Hair & Nails

Nail surgery is an important part of dermatologic training and clinical practice, both for diagnosis and treatment of nail disorders as well as benign and malignant nail tumors. Patient comfort is essential prior to the procedure and while administering local anesthetics. