr. Ortiz said. Specifically, she used a laser at 1.6-2 J/cm2 with a 5- or 6-mm spot size immediately following microdermabrasion for 4 weeks. “She got a good improvement using a skin care regimen of sunscreen, hydroquinone, and tretinoin or vitamin C,” she said. “Remission lasted at least 6 months.”
In a study presented at the 2019 annual meeting of the America Society for Laser Medicine and Surgery, Dr. Ortiz and Tanya Greywal, MD, of the University of California, San Diego, used three passes of the 10764-nm Nd:YAG laser to treat 10 subjects with melasma skin types 2-5. The device has a 650-microsecond pulse duration, a 6-mm spot size, and an energy mode of 11-14 J/cm3. “There was no downtime with these patients, and they saw a mean improvement of 26%-50% as early as 3 weeks,” she said. “Patients did require multiple treatments to see adequate resolution, but no anesthesia or numbing cream was required. This is a good option for patients who need chronic maintenance treatment.”
Topicals also play a key role following the laser treatment of melasma. Dr. Ortiz characterized clobetasol as “kind of like the magic ointment.” She uses one application immediately post procedure “whenever I’m worried about a patient having postinflammatory hyperpigmentation or if I don’t want melasma patients to rebound. It can help reduce swelling and inflammation to decrease the risk of postinflammatory hyperpigmentation.”
Researchers have discovered that there is a vascular component to melasma. Paul M. Friedman, MD, of the Dermatology and Laser Surgery Center, Houston, and his colleagues used spectrocolorimetry to detect an underlying prominent vascular component in 11 patients with melasma (Lasers Surg Med 2017 Jan;49[1]:20-6). They determined that melasma lesions exhibiting subtle or subclinical telangiectatic erythema may be improved by combined vascular-targeted laser therapy together with fractional low-powered diode laser therapy. “A parallel improvement in telangiectatic erythema suggests a relationship between the underlying vasculature and hyperpigmentation,” said Dr. Ortiz, who was not affiliated with the study. “So, patients who have a vascular component to their melasma actually can get improved efficacy.”
Another strategy for melasma patients involves oral treatment with Polypodium leucotomos extract (PLE), a fern from the Polypodiaceae family with antioxidant properties that has been shown to be photoprotective against UVA and UVB radiation. “I like to think of it as an internal sunscreen,” Dr. Ortiz said. “It does not replace your external sunscreen, but it adds extra protection. It has been shown to significantly reduce the severity of sunburn and decrease the risk of UV radiation–induced skin cancer, as well as prevent skin aging.” The purported mechanism of action includes decreasing UV-mediated oxidative damage to DNA, enhancing the activity of endogenous antioxidant systems, increasing the minimal erythema dose, blocking UV radiation–induced cyclooxygenase-2 expression, reducing UV-induced immune suppression, and promoting p53 suppressor gene expression.
In a pilot placebo-controlled study of melasma patients on their normal regimen of hydroquinone and sunscreen, 40 Asian patients with melasma were randomized to receive either oral PLE supplementation or placebo for 12 weeks (J Clin Aesthet Dermatol 2018 Mar;11[3]:14-9). They found that PLE significantly improved and accelerated the outcome reached with hydroquinone and sunscreen from the first month of treatment, compared with placebo.
Dr. Ortiz next discussed the role of oral tranexamic acid, an antifibrinolytic, procoagulant agent that is approved by the Food and Drug Administration for the treatment of menorrhagia and for prevention of hemorrhage in patients with hemophilia undergoing tooth extractions. “It is a synthetic lysine derivative that inhibits plasminogen activation by blocking lysine-binding sites on the plasminogen molecule, and it’s a game changer for melasma treatment,” she said. “One of the side effects is that it inhibits melanogenesis and neovascularization. It’s been effective for melasma, but its use is limited by the risk for thromboembolism. It’s a slight increased risk, something patients should be aware of, but not something that should scare us away from prescribing it.”
In a study of 561 patients with melasma, 90% improved after a median treatment duration of 4 months, and only 7% had side effects (J Am Acad Dermatol 2016;75:385-92). The most common side effects were abdominal bloating and pain. One patient developed a DVT during treatment, but that person was found to have a protein S deficiency.
The daily dosing of tranexamic acid for menorrhagia is 3,900 mg daily, while the dose for melasma has ranged from 500 mg-1,500 mg per day, Dr. Ortiz said. It’s available as a 650-mg pill in the United States. “I prescribe 325 mg twice a day, but studies have shown that 650 mg once a day is just as effective,” she said.
Prior to prescribing tranexamic acid, Dr. Ortiz does not order labs, but she performs an extensive history of present illness. She does not prescribe it in patients with an increased risk of clotting, including people who smoke and those who take oral contraceptives or are on hormone supplementation. Use is also contraindicated in people with a current malignancy, those with a history of stroke or DVT, and those who have any clotting disorder.
She concluded her presentation by noting that she favors a combination approach to treating melasma patients that starts with a broad spectrum sunscreen and PLE. “For bleaching, I like to use 12% hydroquinone with 6% kojic acid in VersaBase,” she said. “Once I get them in better control, then I switch them to 4% hydroquinone for maintenance. I use glycolic peels, low-energy lasers, and tranexamic acid if the melasma is severe, and they have no contraindications. A combination approach really achieves the best results, and counseling is key.”
Dr. Ortiz disclosed having financial relationships with numerous pharmaceutical and device companies. She is also cochair of MOA.
EXPERT ANALYSIS FROM MOA 2020
Bullae and Hyperpigmented Patches on the Legs
The Diagnosis: Lichen Planus Pemphigoides
A skin biopsy from the right thigh demonstrated subepidermal blisters containing neutrophils (Figure 1). Direct immunofluorescence revealed linear basement membrane zone staining with C3 and trace staining with IgG (Figure 2), supporting a diagnosis of lichen planus pemphigoides (LPP). Oral prednisone—starting at 60 mg daily and tapered to 40 mg for a week, 20 mg for a week, then 10 mg for a month—along with triamcinolone ointment 0.1% to affected areas led to improvement. Hydrochlorothiazide and UV light therapy were discontinued. Doxycycline 100 mg twice daily and nicotinamide 500 mg twice daily prescribed as adjunctive therapy also led to improvement. The patient achieved remission with doxycycline and was doing well without prednisone; however, he experienced a flare of his disease about 6 months later and was started on mycophenolate mofetil 1 g twice daily after clearance from his gastroenterologist, given his history of hepatitis B. He has been doing well since starting mycophenolate mofetil.
Lichen planus pemphigoides is a rare autoimmune bullous dermatosis with features of both lichen planus and bullous pemphigoid.1 Violaceous papules and tense bullae may be superimposed or arise independently. The chest, abdomen, back, and upper and lower extremities typically are involved.2 Oral mucosal involvement with white reticular streaks or erosions and nail involvement have been reported.2 Histopathologic and immunologic findings establish the diagnosis. Lichen planus pemphigoides is associated with subepidermal bullae and linear deposits of IgG and C3 on the basement membrane zone.1 Autoantibodies to bullous pemphigoid (BP) antigens BP180 and BP230 are associated with LPP.3 The pathogenesis of LPP remains unclear, but there are associations with chronic diseases, medications, and certain therapies.1,4-6 Several case reports have linked LPP to chronic viral hepatitis infections, as well as malignant tumors of the skin, mucosa, and gastrointestinal tract.2 Lichen planus pemphigoides has been reported in a patient on entecavir for hepatitis B as well as in a patient treated for hepatitis C with interferon and ribavirin.1 Lichen planus pemphigoides has been described in patients treated with the angiotensin-converting enzyme inhibitors enalapril, captopril, and ramipril.4,5,7 UV phototherapy also has been associated with the development of LPP.6 Hydrochlorothiazide previously has been reported as a cause of drug-induced lichen planus.8 A PubMed search of articles indexed for MEDLINE using the terms lichen planus pemphigoides and hydrochlorothiazide revealed no reports of hydrochlorothiazide-induced LPP.
Lichen planus pemphigoides demonstrates overlap with other blistering dermatoses, such as BP, bullous lupus erythematosus, and bullous lichen planus. Although histologically and immunologically similar to BP, LPP can be differentiated clinically by the presence of violaceous papules or plaques typical of lichen planus.9 Bullous pemphigoid is more common in individuals older than 70 years, whereas LPP tends to occur in middle-aged adults.2 Bullous lupus erythematosus usually is associated with manifestations of systemic lupus erythematosus and autoantibodies to collagen type VII.10 Salt-split skin studies demonstrate immunofluorescence on the dermal side of the split. Individuals affected by bullous lupus erythematosus typically have a history of photosensitivity.10 Blisters in LPP may form de novo from unaffected skin, whereas the bullae in bullous lichen planus are limited to existing lichenoid papules.9 The autoantibodies typical of LPP are absent in bullous lichen planus. Lichen planus actinicus is a variant of lichen planus that presents with annular, dyschromic, or violaceous plaques in a photodistributed pattern without bullous lesions.9
Lichen planus pemphigoides most commonly is treated with systemic corticosteroids. Topical steroids, dapsone, erythromycin, tetracycline and nicotinamide, azathioprine, and mycophenolate mofetil have been reported as adjuncts to systemic steroid therapy.2,11 Most reports describe treatment success with resolution of blistering lesions.
- Jang SH, Yun SJ, Lee SC, et al. Lichen planus pemphigoides associated with chronic hepatitis B virus infection. Clin Exp Dermatol. 2015;40:868-871.
- Zaraa I, Mahfoudh A, Sellami MK, et al. Lichen planus pemphigoides: four new cases and a review of the literature. Int J Dermatol. 2013;52:406-412.
- Harting MS, Hsu S. Lichen planus pemphigoides: a case report and review of the literature. Dermatol Online J. 2006;12:10.
- Onprasert W, Chanprapaph K. Lichen planus pemphigoides induced by enalapril: a case report and a review of literature. Case Rep Dermatol. 2017;9:217-224.
- Ben Salem C, Chengeul L, Ghariani N, et al. Captopril-induced lichen planus pemphigoides. Pharmacoepidemiol Drug Saf. 2008;17:722-724.
- Kuramoto N, Kishimoto S, Shibagaki R, et al. PUVA-induced lichen planus pemphigoides. Br J Dermatol. 2000;142:509-512.
- Zhu YI, Fitzpatrick JE, Kornfield BW. Lichen planus pemphigoides associated with Ramipril. Int J Dermatol. 2006;45:1453-1455.
- Sin B, Miller M, Chew E. Hydrochlorothiazide induced lichen planus in the emergency department. J Pharm Pract. 2017;30:266-269.
- Weston G, Payette M. Update on lichen planus and its clinical variants. Int J Women Dermatol. 2015;1:140-149.
- Contestable JJ, Edhegard KD, Meyerle JH. Bullous systemic lupus erythematosus: a review and update to diagnosis and treatment. Am J Clin Dermatol. 2014;15:517-524.
- Fivenson DP, Kimbrough TL. Lichen planus pemphigoides: combination therapy with tetracycline and nicotinamide. J Am Acad Dermatol. 1997;36:638-640.
The Diagnosis: Lichen Planus Pemphigoides
A skin biopsy from the right thigh demonstrated subepidermal blisters containing neutrophils (Figure 1). Direct immunofluorescence revealed linear basement membrane zone staining with C3 and trace staining with IgG (Figure 2), supporting a diagnosis of lichen planus pemphigoides (LPP). Oral prednisone—starting at 60 mg daily and tapered to 40 mg for a week, 20 mg for a week, then 10 mg for a month—along with triamcinolone ointment 0.1% to affected areas led to improvement. Hydrochlorothiazide and UV light therapy were discontinued. Doxycycline 100 mg twice daily and nicotinamide 500 mg twice daily prescribed as adjunctive therapy also led to improvement. The patient achieved remission with doxycycline and was doing well without prednisone; however, he experienced a flare of his disease about 6 months later and was started on mycophenolate mofetil 1 g twice daily after clearance from his gastroenterologist, given his history of hepatitis B. He has been doing well since starting mycophenolate mofetil.
Lichen planus pemphigoides is a rare autoimmune bullous dermatosis with features of both lichen planus and bullous pemphigoid.1 Violaceous papules and tense bullae may be superimposed or arise independently. The chest, abdomen, back, and upper and lower extremities typically are involved.2 Oral mucosal involvement with white reticular streaks or erosions and nail involvement have been reported.2 Histopathologic and immunologic findings establish the diagnosis. Lichen planus pemphigoides is associated with subepidermal bullae and linear deposits of IgG and C3 on the basement membrane zone.1 Autoantibodies to bullous pemphigoid (BP) antigens BP180 and BP230 are associated with LPP.3 The pathogenesis of LPP remains unclear, but there are associations with chronic diseases, medications, and certain therapies.1,4-6 Several case reports have linked LPP to chronic viral hepatitis infections, as well as malignant tumors of the skin, mucosa, and gastrointestinal tract.2 Lichen planus pemphigoides has been reported in a patient on entecavir for hepatitis B as well as in a patient treated for hepatitis C with interferon and ribavirin.1 Lichen planus pemphigoides has been described in patients treated with the angiotensin-converting enzyme inhibitors enalapril, captopril, and ramipril.4,5,7 UV phototherapy also has been associated with the development of LPP.6 Hydrochlorothiazide previously has been reported as a cause of drug-induced lichen planus.8 A PubMed search of articles indexed for MEDLINE using the terms lichen planus pemphigoides and hydrochlorothiazide revealed no reports of hydrochlorothiazide-induced LPP.
Lichen planus pemphigoides demonstrates overlap with other blistering dermatoses, such as BP, bullous lupus erythematosus, and bullous lichen planus. Although histologically and immunologically similar to BP, LPP can be differentiated clinically by the presence of violaceous papules or plaques typical of lichen planus.9 Bullous pemphigoid is more common in individuals older than 70 years, whereas LPP tends to occur in middle-aged adults.2 Bullous lupus erythematosus usually is associated with manifestations of systemic lupus erythematosus and autoantibodies to collagen type VII.10 Salt-split skin studies demonstrate immunofluorescence on the dermal side of the split. Individuals affected by bullous lupus erythematosus typically have a history of photosensitivity.10 Blisters in LPP may form de novo from unaffected skin, whereas the bullae in bullous lichen planus are limited to existing lichenoid papules.9 The autoantibodies typical of LPP are absent in bullous lichen planus. Lichen planus actinicus is a variant of lichen planus that presents with annular, dyschromic, or violaceous plaques in a photodistributed pattern without bullous lesions.9
Lichen planus pemphigoides most commonly is treated with systemic corticosteroids. Topical steroids, dapsone, erythromycin, tetracycline and nicotinamide, azathioprine, and mycophenolate mofetil have been reported as adjuncts to systemic steroid therapy.2,11 Most reports describe treatment success with resolution of blistering lesions.
The Diagnosis: Lichen Planus Pemphigoides
A skin biopsy from the right thigh demonstrated subepidermal blisters containing neutrophils (Figure 1). Direct immunofluorescence revealed linear basement membrane zone staining with C3 and trace staining with IgG (Figure 2), supporting a diagnosis of lichen planus pemphigoides (LPP). Oral prednisone—starting at 60 mg daily and tapered to 40 mg for a week, 20 mg for a week, then 10 mg for a month—along with triamcinolone ointment 0.1% to affected areas led to improvement. Hydrochlorothiazide and UV light therapy were discontinued. Doxycycline 100 mg twice daily and nicotinamide 500 mg twice daily prescribed as adjunctive therapy also led to improvement. The patient achieved remission with doxycycline and was doing well without prednisone; however, he experienced a flare of his disease about 6 months later and was started on mycophenolate mofetil 1 g twice daily after clearance from his gastroenterologist, given his history of hepatitis B. He has been doing well since starting mycophenolate mofetil.
Lichen planus pemphigoides is a rare autoimmune bullous dermatosis with features of both lichen planus and bullous pemphigoid.1 Violaceous papules and tense bullae may be superimposed or arise independently. The chest, abdomen, back, and upper and lower extremities typically are involved.2 Oral mucosal involvement with white reticular streaks or erosions and nail involvement have been reported.2 Histopathologic and immunologic findings establish the diagnosis. Lichen planus pemphigoides is associated with subepidermal bullae and linear deposits of IgG and C3 on the basement membrane zone.1 Autoantibodies to bullous pemphigoid (BP) antigens BP180 and BP230 are associated with LPP.3 The pathogenesis of LPP remains unclear, but there are associations with chronic diseases, medications, and certain therapies.1,4-6 Several case reports have linked LPP to chronic viral hepatitis infections, as well as malignant tumors of the skin, mucosa, and gastrointestinal tract.2 Lichen planus pemphigoides has been reported in a patient on entecavir for hepatitis B as well as in a patient treated for hepatitis C with interferon and ribavirin.1 Lichen planus pemphigoides has been described in patients treated with the angiotensin-converting enzyme inhibitors enalapril, captopril, and ramipril.4,5,7 UV phototherapy also has been associated with the development of LPP.6 Hydrochlorothiazide previously has been reported as a cause of drug-induced lichen planus.8 A PubMed search of articles indexed for MEDLINE using the terms lichen planus pemphigoides and hydrochlorothiazide revealed no reports of hydrochlorothiazide-induced LPP.
Lichen planus pemphigoides demonstrates overlap with other blistering dermatoses, such as BP, bullous lupus erythematosus, and bullous lichen planus. Although histologically and immunologically similar to BP, LPP can be differentiated clinically by the presence of violaceous papules or plaques typical of lichen planus.9 Bullous pemphigoid is more common in individuals older than 70 years, whereas LPP tends to occur in middle-aged adults.2 Bullous lupus erythematosus usually is associated with manifestations of systemic lupus erythematosus and autoantibodies to collagen type VII.10 Salt-split skin studies demonstrate immunofluorescence on the dermal side of the split. Individuals affected by bullous lupus erythematosus typically have a history of photosensitivity.10 Blisters in LPP may form de novo from unaffected skin, whereas the bullae in bullous lichen planus are limited to existing lichenoid papules.9 The autoantibodies typical of LPP are absent in bullous lichen planus. Lichen planus actinicus is a variant of lichen planus that presents with annular, dyschromic, or violaceous plaques in a photodistributed pattern without bullous lesions.9
Lichen planus pemphigoides most commonly is treated with systemic corticosteroids. Topical steroids, dapsone, erythromycin, tetracycline and nicotinamide, azathioprine, and mycophenolate mofetil have been reported as adjuncts to systemic steroid therapy.2,11 Most reports describe treatment success with resolution of blistering lesions.
- Jang SH, Yun SJ, Lee SC, et al. Lichen planus pemphigoides associated with chronic hepatitis B virus infection. Clin Exp Dermatol. 2015;40:868-871.
- Zaraa I, Mahfoudh A, Sellami MK, et al. Lichen planus pemphigoides: four new cases and a review of the literature. Int J Dermatol. 2013;52:406-412.
- Harting MS, Hsu S. Lichen planus pemphigoides: a case report and review of the literature. Dermatol Online J. 2006;12:10.
- Onprasert W, Chanprapaph K. Lichen planus pemphigoides induced by enalapril: a case report and a review of literature. Case Rep Dermatol. 2017;9:217-224.
- Ben Salem C, Chengeul L, Ghariani N, et al. Captopril-induced lichen planus pemphigoides. Pharmacoepidemiol Drug Saf. 2008;17:722-724.
- Kuramoto N, Kishimoto S, Shibagaki R, et al. PUVA-induced lichen planus pemphigoides. Br J Dermatol. 2000;142:509-512.
- Zhu YI, Fitzpatrick JE, Kornfield BW. Lichen planus pemphigoides associated with Ramipril. Int J Dermatol. 2006;45:1453-1455.
- Sin B, Miller M, Chew E. Hydrochlorothiazide induced lichen planus in the emergency department. J Pharm Pract. 2017;30:266-269.
- Weston G, Payette M. Update on lichen planus and its clinical variants. Int J Women Dermatol. 2015;1:140-149.
- Contestable JJ, Edhegard KD, Meyerle JH. Bullous systemic lupus erythematosus: a review and update to diagnosis and treatment. Am J Clin Dermatol. 2014;15:517-524.
- Fivenson DP, Kimbrough TL. Lichen planus pemphigoides: combination therapy with tetracycline and nicotinamide. J Am Acad Dermatol. 1997;36:638-640.
- Jang SH, Yun SJ, Lee SC, et al. Lichen planus pemphigoides associated with chronic hepatitis B virus infection. Clin Exp Dermatol. 2015;40:868-871.
- Zaraa I, Mahfoudh A, Sellami MK, et al. Lichen planus pemphigoides: four new cases and a review of the literature. Int J Dermatol. 2013;52:406-412.
- Harting MS, Hsu S. Lichen planus pemphigoides: a case report and review of the literature. Dermatol Online J. 2006;12:10.
- Onprasert W, Chanprapaph K. Lichen planus pemphigoides induced by enalapril: a case report and a review of literature. Case Rep Dermatol. 2017;9:217-224.
- Ben Salem C, Chengeul L, Ghariani N, et al. Captopril-induced lichen planus pemphigoides. Pharmacoepidemiol Drug Saf. 2008;17:722-724.
- Kuramoto N, Kishimoto S, Shibagaki R, et al. PUVA-induced lichen planus pemphigoides. Br J Dermatol. 2000;142:509-512.
- Zhu YI, Fitzpatrick JE, Kornfield BW. Lichen planus pemphigoides associated with Ramipril. Int J Dermatol. 2006;45:1453-1455.
- Sin B, Miller M, Chew E. Hydrochlorothiazide induced lichen planus in the emergency department. J Pharm Pract. 2017;30:266-269.
- Weston G, Payette M. Update on lichen planus and its clinical variants. Int J Women Dermatol. 2015;1:140-149.
- Contestable JJ, Edhegard KD, Meyerle JH. Bullous systemic lupus erythematosus: a review and update to diagnosis and treatment. Am J Clin Dermatol. 2014;15:517-524.
- Fivenson DP, Kimbrough TL. Lichen planus pemphigoides: combination therapy with tetracycline and nicotinamide. J Am Acad Dermatol. 1997;36:638-640.
A 50-year-old man presented with a pruritic bullous dermatosis on the lower legs, arms, and back of 1 month’s duration. He had an 8-year history of lichen planus, and the lesions recently had worsened despite the addition of UVB phototherapy. His medical history was remarkable for hepatitis B treated with entecavir and the addition of hydrochlorothiazide for essential hypertension 2 weeks prior to the dramatic worsening of the rash. Physical examination revealed multiple bullae on the lower legs associated with violaceous and hyperpigmented papules and patches. He also had violaceous papules on the lower back and eroded lesions on the oral mucosa. Shave biopsies were obtained from the right thigh and mid back, and histopathologic analysis was performed for both routine histology and direct immunofluorescence.
Hyperpigmentation of the Tongue
The Diagnosis: Addison Disease in the Context of Polyglandular Autoimmune Syndrome Type 2
The patient’s hormone levels as well as distinct clinical features led to a diagnosis of Addison disease in the context of polyglandular autoimmune syndrome type 2 (PAS-2). Approximately 50% of PAS-2 cases are familiar, and different modes of inheritance—autosomal recessive, autosomal dominant, and polygenic—have been reported. Women are affected up to 3 times more often than men.1,2 The age of onset ranges from infancy to late adulthood, with most cases occurring in early adulthood. Primary adrenal insufficiency (Addison disease) is the principal manifestation of PAS-2. It appears in approximately 50% of patients, occurring simultaneously with autoimmune thyroid disease or diabetes mellitus in 20% of patients and following them in 30% of patients.1,2 Autoimmune thyroid diseases such as chronic autoimmune thyroiditis and occasionally Graves disease as well as type 1 diabetes mellitus also are common. Polyglandular autoimmune syndrome type 2 with primary adrenal insufficiency and autoimmune thyroid disease was formerly referred to as Schmidt syndrome.3 It must be differentiated from polyglandular autoimmune syndrome type 1, a rare condition that also is referred to as autoimmune polyendocrinopathycandidiasis-ectodermal dystrophy syndrome.1,3 As with any other cause of adrenal insufficiency, the treatment involves hormone replacement therapy up to normal levels and then tapering according to stress levels (ie, surgery or infections that require a dose increase). Our patient was diagnosed according to hormone levels and clinical features and was started on 30 mg daily of hydrocortisone and 50 μg daily of levothyroxine. No improvement in her condition was noted after 6 months of treatment. The patient is still under yearly follow-up, and the mucous hyperpigmentation faded approximately 6 months after hormonal homeostasis was achieved.
Peutz-Jeghers syndrome is inherited in an autosomal-dominant fashion. It is characterized by multiple hamartomatous polyps in the gastrointestinal tract, mucocutaneous pigmentation, and an increased risk for gastrointestinal and nongastrointestinal cancer. Mucocutaneous pigmented macules most commonly occur on the lips and perioral region, buccal mucosa, and the palms and soles. However, mucocutaneous pigmentation usually occurs during the first 1 to 2 years of life, increases in size and number over the ensuing years, and usually fades after puberty.4
Laugier-Hunziker syndrome is an acquired benign disorder presenting in adults with lentigines on the lips and buccal mucosa. It frequently is accompaniedby longitudinal melanonychia, macular pigmentation of the genitals, and involvement of the palms and soles. The diagnosis of Laugier-Hunziker syndrome is one of exclusion and is made after ruling out other causes of oral and labial hyperpigmentation, including physiologic pigmentation seen in darker-skinned individuals as well as inherited diseases associated with lentiginosis, requiring complete physical examination, endoscopy, and colonscopy.5
A wide variety of drugs and chemicals can lead to diffuse cutaneous hyperpigmentation. Increased production of melanin and/or the deposition of drug complexes or metals in the dermis is responsible for the skin discoloration. Drugs that most often cause hyperpigmentation on mucosal surfaces are hydroxychloroquine, minocycline, nicotine, silver, and some chemotherapy agents. The hyperpigmentation usually resolves with discontinuation of the offending agent, but the course may be prolonged over months to years.6
Changes in the skin and subcutaneous tissue occur in patients with Cushing syndrome. Hyperpigmentation is induced by increased secretion of adrenocorticotropic hormone, not cortisol, and occurs most often in patients with the ectopic adrenocorticotropic hormone syndrome. Hyperpigmentation may be generalized but is more intense in areas exposed to light (eg, face, neck, dorsal aspects of the hands) or to chronic mild trauma, friction, or pressure (eg, elbows, knees, spine, knuckles). Patchy pigmentation may occur on the inner surface of the lips and the buccal mucosa along the line of dental occlusion. Acanthosis nigricans also can be present in the axillae and around the neck.7
- Ferre EM, Rose SR, Rosenzweig SD, et al. Redefined clinical features and diagnostic criteria in autoimmune polyendocrinopathycandidiasis-ectodermal dystrophy. JCI Insight. 2016;1:E88782.
- Orlova EM, Sozaeva LS, Kareva MA, et al. Expanding the phenotypic and genotypic landscape of autoimmune polyendocrine syndrome type 1. J Clin Endocrinol Metab. 2017;102:3546-3556.
- Ahonen P, Myllärniemi S, Sipilä I, et al. Clinical variation of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) in a series of 68 patients. N Engl J Med. 1990;322:1829-1836.
- Utsunomiya J, Gocho H, Miyanaga T, et al. Peutz-Jeghers syndrome: its natural course and management. Johns Hopkins Med J. 1975;136:71-82.
- Nayak RS, Kotrashetti VS, Hosmani JV. Laugier-Hunziker syndrome. J Oral Maxillofac Pathol. 2012;16:245-250.
- Krause W. Drug-induced hyperpigmentation: a systematic review. J Dtsch Dermatol Ges. 2013;11:644-651.
- Newell-Price J, Trainer P, Besser M, et al. The diagnosis and differential diagnosis of Cushing’s syndrome and pseudo-Cushing’s states. Endocr Rev. 1998;19:647-672.
The Diagnosis: Addison Disease in the Context of Polyglandular Autoimmune Syndrome Type 2
The patient’s hormone levels as well as distinct clinical features led to a diagnosis of Addison disease in the context of polyglandular autoimmune syndrome type 2 (PAS-2). Approximately 50% of PAS-2 cases are familiar, and different modes of inheritance—autosomal recessive, autosomal dominant, and polygenic—have been reported. Women are affected up to 3 times more often than men.1,2 The age of onset ranges from infancy to late adulthood, with most cases occurring in early adulthood. Primary adrenal insufficiency (Addison disease) is the principal manifestation of PAS-2. It appears in approximately 50% of patients, occurring simultaneously with autoimmune thyroid disease or diabetes mellitus in 20% of patients and following them in 30% of patients.1,2 Autoimmune thyroid diseases such as chronic autoimmune thyroiditis and occasionally Graves disease as well as type 1 diabetes mellitus also are common. Polyglandular autoimmune syndrome type 2 with primary adrenal insufficiency and autoimmune thyroid disease was formerly referred to as Schmidt syndrome.3 It must be differentiated from polyglandular autoimmune syndrome type 1, a rare condition that also is referred to as autoimmune polyendocrinopathycandidiasis-ectodermal dystrophy syndrome.1,3 As with any other cause of adrenal insufficiency, the treatment involves hormone replacement therapy up to normal levels and then tapering according to stress levels (ie, surgery or infections that require a dose increase). Our patient was diagnosed according to hormone levels and clinical features and was started on 30 mg daily of hydrocortisone and 50 μg daily of levothyroxine. No improvement in her condition was noted after 6 months of treatment. The patient is still under yearly follow-up, and the mucous hyperpigmentation faded approximately 6 months after hormonal homeostasis was achieved.
Peutz-Jeghers syndrome is inherited in an autosomal-dominant fashion. It is characterized by multiple hamartomatous polyps in the gastrointestinal tract, mucocutaneous pigmentation, and an increased risk for gastrointestinal and nongastrointestinal cancer. Mucocutaneous pigmented macules most commonly occur on the lips and perioral region, buccal mucosa, and the palms and soles. However, mucocutaneous pigmentation usually occurs during the first 1 to 2 years of life, increases in size and number over the ensuing years, and usually fades after puberty.4
Laugier-Hunziker syndrome is an acquired benign disorder presenting in adults with lentigines on the lips and buccal mucosa. It frequently is accompaniedby longitudinal melanonychia, macular pigmentation of the genitals, and involvement of the palms and soles. The diagnosis of Laugier-Hunziker syndrome is one of exclusion and is made after ruling out other causes of oral and labial hyperpigmentation, including physiologic pigmentation seen in darker-skinned individuals as well as inherited diseases associated with lentiginosis, requiring complete physical examination, endoscopy, and colonscopy.5
A wide variety of drugs and chemicals can lead to diffuse cutaneous hyperpigmentation. Increased production of melanin and/or the deposition of drug complexes or metals in the dermis is responsible for the skin discoloration. Drugs that most often cause hyperpigmentation on mucosal surfaces are hydroxychloroquine, minocycline, nicotine, silver, and some chemotherapy agents. The hyperpigmentation usually resolves with discontinuation of the offending agent, but the course may be prolonged over months to years.6
Changes in the skin and subcutaneous tissue occur in patients with Cushing syndrome. Hyperpigmentation is induced by increased secretion of adrenocorticotropic hormone, not cortisol, and occurs most often in patients with the ectopic adrenocorticotropic hormone syndrome. Hyperpigmentation may be generalized but is more intense in areas exposed to light (eg, face, neck, dorsal aspects of the hands) or to chronic mild trauma, friction, or pressure (eg, elbows, knees, spine, knuckles). Patchy pigmentation may occur on the inner surface of the lips and the buccal mucosa along the line of dental occlusion. Acanthosis nigricans also can be present in the axillae and around the neck.7
The Diagnosis: Addison Disease in the Context of Polyglandular Autoimmune Syndrome Type 2
The patient’s hormone levels as well as distinct clinical features led to a diagnosis of Addison disease in the context of polyglandular autoimmune syndrome type 2 (PAS-2). Approximately 50% of PAS-2 cases are familiar, and different modes of inheritance—autosomal recessive, autosomal dominant, and polygenic—have been reported. Women are affected up to 3 times more often than men.1,2 The age of onset ranges from infancy to late adulthood, with most cases occurring in early adulthood. Primary adrenal insufficiency (Addison disease) is the principal manifestation of PAS-2. It appears in approximately 50% of patients, occurring simultaneously with autoimmune thyroid disease or diabetes mellitus in 20% of patients and following them in 30% of patients.1,2 Autoimmune thyroid diseases such as chronic autoimmune thyroiditis and occasionally Graves disease as well as type 1 diabetes mellitus also are common. Polyglandular autoimmune syndrome type 2 with primary adrenal insufficiency and autoimmune thyroid disease was formerly referred to as Schmidt syndrome.3 It must be differentiated from polyglandular autoimmune syndrome type 1, a rare condition that also is referred to as autoimmune polyendocrinopathycandidiasis-ectodermal dystrophy syndrome.1,3 As with any other cause of adrenal insufficiency, the treatment involves hormone replacement therapy up to normal levels and then tapering according to stress levels (ie, surgery or infections that require a dose increase). Our patient was diagnosed according to hormone levels and clinical features and was started on 30 mg daily of hydrocortisone and 50 μg daily of levothyroxine. No improvement in her condition was noted after 6 months of treatment. The patient is still under yearly follow-up, and the mucous hyperpigmentation faded approximately 6 months after hormonal homeostasis was achieved.
Peutz-Jeghers syndrome is inherited in an autosomal-dominant fashion. It is characterized by multiple hamartomatous polyps in the gastrointestinal tract, mucocutaneous pigmentation, and an increased risk for gastrointestinal and nongastrointestinal cancer. Mucocutaneous pigmented macules most commonly occur on the lips and perioral region, buccal mucosa, and the palms and soles. However, mucocutaneous pigmentation usually occurs during the first 1 to 2 years of life, increases in size and number over the ensuing years, and usually fades after puberty.4
Laugier-Hunziker syndrome is an acquired benign disorder presenting in adults with lentigines on the lips and buccal mucosa. It frequently is accompaniedby longitudinal melanonychia, macular pigmentation of the genitals, and involvement of the palms and soles. The diagnosis of Laugier-Hunziker syndrome is one of exclusion and is made after ruling out other causes of oral and labial hyperpigmentation, including physiologic pigmentation seen in darker-skinned individuals as well as inherited diseases associated with lentiginosis, requiring complete physical examination, endoscopy, and colonscopy.5
A wide variety of drugs and chemicals can lead to diffuse cutaneous hyperpigmentation. Increased production of melanin and/or the deposition of drug complexes or metals in the dermis is responsible for the skin discoloration. Drugs that most often cause hyperpigmentation on mucosal surfaces are hydroxychloroquine, minocycline, nicotine, silver, and some chemotherapy agents. The hyperpigmentation usually resolves with discontinuation of the offending agent, but the course may be prolonged over months to years.6
Changes in the skin and subcutaneous tissue occur in patients with Cushing syndrome. Hyperpigmentation is induced by increased secretion of adrenocorticotropic hormone, not cortisol, and occurs most often in patients with the ectopic adrenocorticotropic hormone syndrome. Hyperpigmentation may be generalized but is more intense in areas exposed to light (eg, face, neck, dorsal aspects of the hands) or to chronic mild trauma, friction, or pressure (eg, elbows, knees, spine, knuckles). Patchy pigmentation may occur on the inner surface of the lips and the buccal mucosa along the line of dental occlusion. Acanthosis nigricans also can be present in the axillae and around the neck.7
- Ferre EM, Rose SR, Rosenzweig SD, et al. Redefined clinical features and diagnostic criteria in autoimmune polyendocrinopathycandidiasis-ectodermal dystrophy. JCI Insight. 2016;1:E88782.
- Orlova EM, Sozaeva LS, Kareva MA, et al. Expanding the phenotypic and genotypic landscape of autoimmune polyendocrine syndrome type 1. J Clin Endocrinol Metab. 2017;102:3546-3556.
- Ahonen P, Myllärniemi S, Sipilä I, et al. Clinical variation of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) in a series of 68 patients. N Engl J Med. 1990;322:1829-1836.
- Utsunomiya J, Gocho H, Miyanaga T, et al. Peutz-Jeghers syndrome: its natural course and management. Johns Hopkins Med J. 1975;136:71-82.
- Nayak RS, Kotrashetti VS, Hosmani JV. Laugier-Hunziker syndrome. J Oral Maxillofac Pathol. 2012;16:245-250.
- Krause W. Drug-induced hyperpigmentation: a systematic review. J Dtsch Dermatol Ges. 2013;11:644-651.
- Newell-Price J, Trainer P, Besser M, et al. The diagnosis and differential diagnosis of Cushing’s syndrome and pseudo-Cushing’s states. Endocr Rev. 1998;19:647-672.
- Ferre EM, Rose SR, Rosenzweig SD, et al. Redefined clinical features and diagnostic criteria in autoimmune polyendocrinopathycandidiasis-ectodermal dystrophy. JCI Insight. 2016;1:E88782.
- Orlova EM, Sozaeva LS, Kareva MA, et al. Expanding the phenotypic and genotypic landscape of autoimmune polyendocrine syndrome type 1. J Clin Endocrinol Metab. 2017;102:3546-3556.
- Ahonen P, Myllärniemi S, Sipilä I, et al. Clinical variation of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) in a series of 68 patients. N Engl J Med. 1990;322:1829-1836.
- Utsunomiya J, Gocho H, Miyanaga T, et al. Peutz-Jeghers syndrome: its natural course and management. Johns Hopkins Med J. 1975;136:71-82.
- Nayak RS, Kotrashetti VS, Hosmani JV. Laugier-Hunziker syndrome. J Oral Maxillofac Pathol. 2012;16:245-250.
- Krause W. Drug-induced hyperpigmentation: a systematic review. J Dtsch Dermatol Ges. 2013;11:644-651.
- Newell-Price J, Trainer P, Besser M, et al. The diagnosis and differential diagnosis of Cushing’s syndrome and pseudo-Cushing’s states. Endocr Rev. 1998;19:647-672.
An otherwise healthy 17-year-old adolescent girl from Spain presented with hyperpigmentation on the tongue of several weeks’ duration. She denied licking graphite pencils or pens. Physical examination revealed pigmentation in the palmar creases and a slight generalized tan. The patient denied sun exposure. Neither melanonychia nor genital hyperpigmented lesions were noted. Blood tests showed overt hypothyroidism.
Granular Parakeratosis
To the Editor:
A 46-year-old overweight woman presented with a rash in the axillae of 2 months’ duration. She did not report any additional symptoms such as pruritus or pain. She reported changing her deodorant recently from Secret Original to Secret Clinical Strength (both Procter & Gamble). Her medical history was remarkable for asthma and gastroesophageal reflux disease. Clinical examination revealed erythematous-brown, stuccolike, hyperkeratotic papules coalescing into plaques in recently shaved axillae, affecting the left axilla more than the right axilla (Figure 1). The clinical differential diagnosis included granular parakeratosis, intertrigo, Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, acanthosis nigricans, seborrheic keratoses, and irritant or allergic contact dermatitis. A punch biopsy revealed a marked compact parakeratotic horn with retention of keratohyalin granules (Figure 2). The subjacent epidermis showed some acanthosis and spongiosis with mild chronic inflammation of the dermal rim. Based on histopathology, granular parakeratosis was diagnosed.
At a subsequent visit 2 weeks later, we prescribed glycolic acid lotion 10% applied to the axillae twice daily, plus tretinoin gel 0.05% applied to the axillae each evening. She reported clearing after 1 week of therapy. She also had changed her deodorant from Secret Clinical Strength back to the usual Secret Original. The patient discontinued topical treatment after clearing of the lesions. Three weeks later, clinical examination revealed postinflammatory hyperpigmentation in the axillae, and the prior lesions had resolved (Figure 3).
Granular parakeratosis is an unusual condition most commonly presenting in middle-aged women in the axillae, with a clinical presentation of erythematous to brownish hyperkeratotic papules coalescing into plaques. Although few cases have been reported, granular parakeratosis likely is more common than has been reported. There have been reports involving the scalp, cheeks, abdomen, thighs, and other intertriginous areas including inguinal folds and the submammary region.1-4 There also is an infantile form related to diapers and zinc oxide paste.5 Although uncommon, granular parakeratosis can occur as a single papule or plaque and is termed granular parakeratotic acanthoma.6 Lesions may persist for months, spontaneously resolve and recur, and occasionally evolve into fissures and erosions due to irritation. Pruritus is a common concern. Histology of granular parakeratosis reveals hyperkeratosis with eosinophilic staining, compact parakeratosis with retention of basophilic keratohyalin granules, and vascular proliferation and ectasia.5
The cause is unknown but possibly related to irritation from rubbing, occlusion, sweating, or deodorants.5,7 Cases indicate a link to obesity. Hypotheses as to the etiology include the disruption of cornification. Normally, filaggrin maintains the keratohyaline granules in the stratum corneum during cornification. Therefore, the retention of keratohyaline granules in granular parakeratosis may be due to a defect in processing profilaggrin to filaggrin, which has been proposed based on ultrastructural and immunohistochemical studies.8
The differential diagnosis includes granular parakeratosis, intertrigo (caused by seborrheic dermatitis, candidiasis, inverse psoriasis, or erythrasma), Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, and irritant or allergic contact dermatitis. The papules may resemble seborrheic keratoses, while the plaques can be mistaken for acanthosis nigricans.
Therapeutic success has been reported with topical corticosteroids, vitamin D analogues, topical or oral retinoids, ammonium lactate, calcineurin inhibitors, topical or oral antifungals, cryotherapy, and botulinum toxin injections.3,9-11 In addition, parakeratosis has decreased in biopsies from psoriatic patients after acitretin, methotrexate, and phototherapy, which may be alternative treatments for unusually difficult or recalcitrant cases of granular parakeratosis. To minimize side effects and resolve the papules quickly, we combined 2 synergistic agents—glycolic acid and tretinoin—each with different mechanisms of action, and we observed excellent clinical response.
Granular parakeratosis is possibly related to a combination of topical products that potentiate irritation, rubbing, and occlusion of sweat. Multiple treatment modalities likely contribute to clearing, the most important being removal of any triggering topical products. Our patient’s change in deodorant may have been the inciting factor for the disease. Withdrawal of the Secret Clinical Strength deodorant prompted clearing, though topical retinoid and glycolic acid acted as facilitating therapies for timely results. A thorough history, as highlighted by this case, may help pinpoint etiologic factors. By identifying a seemingly innocuous change in hygienic routine, we were able to minimize the need for ongoing therapy.
- Graham R. Intertriginous granular parakeratosis: a case report and review of the literature. J Am Acad Dermatol. 2011;64:AB45-AB45.
- Compton AK, Jackson JM. Isotretinoin as a treatment for axillary granular parakeratosis. Cutis. 2007;80:55-56.
- Channual J, Fife DJ, Wu JJ. Axillary granular parakeratosis. Cutis. 2013;92;61, 65-66.
- Streams S, Gottwald L, Zaher A, et al. Granular parakeratosis of the scalp: a case report. J Am Acad Dermatol. 2007;56:AB81-AB81.
- James WD, Berger T, Elston D. Andrews’ Diseases of the Skin. 12th ed. Philadelphia, PA: Elsevier, Inc; 2015.
- Resnik KS, Kantor GR, DiLeonardo M. Granular parakeratotic acanthoma. Am J Dermatopathol. 2005;27:393-396.
- Naylor E, Wartman D, Telang G, et al. Granular parakeratosis secondary to postsurgical occlusion. J Am Acad Dermatol. 2008;58:AB126.
- Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. Philadelphia, PA: Elsevier, Inc; 2012.
- Baum B, Skopit S. Granular parakeratosis treatment with tacrolimus 0.1% ointment: a case presentation and discussion. J Am Osteo Coll Dermatol. 2013;26:40-41.
- Brown SK, Heilman ER. Granular parakeratosis: resolution with topical tretinoin. J Am Acad Dermatol. 2002;47:S279-S280.
- Webster CG, Resnik KS, Webster GF. Axillary granular parakeratosis: response to isotretinoin. J Am Acad Dermatol. 1997;37:789790.
To the Editor:
A 46-year-old overweight woman presented with a rash in the axillae of 2 months’ duration. She did not report any additional symptoms such as pruritus or pain. She reported changing her deodorant recently from Secret Original to Secret Clinical Strength (both Procter & Gamble). Her medical history was remarkable for asthma and gastroesophageal reflux disease. Clinical examination revealed erythematous-brown, stuccolike, hyperkeratotic papules coalescing into plaques in recently shaved axillae, affecting the left axilla more than the right axilla (Figure 1). The clinical differential diagnosis included granular parakeratosis, intertrigo, Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, acanthosis nigricans, seborrheic keratoses, and irritant or allergic contact dermatitis. A punch biopsy revealed a marked compact parakeratotic horn with retention of keratohyalin granules (Figure 2). The subjacent epidermis showed some acanthosis and spongiosis with mild chronic inflammation of the dermal rim. Based on histopathology, granular parakeratosis was diagnosed.
At a subsequent visit 2 weeks later, we prescribed glycolic acid lotion 10% applied to the axillae twice daily, plus tretinoin gel 0.05% applied to the axillae each evening. She reported clearing after 1 week of therapy. She also had changed her deodorant from Secret Clinical Strength back to the usual Secret Original. The patient discontinued topical treatment after clearing of the lesions. Three weeks later, clinical examination revealed postinflammatory hyperpigmentation in the axillae, and the prior lesions had resolved (Figure 3).
Granular parakeratosis is an unusual condition most commonly presenting in middle-aged women in the axillae, with a clinical presentation of erythematous to brownish hyperkeratotic papules coalescing into plaques. Although few cases have been reported, granular parakeratosis likely is more common than has been reported. There have been reports involving the scalp, cheeks, abdomen, thighs, and other intertriginous areas including inguinal folds and the submammary region.1-4 There also is an infantile form related to diapers and zinc oxide paste.5 Although uncommon, granular parakeratosis can occur as a single papule or plaque and is termed granular parakeratotic acanthoma.6 Lesions may persist for months, spontaneously resolve and recur, and occasionally evolve into fissures and erosions due to irritation. Pruritus is a common concern. Histology of granular parakeratosis reveals hyperkeratosis with eosinophilic staining, compact parakeratosis with retention of basophilic keratohyalin granules, and vascular proliferation and ectasia.5
The cause is unknown but possibly related to irritation from rubbing, occlusion, sweating, or deodorants.5,7 Cases indicate a link to obesity. Hypotheses as to the etiology include the disruption of cornification. Normally, filaggrin maintains the keratohyaline granules in the stratum corneum during cornification. Therefore, the retention of keratohyaline granules in granular parakeratosis may be due to a defect in processing profilaggrin to filaggrin, which has been proposed based on ultrastructural and immunohistochemical studies.8
The differential diagnosis includes granular parakeratosis, intertrigo (caused by seborrheic dermatitis, candidiasis, inverse psoriasis, or erythrasma), Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, and irritant or allergic contact dermatitis. The papules may resemble seborrheic keratoses, while the plaques can be mistaken for acanthosis nigricans.
Therapeutic success has been reported with topical corticosteroids, vitamin D analogues, topical or oral retinoids, ammonium lactate, calcineurin inhibitors, topical or oral antifungals, cryotherapy, and botulinum toxin injections.3,9-11 In addition, parakeratosis has decreased in biopsies from psoriatic patients after acitretin, methotrexate, and phototherapy, which may be alternative treatments for unusually difficult or recalcitrant cases of granular parakeratosis. To minimize side effects and resolve the papules quickly, we combined 2 synergistic agents—glycolic acid and tretinoin—each with different mechanisms of action, and we observed excellent clinical response.
Granular parakeratosis is possibly related to a combination of topical products that potentiate irritation, rubbing, and occlusion of sweat. Multiple treatment modalities likely contribute to clearing, the most important being removal of any triggering topical products. Our patient’s change in deodorant may have been the inciting factor for the disease. Withdrawal of the Secret Clinical Strength deodorant prompted clearing, though topical retinoid and glycolic acid acted as facilitating therapies for timely results. A thorough history, as highlighted by this case, may help pinpoint etiologic factors. By identifying a seemingly innocuous change in hygienic routine, we were able to minimize the need for ongoing therapy.
To the Editor:
A 46-year-old overweight woman presented with a rash in the axillae of 2 months’ duration. She did not report any additional symptoms such as pruritus or pain. She reported changing her deodorant recently from Secret Original to Secret Clinical Strength (both Procter & Gamble). Her medical history was remarkable for asthma and gastroesophageal reflux disease. Clinical examination revealed erythematous-brown, stuccolike, hyperkeratotic papules coalescing into plaques in recently shaved axillae, affecting the left axilla more than the right axilla (Figure 1). The clinical differential diagnosis included granular parakeratosis, intertrigo, Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, acanthosis nigricans, seborrheic keratoses, and irritant or allergic contact dermatitis. A punch biopsy revealed a marked compact parakeratotic horn with retention of keratohyalin granules (Figure 2). The subjacent epidermis showed some acanthosis and spongiosis with mild chronic inflammation of the dermal rim. Based on histopathology, granular parakeratosis was diagnosed.
At a subsequent visit 2 weeks later, we prescribed glycolic acid lotion 10% applied to the axillae twice daily, plus tretinoin gel 0.05% applied to the axillae each evening. She reported clearing after 1 week of therapy. She also had changed her deodorant from Secret Clinical Strength back to the usual Secret Original. The patient discontinued topical treatment after clearing of the lesions. Three weeks later, clinical examination revealed postinflammatory hyperpigmentation in the axillae, and the prior lesions had resolved (Figure 3).
Granular parakeratosis is an unusual condition most commonly presenting in middle-aged women in the axillae, with a clinical presentation of erythematous to brownish hyperkeratotic papules coalescing into plaques. Although few cases have been reported, granular parakeratosis likely is more common than has been reported. There have been reports involving the scalp, cheeks, abdomen, thighs, and other intertriginous areas including inguinal folds and the submammary region.1-4 There also is an infantile form related to diapers and zinc oxide paste.5 Although uncommon, granular parakeratosis can occur as a single papule or plaque and is termed granular parakeratotic acanthoma.6 Lesions may persist for months, spontaneously resolve and recur, and occasionally evolve into fissures and erosions due to irritation. Pruritus is a common concern. Histology of granular parakeratosis reveals hyperkeratosis with eosinophilic staining, compact parakeratosis with retention of basophilic keratohyalin granules, and vascular proliferation and ectasia.5
The cause is unknown but possibly related to irritation from rubbing, occlusion, sweating, or deodorants.5,7 Cases indicate a link to obesity. Hypotheses as to the etiology include the disruption of cornification. Normally, filaggrin maintains the keratohyaline granules in the stratum corneum during cornification. Therefore, the retention of keratohyaline granules in granular parakeratosis may be due to a defect in processing profilaggrin to filaggrin, which has been proposed based on ultrastructural and immunohistochemical studies.8
The differential diagnosis includes granular parakeratosis, intertrigo (caused by seborrheic dermatitis, candidiasis, inverse psoriasis, or erythrasma), Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, and irritant or allergic contact dermatitis. The papules may resemble seborrheic keratoses, while the plaques can be mistaken for acanthosis nigricans.
Therapeutic success has been reported with topical corticosteroids, vitamin D analogues, topical or oral retinoids, ammonium lactate, calcineurin inhibitors, topical or oral antifungals, cryotherapy, and botulinum toxin injections.3,9-11 In addition, parakeratosis has decreased in biopsies from psoriatic patients after acitretin, methotrexate, and phototherapy, which may be alternative treatments for unusually difficult or recalcitrant cases of granular parakeratosis. To minimize side effects and resolve the papules quickly, we combined 2 synergistic agents—glycolic acid and tretinoin—each with different mechanisms of action, and we observed excellent clinical response.
Granular parakeratosis is possibly related to a combination of topical products that potentiate irritation, rubbing, and occlusion of sweat. Multiple treatment modalities likely contribute to clearing, the most important being removal of any triggering topical products. Our patient’s change in deodorant may have been the inciting factor for the disease. Withdrawal of the Secret Clinical Strength deodorant prompted clearing, though topical retinoid and glycolic acid acted as facilitating therapies for timely results. A thorough history, as highlighted by this case, may help pinpoint etiologic factors. By identifying a seemingly innocuous change in hygienic routine, we were able to minimize the need for ongoing therapy.
- Graham R. Intertriginous granular parakeratosis: a case report and review of the literature. J Am Acad Dermatol. 2011;64:AB45-AB45.
- Compton AK, Jackson JM. Isotretinoin as a treatment for axillary granular parakeratosis. Cutis. 2007;80:55-56.
- Channual J, Fife DJ, Wu JJ. Axillary granular parakeratosis. Cutis. 2013;92;61, 65-66.
- Streams S, Gottwald L, Zaher A, et al. Granular parakeratosis of the scalp: a case report. J Am Acad Dermatol. 2007;56:AB81-AB81.
- James WD, Berger T, Elston D. Andrews’ Diseases of the Skin. 12th ed. Philadelphia, PA: Elsevier, Inc; 2015.
- Resnik KS, Kantor GR, DiLeonardo M. Granular parakeratotic acanthoma. Am J Dermatopathol. 2005;27:393-396.
- Naylor E, Wartman D, Telang G, et al. Granular parakeratosis secondary to postsurgical occlusion. J Am Acad Dermatol. 2008;58:AB126.
- Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. Philadelphia, PA: Elsevier, Inc; 2012.
- Baum B, Skopit S. Granular parakeratosis treatment with tacrolimus 0.1% ointment: a case presentation and discussion. J Am Osteo Coll Dermatol. 2013;26:40-41.
- Brown SK, Heilman ER. Granular parakeratosis: resolution with topical tretinoin. J Am Acad Dermatol. 2002;47:S279-S280.
- Webster CG, Resnik KS, Webster GF. Axillary granular parakeratosis: response to isotretinoin. J Am Acad Dermatol. 1997;37:789790.
- Graham R. Intertriginous granular parakeratosis: a case report and review of the literature. J Am Acad Dermatol. 2011;64:AB45-AB45.
- Compton AK, Jackson JM. Isotretinoin as a treatment for axillary granular parakeratosis. Cutis. 2007;80:55-56.
- Channual J, Fife DJ, Wu JJ. Axillary granular parakeratosis. Cutis. 2013;92;61, 65-66.
- Streams S, Gottwald L, Zaher A, et al. Granular parakeratosis of the scalp: a case report. J Am Acad Dermatol. 2007;56:AB81-AB81.
- James WD, Berger T, Elston D. Andrews’ Diseases of the Skin. 12th ed. Philadelphia, PA: Elsevier, Inc; 2015.
- Resnik KS, Kantor GR, DiLeonardo M. Granular parakeratotic acanthoma. Am J Dermatopathol. 2005;27:393-396.
- Naylor E, Wartman D, Telang G, et al. Granular parakeratosis secondary to postsurgical occlusion. J Am Acad Dermatol. 2008;58:AB126.
- Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. Philadelphia, PA: Elsevier, Inc; 2012.
- Baum B, Skopit S. Granular parakeratosis treatment with tacrolimus 0.1% ointment: a case presentation and discussion. J Am Osteo Coll Dermatol. 2013;26:40-41.
- Brown SK, Heilman ER. Granular parakeratosis: resolution with topical tretinoin. J Am Acad Dermatol. 2002;47:S279-S280.
- Webster CG, Resnik KS, Webster GF. Axillary granular parakeratosis: response to isotretinoin. J Am Acad Dermatol. 1997;37:789790.
Practice Points
- Granular parakeratosis most commonly presents in middle-aged women in the axillae.
- The cause is unknown but possibly related to irritation from rubbing, occlusion, sweating, or deodorants.
- Multiple treatment modalities likely contribute to clearing, the most important being removal of any triggering topical products.
Microneedling plus 10% TCA peels bests CO2 laser alone for infraorbital dark circles
In a study of patients with mild to moderate infraorbital dark circles, treatment with carbon dioxide laser resurfacing did not produce a significant improvement in infraorbital hyperpigmentation. However, the combination of microneedling and 10% trichloroacetic acid peels did.
The finding comes from what is believed to be the first head-to-head comparison of the two procedures for infraorbital dark circles, which are a common cosmetic concern with increased age.
During a late-breaking abstract session at the virtual annual meeting of the American Academy of Dermatology, lead study author Banu Farabi, MD, said that dark circles seen in the periorbital area are defined as bilateral, round homogeneous pigmented macules whose etiology is thought to be multifactorial. Available treatments include bleaching creams, topical retinoids, chemical peels, lasers, autologous fat transplantation, injectable fillers, and blepharoplasty.
“Microneedling has been recently suggested as an effective and efficient method for reducing infraorbital dark circles,” Dr. Farabi said. “This technique is based on creating microchannels that can stimulate the production of subcutaneous collagen and elastin. It also enhances the revascularization and fibroblast activity, which increases the skin thickness and gives a shiny appearance to the skin. The fractional CO2 has also been introduced as an effective procedure to remove infraorbital dark circles. However, there are some potential complications with that therapy.”
For the current study, Dr. Farabi, of the department of dermatology at Ankara (Turkey) University, and Mohamad Goldust, MD, of University Hospital Basel (Switzerland), They used the handheld Automatic Microneedle Therapy System-Handhold from MCure. After creating microchannels, the investigators topically applied 10% trichloroacetic acid peels to each infraorbital area and waited for 5 minutes.
In the carbon dioxide laser group, a Lutronic CO2 laser was used with a pulse energy of 10 J/cm2, a 100-microsecond pulse rate, 30 W of power, and a pulse width of 4 mm. The treatment outcome was assessed with the patient’s satisfaction and the physician’s judgment, which were no response, partial response, and complete response. Patients in both study groups were followed up for blinded-investigator assessment of infraorbital hyperpigmentation, adverse events, and improvement, compared with baseline.
The mean age of patients was 40 years, with a range between 27 and 58 years. About one-third of patients in each group had Fitzpatrick skin types II, III, and IV, respectively. In the blinded investigator assessment, the laser-resurfacing procedure did not demonstrate a significant improvement in infraorbital hyperpigmentation at day 90 (P = .24). However, the combination of microneedling and 10% trichloroacetic acid peels significantly improved infraorbital hyperpigmentation by day 90, with improvement maintained through day 180 (P = .012 and .002, respectively).
Adverse events were mild and temporary in both groups. In the laser-resurfacing group, 7 of the patients (22.5%) developed transient infraorbital hyperpigmentation postoperatively that lasted 4 weeks. In the combination treatment group, 18 patients (58%) developed transient erythema that lasted for up to 1 week.
“We suggest using microneedling plus 10% [trichloroacetic acid] as a cost-effective and efficient method for reducing infraorbital dark circles,” Dr. Farabi concluded.
The researchers reported having no financial disclosures.
In a study of patients with mild to moderate infraorbital dark circles, treatment with carbon dioxide laser resurfacing did not produce a significant improvement in infraorbital hyperpigmentation. However, the combination of microneedling and 10% trichloroacetic acid peels did.
The finding comes from what is believed to be the first head-to-head comparison of the two procedures for infraorbital dark circles, which are a common cosmetic concern with increased age.
During a late-breaking abstract session at the virtual annual meeting of the American Academy of Dermatology, lead study author Banu Farabi, MD, said that dark circles seen in the periorbital area are defined as bilateral, round homogeneous pigmented macules whose etiology is thought to be multifactorial. Available treatments include bleaching creams, topical retinoids, chemical peels, lasers, autologous fat transplantation, injectable fillers, and blepharoplasty.
“Microneedling has been recently suggested as an effective and efficient method for reducing infraorbital dark circles,” Dr. Farabi said. “This technique is based on creating microchannels that can stimulate the production of subcutaneous collagen and elastin. It also enhances the revascularization and fibroblast activity, which increases the skin thickness and gives a shiny appearance to the skin. The fractional CO2 has also been introduced as an effective procedure to remove infraorbital dark circles. However, there are some potential complications with that therapy.”
For the current study, Dr. Farabi, of the department of dermatology at Ankara (Turkey) University, and Mohamad Goldust, MD, of University Hospital Basel (Switzerland), They used the handheld Automatic Microneedle Therapy System-Handhold from MCure. After creating microchannels, the investigators topically applied 10% trichloroacetic acid peels to each infraorbital area and waited for 5 minutes.
In the carbon dioxide laser group, a Lutronic CO2 laser was used with a pulse energy of 10 J/cm2, a 100-microsecond pulse rate, 30 W of power, and a pulse width of 4 mm. The treatment outcome was assessed with the patient’s satisfaction and the physician’s judgment, which were no response, partial response, and complete response. Patients in both study groups were followed up for blinded-investigator assessment of infraorbital hyperpigmentation, adverse events, and improvement, compared with baseline.
The mean age of patients was 40 years, with a range between 27 and 58 years. About one-third of patients in each group had Fitzpatrick skin types II, III, and IV, respectively. In the blinded investigator assessment, the laser-resurfacing procedure did not demonstrate a significant improvement in infraorbital hyperpigmentation at day 90 (P = .24). However, the combination of microneedling and 10% trichloroacetic acid peels significantly improved infraorbital hyperpigmentation by day 90, with improvement maintained through day 180 (P = .012 and .002, respectively).
Adverse events were mild and temporary in both groups. In the laser-resurfacing group, 7 of the patients (22.5%) developed transient infraorbital hyperpigmentation postoperatively that lasted 4 weeks. In the combination treatment group, 18 patients (58%) developed transient erythema that lasted for up to 1 week.
“We suggest using microneedling plus 10% [trichloroacetic acid] as a cost-effective and efficient method for reducing infraorbital dark circles,” Dr. Farabi concluded.
The researchers reported having no financial disclosures.
In a study of patients with mild to moderate infraorbital dark circles, treatment with carbon dioxide laser resurfacing did not produce a significant improvement in infraorbital hyperpigmentation. However, the combination of microneedling and 10% trichloroacetic acid peels did.
The finding comes from what is believed to be the first head-to-head comparison of the two procedures for infraorbital dark circles, which are a common cosmetic concern with increased age.
During a late-breaking abstract session at the virtual annual meeting of the American Academy of Dermatology, lead study author Banu Farabi, MD, said that dark circles seen in the periorbital area are defined as bilateral, round homogeneous pigmented macules whose etiology is thought to be multifactorial. Available treatments include bleaching creams, topical retinoids, chemical peels, lasers, autologous fat transplantation, injectable fillers, and blepharoplasty.
“Microneedling has been recently suggested as an effective and efficient method for reducing infraorbital dark circles,” Dr. Farabi said. “This technique is based on creating microchannels that can stimulate the production of subcutaneous collagen and elastin. It also enhances the revascularization and fibroblast activity, which increases the skin thickness and gives a shiny appearance to the skin. The fractional CO2 has also been introduced as an effective procedure to remove infraorbital dark circles. However, there are some potential complications with that therapy.”
For the current study, Dr. Farabi, of the department of dermatology at Ankara (Turkey) University, and Mohamad Goldust, MD, of University Hospital Basel (Switzerland), They used the handheld Automatic Microneedle Therapy System-Handhold from MCure. After creating microchannels, the investigators topically applied 10% trichloroacetic acid peels to each infraorbital area and waited for 5 minutes.
In the carbon dioxide laser group, a Lutronic CO2 laser was used with a pulse energy of 10 J/cm2, a 100-microsecond pulse rate, 30 W of power, and a pulse width of 4 mm. The treatment outcome was assessed with the patient’s satisfaction and the physician’s judgment, which were no response, partial response, and complete response. Patients in both study groups were followed up for blinded-investigator assessment of infraorbital hyperpigmentation, adverse events, and improvement, compared with baseline.
The mean age of patients was 40 years, with a range between 27 and 58 years. About one-third of patients in each group had Fitzpatrick skin types II, III, and IV, respectively. In the blinded investigator assessment, the laser-resurfacing procedure did not demonstrate a significant improvement in infraorbital hyperpigmentation at day 90 (P = .24). However, the combination of microneedling and 10% trichloroacetic acid peels significantly improved infraorbital hyperpigmentation by day 90, with improvement maintained through day 180 (P = .012 and .002, respectively).
Adverse events were mild and temporary in both groups. In the laser-resurfacing group, 7 of the patients (22.5%) developed transient infraorbital hyperpigmentation postoperatively that lasted 4 weeks. In the combination treatment group, 18 patients (58%) developed transient erythema that lasted for up to 1 week.
“We suggest using microneedling plus 10% [trichloroacetic acid] as a cost-effective and efficient method for reducing infraorbital dark circles,” Dr. Farabi concluded.
The researchers reported having no financial disclosures.
FROM AAD 20
Multiethnic Training in Residency: A Survey of Dermatology Residents
Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,1 which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.4
Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.
Methods
A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education.
Results
When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).
Comment
Responses varied by practicing region
Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.9 Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.
Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.6 In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al6 and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.
One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.6 These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.6 Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.10
This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.
Conclusion
In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.12
- Luther N, Darvin ME, Sterry W, et al. Ethnic differences in skin physiology, hair follicle morphology and follicular penetration. Skin Pharmacol Physiol. 2012;25:182-191.
- Shokeen D. Postinflammatory hyperpigmentation in patients with skin of color. Cutis. 2016;97:E9-E11.
- Lawson CN, Hollinger J, Sethi S, et al. Updates in the understanding and treatments of skin & hair disorders in women of color. Int J Women’s Dermatol. 2017;3:S21-S37.
- Hu S, Parmet Y, Allen G, et al. Disparity in melanoma: a trend analysis of melanoma incidence and stage at diagnosis among whites, Hispanics, and blacks in Florida. Arch Dermatol. 2009;145:1369-1374.
- Colby SL, Ortman JM; US Census Bureau. Projections of the Size and Composition of the U.S. Population: 2014 to 2060. Washington, DC: US Census Bureau; 2014. Current Population Reports, P25-1143. https://census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf. Published March 2015. Accessed May 13, 2020.
- Nijhawan RI, Jacob SE, Woolery-Lloyd H. Skin of color education in dermatology residency programs: does residency training reflect the changing demographics of the United States? J Am Acad Dermatol. 2008;59:615-618.
- Pritchett EN, Pandya AG, Ferguson NN, et al. Diversity in dermatology: roadmap for improvement. J Am Acad Dermatol. 2018;79:337-341.
- Pandya AG, Alexis AF, Berger TG, et al. Increasing racial and ethnic diversity in dermatology: a call to action. J Am Acad Dermatol. 2016;74:584-587.
- Ernst H, Colthorpe K. The efficacy of interactive lecturing for students with diverse science backgrounds. Adv Physiol Educ. 2007;31:41-44.
- Allday E. UCSF opens ‘skin of color’ dermatology clinic to address disparity in care. San Francisco Chronicle. March 20, 2019. https://www.sfchronicle.com/health/article/UCSF-opens-skin-of-color-dermatology-clinic-13704387.php. Accessed May 13, 2020.
- Van Voorhees AS, Enos CW. Diversity in dermatology residency programs. J Investig Dermatol Symp Proc. 2017;18:S46-S49.
- Enos CW, Harvey VM. From bench to bedside: the Hampton University Skin of Color Research Institute 2015 Skin of Color Symposium. J Investig Dermatol Symp Proc. 2017;18:S29-S30.
Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,1 which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.4
Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.
Methods
A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education.
Results
When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).
Comment
Responses varied by practicing region
Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.9 Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.
Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.6 In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al6 and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.
One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.6 These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.6 Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.10
This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.
Conclusion
In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.12
Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,1 which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.4
Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.
Methods
A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education.
Results
When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).
Comment
Responses varied by practicing region
Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.9 Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.
Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.6 In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al6 and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.
One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.6 These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.6 Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.10
This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.
Conclusion
In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.12
- Luther N, Darvin ME, Sterry W, et al. Ethnic differences in skin physiology, hair follicle morphology and follicular penetration. Skin Pharmacol Physiol. 2012;25:182-191.
- Shokeen D. Postinflammatory hyperpigmentation in patients with skin of color. Cutis. 2016;97:E9-E11.
- Lawson CN, Hollinger J, Sethi S, et al. Updates in the understanding and treatments of skin & hair disorders in women of color. Int J Women’s Dermatol. 2017;3:S21-S37.
- Hu S, Parmet Y, Allen G, et al. Disparity in melanoma: a trend analysis of melanoma incidence and stage at diagnosis among whites, Hispanics, and blacks in Florida. Arch Dermatol. 2009;145:1369-1374.
- Colby SL, Ortman JM; US Census Bureau. Projections of the Size and Composition of the U.S. Population: 2014 to 2060. Washington, DC: US Census Bureau; 2014. Current Population Reports, P25-1143. https://census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf. Published March 2015. Accessed May 13, 2020.
- Nijhawan RI, Jacob SE, Woolery-Lloyd H. Skin of color education in dermatology residency programs: does residency training reflect the changing demographics of the United States? J Am Acad Dermatol. 2008;59:615-618.
- Pritchett EN, Pandya AG, Ferguson NN, et al. Diversity in dermatology: roadmap for improvement. J Am Acad Dermatol. 2018;79:337-341.
- Pandya AG, Alexis AF, Berger TG, et al. Increasing racial and ethnic diversity in dermatology: a call to action. J Am Acad Dermatol. 2016;74:584-587.
- Ernst H, Colthorpe K. The efficacy of interactive lecturing for students with diverse science backgrounds. Adv Physiol Educ. 2007;31:41-44.
- Allday E. UCSF opens ‘skin of color’ dermatology clinic to address disparity in care. San Francisco Chronicle. March 20, 2019. https://www.sfchronicle.com/health/article/UCSF-opens-skin-of-color-dermatology-clinic-13704387.php. Accessed May 13, 2020.
- Van Voorhees AS, Enos CW. Diversity in dermatology residency programs. J Investig Dermatol Symp Proc. 2017;18:S46-S49.
- Enos CW, Harvey VM. From bench to bedside: the Hampton University Skin of Color Research Institute 2015 Skin of Color Symposium. J Investig Dermatol Symp Proc. 2017;18:S29-S30.
- Luther N, Darvin ME, Sterry W, et al. Ethnic differences in skin physiology, hair follicle morphology and follicular penetration. Skin Pharmacol Physiol. 2012;25:182-191.
- Shokeen D. Postinflammatory hyperpigmentation in patients with skin of color. Cutis. 2016;97:E9-E11.
- Lawson CN, Hollinger J, Sethi S, et al. Updates in the understanding and treatments of skin & hair disorders in women of color. Int J Women’s Dermatol. 2017;3:S21-S37.
- Hu S, Parmet Y, Allen G, et al. Disparity in melanoma: a trend analysis of melanoma incidence and stage at diagnosis among whites, Hispanics, and blacks in Florida. Arch Dermatol. 2009;145:1369-1374.
- Colby SL, Ortman JM; US Census Bureau. Projections of the Size and Composition of the U.S. Population: 2014 to 2060. Washington, DC: US Census Bureau; 2014. Current Population Reports, P25-1143. https://census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf. Published March 2015. Accessed May 13, 2020.
- Nijhawan RI, Jacob SE, Woolery-Lloyd H. Skin of color education in dermatology residency programs: does residency training reflect the changing demographics of the United States? J Am Acad Dermatol. 2008;59:615-618.
- Pritchett EN, Pandya AG, Ferguson NN, et al. Diversity in dermatology: roadmap for improvement. J Am Acad Dermatol. 2018;79:337-341.
- Pandya AG, Alexis AF, Berger TG, et al. Increasing racial and ethnic diversity in dermatology: a call to action. J Am Acad Dermatol. 2016;74:584-587.
- Ernst H, Colthorpe K. The efficacy of interactive lecturing for students with diverse science backgrounds. Adv Physiol Educ. 2007;31:41-44.
- Allday E. UCSF opens ‘skin of color’ dermatology clinic to address disparity in care. San Francisco Chronicle. March 20, 2019. https://www.sfchronicle.com/health/article/UCSF-opens-skin-of-color-dermatology-clinic-13704387.php. Accessed May 13, 2020.
- Van Voorhees AS, Enos CW. Diversity in dermatology residency programs. J Investig Dermatol Symp Proc. 2017;18:S46-S49.
- Enos CW, Harvey VM. From bench to bedside: the Hampton University Skin of Color Research Institute 2015 Skin of Color Symposium. J Investig Dermatol Symp Proc. 2017;18:S29-S30.
Practice Points
- To treat the ever-changing demographics of patients in the United States, dermatologists must receive adequate exposure and education regarding dermatologic conditions in patients from various ethnic backgrounds.
- Dermatology residents from less diverse regions are more likely to agree that dedicated clinics and rotations are important to gain competence compared to those from more diverse regions.
- In areas with less diversity, dedicated multiethnic skin clinics and faculty may be more important for assuring an adequate residency experience.
Comment on “Racial Limitations of Fitzpatrick Skin Type”
To the Editor:
It is with great interest that I read the article by Ware et al,1 “Racial Limitations of Fitzpatrick Skin Type.” Within my own department, the issue of the appropriateness of using Fitzpatrick skin type (FST) as a surrogate to describe skin color has been raised with mixed responses.
As in many dermatology residency programs across the country, first-year dermatology residents are asked to describe the morphology of a lesion/eruption seen on a patient during Grand Rounds. Preceding the morphologic description, many providers describe the appearance of the patient including their skin color, as constitutive skin color can impact understanding of the morphologic descriptions, favor different diagnoses based on disease epidemiology, and guide subsequent treatment recommendations.2,3 During one of my first Grand Rounds as an early dermatology resident, a patient was described as a “well-appearing brown boy,” which led to a lively discussion regarding the terms that should be used to describe skin color, with some in the audience preferring FST, others including myself preferring degree of pigmentation (eg, light, moderate, dark), and lastly others preferring an inferred ethnicity based on the patient’s appearance. One audience member commented, “I am brown, therefore I think it is fine to say ‘brown boy,’” which adds to findings from Ware et al1 that there may be differences in what providers prefer to utilize to describe a patient’s skin color based on their own constitutive skin color.
I inquired with 2 other first-year dermatology residents with skin of color at other programs. When asked what terminology they use to describe a patient for Grand Rounds or in clinic, one resident replied, “It’s stylistic but if it’s your one liner [for assessment and plan] use their ethnicity [whereas] if it’s [for] a physical exam use their Fitzpatrick skin type.” The other resident replied, “I use Fitzpatrick skin type even though it’s technically subjective and therefore not appropriate for use within objective data, such as the physical exam, however it’s a language that most colleagues understand as a substitute for skin color.” I also raised the same question to an attending dermatologist at a primarily skin-of-color community hospital. She replied, “I think when unsure about ethnicity, Fitzpatrick type is an appropriate way to describe someone. It’s not really correct to say [a patient’s ethnicity] when you don’t know for sure.”
Unfortunately, as Ware and colleagues1 indicated, there is no consensus by which to objectively classify nonwhite skin color. Within the dermatology literature, it has been proposed that race should not be used to express skin color, and this article proposes that FST is an inappropriate surrogate for race/ethnicity.4 Although I agree that appropriate use of FST should be emphasized in training, is there a vocabulary that Ware et al1 recommend we use instead? Does the Skin of Color Society have suggestions on preferred language among its members? Finally, what efforts are being made to develop “culturally appropriate and clinically relevant methods for describing skin of color,” as the authors stated, within our own Skin of Color Society, or to whom does this responsibility ultimately fall?
References
1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.
2. Sachdeva S. Fitzpatrick skin typing: applications in dermatology. Indian J Dermatol Venereol Leprol. 2009;75:93-96.
3. Kelly AP, Taylor SC, Lim HW, et al. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.
4. Bigby M, Thaler D. Describing patients’ “race” in clinical presentations should be abandoned. J Am Acad Dermatol. 2006;54:1074-1076.
Author’s Response
My colleagues and I thank Dr. Pimentel for his insights regarding the article, “Racial Limitations of Fitzpatrick Skin Type.”1 The conundrum on how to appropriately categorize skin color for descriptive and epidemiologic purposes continues to remain unsolved today. However, attempts have been made in the past. For example, in September 2006, Dr. Susan C. Taylor (Philadelphia, Pennsylvania), formed and chaired a workshop session titled “A New Classification System for All Skin Types.” Dermatology leaders with skin of color expertise were invited from around the world for a weekend in New York, New York, to brainstorm a new skin color classification system. This endeavor did not produce any successful alternatives, but it has remained a pertinent topic of discussion in academic dermatology, including the Skin of Color Society, since then.
When unsure about ethnicity, my colleagues and I continue to advocate that the Fitzpatrick scale is not an appropriate substitute to describe skin color. This usage of Fitzpatrick skin type (FST) perpetuates the idea that the Fitzpatrick scale is a suitable proxy to describe ethnicity or race, which it is not. It is important to remember that race is a social classification construct, not a biological one.2 The topic of race in contemporary culture undoubtedly invokes strong emotional connotations. The language around race is constantly evolving. I would argue that fear and discomfort of using incorrect racial language promotes the inappropriate use of FST, as the FST may be perceived as a more scientific and pseudoapplicable form of classification. To gain knowledge about a patient’s ethnicity/race to assess epidemiologic ethnic trends, we recommend asking the patient in an intake form or during consultation to self-identify his/her ethnicity or race,3 which takes the guesswork out for providers. However, caution must be exercised to avoid using race and ethnicity to later describe skin color.
Until a more culturally and medically relevant method of skin color classification is created, my colleagues and I recommend using basic color adjectives such as brown, black, pink, tan, or white supplemented with light, medium, or dark predescriptors. For example, “A 35-year-old self-identified African American woman with a dark brown skin hue presents with a 2-week flare of itchy, dark purple plaques with white scale on the scalp and extensor surfaces of the knees and elbows.” These basic descriptions for constitutive skin color conjure ample visual information for the listener/reader to understand morphologic descriptions, presentation of erythema, changes in pigmentation, and more. For a more specific skin color classification, we recommend developing a user-friendly Pantone-like color system to classify constitutive skin color.4
Jessica E. Dawson, MD
From the University of Washington School of Medicine, Seattle.
The author reports no conflict of interest.
Correspondence: Jessica E. Dawson, MD, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 ([email protected]).
References
1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.
2. Ifekwunigwe JO, Wagner JK, Yu JH, et al. A qualitative analysis of how anthropologists interpret the race construct. Am Anthropol. 2017;119:422-434.
3. Hasnain-Wynia R, Baker DW. Obtaining data on patient race, ethnicity, and primary language in health care organizations: current challenges and proposed solutions. Health Serv Res. 2006;41:1501-1518.
4. What is the Pantone color system? Pantone website. https://www.pantone.com/color-systems/pantone-color-systems-explained. Accesed May 13, 2020.
To the Editor:
It is with great interest that I read the article by Ware et al,1 “Racial Limitations of Fitzpatrick Skin Type.” Within my own department, the issue of the appropriateness of using Fitzpatrick skin type (FST) as a surrogate to describe skin color has been raised with mixed responses.
As in many dermatology residency programs across the country, first-year dermatology residents are asked to describe the morphology of a lesion/eruption seen on a patient during Grand Rounds. Preceding the morphologic description, many providers describe the appearance of the patient including their skin color, as constitutive skin color can impact understanding of the morphologic descriptions, favor different diagnoses based on disease epidemiology, and guide subsequent treatment recommendations.2,3 During one of my first Grand Rounds as an early dermatology resident, a patient was described as a “well-appearing brown boy,” which led to a lively discussion regarding the terms that should be used to describe skin color, with some in the audience preferring FST, others including myself preferring degree of pigmentation (eg, light, moderate, dark), and lastly others preferring an inferred ethnicity based on the patient’s appearance. One audience member commented, “I am brown, therefore I think it is fine to say ‘brown boy,’” which adds to findings from Ware et al1 that there may be differences in what providers prefer to utilize to describe a patient’s skin color based on their own constitutive skin color.
I inquired with 2 other first-year dermatology residents with skin of color at other programs. When asked what terminology they use to describe a patient for Grand Rounds or in clinic, one resident replied, “It’s stylistic but if it’s your one liner [for assessment and plan] use their ethnicity [whereas] if it’s [for] a physical exam use their Fitzpatrick skin type.” The other resident replied, “I use Fitzpatrick skin type even though it’s technically subjective and therefore not appropriate for use within objective data, such as the physical exam, however it’s a language that most colleagues understand as a substitute for skin color.” I also raised the same question to an attending dermatologist at a primarily skin-of-color community hospital. She replied, “I think when unsure about ethnicity, Fitzpatrick type is an appropriate way to describe someone. It’s not really correct to say [a patient’s ethnicity] when you don’t know for sure.”
Unfortunately, as Ware and colleagues1 indicated, there is no consensus by which to objectively classify nonwhite skin color. Within the dermatology literature, it has been proposed that race should not be used to express skin color, and this article proposes that FST is an inappropriate surrogate for race/ethnicity.4 Although I agree that appropriate use of FST should be emphasized in training, is there a vocabulary that Ware et al1 recommend we use instead? Does the Skin of Color Society have suggestions on preferred language among its members? Finally, what efforts are being made to develop “culturally appropriate and clinically relevant methods for describing skin of color,” as the authors stated, within our own Skin of Color Society, or to whom does this responsibility ultimately fall?
References
1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.
2. Sachdeva S. Fitzpatrick skin typing: applications in dermatology. Indian J Dermatol Venereol Leprol. 2009;75:93-96.
3. Kelly AP, Taylor SC, Lim HW, et al. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.
4. Bigby M, Thaler D. Describing patients’ “race” in clinical presentations should be abandoned. J Am Acad Dermatol. 2006;54:1074-1076.
Author’s Response
My colleagues and I thank Dr. Pimentel for his insights regarding the article, “Racial Limitations of Fitzpatrick Skin Type.”1 The conundrum on how to appropriately categorize skin color for descriptive and epidemiologic purposes continues to remain unsolved today. However, attempts have been made in the past. For example, in September 2006, Dr. Susan C. Taylor (Philadelphia, Pennsylvania), formed and chaired a workshop session titled “A New Classification System for All Skin Types.” Dermatology leaders with skin of color expertise were invited from around the world for a weekend in New York, New York, to brainstorm a new skin color classification system. This endeavor did not produce any successful alternatives, but it has remained a pertinent topic of discussion in academic dermatology, including the Skin of Color Society, since then.
When unsure about ethnicity, my colleagues and I continue to advocate that the Fitzpatrick scale is not an appropriate substitute to describe skin color. This usage of Fitzpatrick skin type (FST) perpetuates the idea that the Fitzpatrick scale is a suitable proxy to describe ethnicity or race, which it is not. It is important to remember that race is a social classification construct, not a biological one.2 The topic of race in contemporary culture undoubtedly invokes strong emotional connotations. The language around race is constantly evolving. I would argue that fear and discomfort of using incorrect racial language promotes the inappropriate use of FST, as the FST may be perceived as a more scientific and pseudoapplicable form of classification. To gain knowledge about a patient’s ethnicity/race to assess epidemiologic ethnic trends, we recommend asking the patient in an intake form or during consultation to self-identify his/her ethnicity or race,3 which takes the guesswork out for providers. However, caution must be exercised to avoid using race and ethnicity to later describe skin color.
Until a more culturally and medically relevant method of skin color classification is created, my colleagues and I recommend using basic color adjectives such as brown, black, pink, tan, or white supplemented with light, medium, or dark predescriptors. For example, “A 35-year-old self-identified African American woman with a dark brown skin hue presents with a 2-week flare of itchy, dark purple plaques with white scale on the scalp and extensor surfaces of the knees and elbows.” These basic descriptions for constitutive skin color conjure ample visual information for the listener/reader to understand morphologic descriptions, presentation of erythema, changes in pigmentation, and more. For a more specific skin color classification, we recommend developing a user-friendly Pantone-like color system to classify constitutive skin color.4
Jessica E. Dawson, MD
From the University of Washington School of Medicine, Seattle.
The author reports no conflict of interest.
Correspondence: Jessica E. Dawson, MD, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 ([email protected]).
References
1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.
2. Ifekwunigwe JO, Wagner JK, Yu JH, et al. A qualitative analysis of how anthropologists interpret the race construct. Am Anthropol. 2017;119:422-434.
3. Hasnain-Wynia R, Baker DW. Obtaining data on patient race, ethnicity, and primary language in health care organizations: current challenges and proposed solutions. Health Serv Res. 2006;41:1501-1518.
4. What is the Pantone color system? Pantone website. https://www.pantone.com/color-systems/pantone-color-systems-explained. Accesed May 13, 2020.
To the Editor:
It is with great interest that I read the article by Ware et al,1 “Racial Limitations of Fitzpatrick Skin Type.” Within my own department, the issue of the appropriateness of using Fitzpatrick skin type (FST) as a surrogate to describe skin color has been raised with mixed responses.
As in many dermatology residency programs across the country, first-year dermatology residents are asked to describe the morphology of a lesion/eruption seen on a patient during Grand Rounds. Preceding the morphologic description, many providers describe the appearance of the patient including their skin color, as constitutive skin color can impact understanding of the morphologic descriptions, favor different diagnoses based on disease epidemiology, and guide subsequent treatment recommendations.2,3 During one of my first Grand Rounds as an early dermatology resident, a patient was described as a “well-appearing brown boy,” which led to a lively discussion regarding the terms that should be used to describe skin color, with some in the audience preferring FST, others including myself preferring degree of pigmentation (eg, light, moderate, dark), and lastly others preferring an inferred ethnicity based on the patient’s appearance. One audience member commented, “I am brown, therefore I think it is fine to say ‘brown boy,’” which adds to findings from Ware et al1 that there may be differences in what providers prefer to utilize to describe a patient’s skin color based on their own constitutive skin color.
I inquired with 2 other first-year dermatology residents with skin of color at other programs. When asked what terminology they use to describe a patient for Grand Rounds or in clinic, one resident replied, “It’s stylistic but if it’s your one liner [for assessment and plan] use their ethnicity [whereas] if it’s [for] a physical exam use their Fitzpatrick skin type.” The other resident replied, “I use Fitzpatrick skin type even though it’s technically subjective and therefore not appropriate for use within objective data, such as the physical exam, however it’s a language that most colleagues understand as a substitute for skin color.” I also raised the same question to an attending dermatologist at a primarily skin-of-color community hospital. She replied, “I think when unsure about ethnicity, Fitzpatrick type is an appropriate way to describe someone. It’s not really correct to say [a patient’s ethnicity] when you don’t know for sure.”
Unfortunately, as Ware and colleagues1 indicated, there is no consensus by which to objectively classify nonwhite skin color. Within the dermatology literature, it has been proposed that race should not be used to express skin color, and this article proposes that FST is an inappropriate surrogate for race/ethnicity.4 Although I agree that appropriate use of FST should be emphasized in training, is there a vocabulary that Ware et al1 recommend we use instead? Does the Skin of Color Society have suggestions on preferred language among its members? Finally, what efforts are being made to develop “culturally appropriate and clinically relevant methods for describing skin of color,” as the authors stated, within our own Skin of Color Society, or to whom does this responsibility ultimately fall?
References
1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.
2. Sachdeva S. Fitzpatrick skin typing: applications in dermatology. Indian J Dermatol Venereol Leprol. 2009;75:93-96.
3. Kelly AP, Taylor SC, Lim HW, et al. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.
4. Bigby M, Thaler D. Describing patients’ “race” in clinical presentations should be abandoned. J Am Acad Dermatol. 2006;54:1074-1076.
Author’s Response
My colleagues and I thank Dr. Pimentel for his insights regarding the article, “Racial Limitations of Fitzpatrick Skin Type.”1 The conundrum on how to appropriately categorize skin color for descriptive and epidemiologic purposes continues to remain unsolved today. However, attempts have been made in the past. For example, in September 2006, Dr. Susan C. Taylor (Philadelphia, Pennsylvania), formed and chaired a workshop session titled “A New Classification System for All Skin Types.” Dermatology leaders with skin of color expertise were invited from around the world for a weekend in New York, New York, to brainstorm a new skin color classification system. This endeavor did not produce any successful alternatives, but it has remained a pertinent topic of discussion in academic dermatology, including the Skin of Color Society, since then.
When unsure about ethnicity, my colleagues and I continue to advocate that the Fitzpatrick scale is not an appropriate substitute to describe skin color. This usage of Fitzpatrick skin type (FST) perpetuates the idea that the Fitzpatrick scale is a suitable proxy to describe ethnicity or race, which it is not. It is important to remember that race is a social classification construct, not a biological one.2 The topic of race in contemporary culture undoubtedly invokes strong emotional connotations. The language around race is constantly evolving. I would argue that fear and discomfort of using incorrect racial language promotes the inappropriate use of FST, as the FST may be perceived as a more scientific and pseudoapplicable form of classification. To gain knowledge about a patient’s ethnicity/race to assess epidemiologic ethnic trends, we recommend asking the patient in an intake form or during consultation to self-identify his/her ethnicity or race,3 which takes the guesswork out for providers. However, caution must be exercised to avoid using race and ethnicity to later describe skin color.
Until a more culturally and medically relevant method of skin color classification is created, my colleagues and I recommend using basic color adjectives such as brown, black, pink, tan, or white supplemented with light, medium, or dark predescriptors. For example, “A 35-year-old self-identified African American woman with a dark brown skin hue presents with a 2-week flare of itchy, dark purple plaques with white scale on the scalp and extensor surfaces of the knees and elbows.” These basic descriptions for constitutive skin color conjure ample visual information for the listener/reader to understand morphologic descriptions, presentation of erythema, changes in pigmentation, and more. For a more specific skin color classification, we recommend developing a user-friendly Pantone-like color system to classify constitutive skin color.4
Jessica E. Dawson, MD
From the University of Washington School of Medicine, Seattle.
The author reports no conflict of interest.
Correspondence: Jessica E. Dawson, MD, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 ([email protected]).
References
1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.
2. Ifekwunigwe JO, Wagner JK, Yu JH, et al. A qualitative analysis of how anthropologists interpret the race construct. Am Anthropol. 2017;119:422-434.
3. Hasnain-Wynia R, Baker DW. Obtaining data on patient race, ethnicity, and primary language in health care organizations: current challenges and proposed solutions. Health Serv Res. 2006;41:1501-1518.
4. What is the Pantone color system? Pantone website. https://www.pantone.com/color-systems/pantone-color-systems-explained. Accesed May 13, 2020.
Asymptomatic Transient Lingual Hyperpigmentation
The Diagnosis: Pseudo-Black Hairy Tongue
Pseudo-black hairy tongue is a benign and painless disorder characterized by transient hyperpigmentation of the tongue with a substance that can be easily scraped off. In this case, the patient's lingual discoloration was secondary to the ingestion of bismuth salicylate. The phenomenon is thought to occur due to a reaction between bismuth and sulfur-containing compounds in the saliva, resulting in the characteristic black substance on the surface of the tongue that nestles between the lingual papillae.1 An associated feature may include black stools. Other etiologic factors involved in pseudo-black hairy tongue include food coloring, tobacco, and other drugs such antibiotics and antidepressants.2
The differential diagnosis of lingual hyperpigmentation includes lingua villosa nigra (also known as black hairy tongue), pigmented fungiform papillae of the tongue, acanthosis nigricans, and oral hairy leukoplakia. Lingua villosa nigra is a similar condition in which individuals present with a black tongue; however, the tongue also appears hairy. The tongue may appear as other colors such as brown, yellow, or green. Patients additionally may have symptoms of burning, dysgeusia, halitosis, or gagging. Poor oral hygiene, xerostomia, use of tobacco or alcohol, and different medications including antibiotics and antipsychotic medications increase the risk for developing lingua villosa nigra.2,3 This condition is distinguished from pseudo-black hairy tongue by proliferation and elongation of the filiform papillae.3 Pigmented fungiform papillae of the tongue is a normal variant of tongue morphology, is more common in individuals with darker skin types, and primarily affects the lateral aspect and apex of the tongue.4 Acanthosis nigricans can appear in the oral cavity as multiple pigmented papillary lesions on the dorsal and lateral regions of the tongue and frequently involves the lips; this condition may be associated with metabolic disorders or underlying malignancy.2,3 Oral hairy leukoplakia is caused by Epstein-Barr virus infection and typically presents as white plaques on the dorsal and ventral surfaces of the tongue; this condition largely is found in immunocompromised patients.5
In our patient there was an acute onset of tongue discoloration associated with ingestion of bismuth salicylate, no hypertrophy or lengthening of the lingual papillae, and no involvement of the patient's lips, which was consistent with the diagnosis of pseudo-black hairy tongue. Pseudo-black hairy tongue is transient and treated by discontinuation of offending agents and proper hygiene practices.
- Bradley B, Singleton M, Lin Wan Po A. Bismuth toxicity--a reassessment. J Clin Pharm Ther. 1989;14:423-441.
- Gurvits GE, Tan A. Black hairy tongue syndrome. World J Gastroenterol. 2014;20:10845-10850.
- Schlager E, St Claire C, Ashack K, et al. Black hairy tongue: predisposing factors, diagnosis, and treatment. Am J Clin Dermatol. 2017;18:563-569.
- Mangold AR, Torgerson RR, Rogers RS. Diseases of the tongue. Clin Dermatol. 2016;34:458-469.
- Husak R, Garbe C, Orfanos CE. Oral hairy leukoplakia in 71 HIV-seropositive patients: clinical symptoms, relation to immunologic status, and prognostic significance. J Am Acad Dermatol. 1996;35:928-934.
The Diagnosis: Pseudo-Black Hairy Tongue
Pseudo-black hairy tongue is a benign and painless disorder characterized by transient hyperpigmentation of the tongue with a substance that can be easily scraped off. In this case, the patient's lingual discoloration was secondary to the ingestion of bismuth salicylate. The phenomenon is thought to occur due to a reaction between bismuth and sulfur-containing compounds in the saliva, resulting in the characteristic black substance on the surface of the tongue that nestles between the lingual papillae.1 An associated feature may include black stools. Other etiologic factors involved in pseudo-black hairy tongue include food coloring, tobacco, and other drugs such antibiotics and antidepressants.2
The differential diagnosis of lingual hyperpigmentation includes lingua villosa nigra (also known as black hairy tongue), pigmented fungiform papillae of the tongue, acanthosis nigricans, and oral hairy leukoplakia. Lingua villosa nigra is a similar condition in which individuals present with a black tongue; however, the tongue also appears hairy. The tongue may appear as other colors such as brown, yellow, or green. Patients additionally may have symptoms of burning, dysgeusia, halitosis, or gagging. Poor oral hygiene, xerostomia, use of tobacco or alcohol, and different medications including antibiotics and antipsychotic medications increase the risk for developing lingua villosa nigra.2,3 This condition is distinguished from pseudo-black hairy tongue by proliferation and elongation of the filiform papillae.3 Pigmented fungiform papillae of the tongue is a normal variant of tongue morphology, is more common in individuals with darker skin types, and primarily affects the lateral aspect and apex of the tongue.4 Acanthosis nigricans can appear in the oral cavity as multiple pigmented papillary lesions on the dorsal and lateral regions of the tongue and frequently involves the lips; this condition may be associated with metabolic disorders or underlying malignancy.2,3 Oral hairy leukoplakia is caused by Epstein-Barr virus infection and typically presents as white plaques on the dorsal and ventral surfaces of the tongue; this condition largely is found in immunocompromised patients.5
In our patient there was an acute onset of tongue discoloration associated with ingestion of bismuth salicylate, no hypertrophy or lengthening of the lingual papillae, and no involvement of the patient's lips, which was consistent with the diagnosis of pseudo-black hairy tongue. Pseudo-black hairy tongue is transient and treated by discontinuation of offending agents and proper hygiene practices.
The Diagnosis: Pseudo-Black Hairy Tongue
Pseudo-black hairy tongue is a benign and painless disorder characterized by transient hyperpigmentation of the tongue with a substance that can be easily scraped off. In this case, the patient's lingual discoloration was secondary to the ingestion of bismuth salicylate. The phenomenon is thought to occur due to a reaction between bismuth and sulfur-containing compounds in the saliva, resulting in the characteristic black substance on the surface of the tongue that nestles between the lingual papillae.1 An associated feature may include black stools. Other etiologic factors involved in pseudo-black hairy tongue include food coloring, tobacco, and other drugs such antibiotics and antidepressants.2
The differential diagnosis of lingual hyperpigmentation includes lingua villosa nigra (also known as black hairy tongue), pigmented fungiform papillae of the tongue, acanthosis nigricans, and oral hairy leukoplakia. Lingua villosa nigra is a similar condition in which individuals present with a black tongue; however, the tongue also appears hairy. The tongue may appear as other colors such as brown, yellow, or green. Patients additionally may have symptoms of burning, dysgeusia, halitosis, or gagging. Poor oral hygiene, xerostomia, use of tobacco or alcohol, and different medications including antibiotics and antipsychotic medications increase the risk for developing lingua villosa nigra.2,3 This condition is distinguished from pseudo-black hairy tongue by proliferation and elongation of the filiform papillae.3 Pigmented fungiform papillae of the tongue is a normal variant of tongue morphology, is more common in individuals with darker skin types, and primarily affects the lateral aspect and apex of the tongue.4 Acanthosis nigricans can appear in the oral cavity as multiple pigmented papillary lesions on the dorsal and lateral regions of the tongue and frequently involves the lips; this condition may be associated with metabolic disorders or underlying malignancy.2,3 Oral hairy leukoplakia is caused by Epstein-Barr virus infection and typically presents as white plaques on the dorsal and ventral surfaces of the tongue; this condition largely is found in immunocompromised patients.5
In our patient there was an acute onset of tongue discoloration associated with ingestion of bismuth salicylate, no hypertrophy or lengthening of the lingual papillae, and no involvement of the patient's lips, which was consistent with the diagnosis of pseudo-black hairy tongue. Pseudo-black hairy tongue is transient and treated by discontinuation of offending agents and proper hygiene practices.
- Bradley B, Singleton M, Lin Wan Po A. Bismuth toxicity--a reassessment. J Clin Pharm Ther. 1989;14:423-441.
- Gurvits GE, Tan A. Black hairy tongue syndrome. World J Gastroenterol. 2014;20:10845-10850.
- Schlager E, St Claire C, Ashack K, et al. Black hairy tongue: predisposing factors, diagnosis, and treatment. Am J Clin Dermatol. 2017;18:563-569.
- Mangold AR, Torgerson RR, Rogers RS. Diseases of the tongue. Clin Dermatol. 2016;34:458-469.
- Husak R, Garbe C, Orfanos CE. Oral hairy leukoplakia in 71 HIV-seropositive patients: clinical symptoms, relation to immunologic status, and prognostic significance. J Am Acad Dermatol. 1996;35:928-934.
- Bradley B, Singleton M, Lin Wan Po A. Bismuth toxicity--a reassessment. J Clin Pharm Ther. 1989;14:423-441.
- Gurvits GE, Tan A. Black hairy tongue syndrome. World J Gastroenterol. 2014;20:10845-10850.
- Schlager E, St Claire C, Ashack K, et al. Black hairy tongue: predisposing factors, diagnosis, and treatment. Am J Clin Dermatol. 2017;18:563-569.
- Mangold AR, Torgerson RR, Rogers RS. Diseases of the tongue. Clin Dermatol. 2016;34:458-469.
- Husak R, Garbe C, Orfanos CE. Oral hairy leukoplakia in 71 HIV-seropositive patients: clinical symptoms, relation to immunologic status, and prognostic significance. J Am Acad Dermatol. 1996;35:928-934.
A 77-year-old woman incidentally was noted to have black discoloration of the tongue during a routine dermatologic examination. The patient was unaware of the tongue discoloration and reported that her tongue appeared normal the day prior. The tongue was asymptomatic. Clinical examination revealed black hyperpigmentation on the dorsal aspect of the tongue without appreciable hypertrophy or hyperkeratosis of the filiform papillae. The patient had a half-pack daily smoking habit for many years but had abstained from any smoking or tobacco use for the last 15 years. The patient endorsed good oral hygiene. Upon further questioning, the patient revealed that she had ingested 1 tablet of bismuth salicylate the prior night to relieve postprandial dyspepsia. A cotton-tipped applicator was rubbed gently against the affected area and removed some of the black pigment.
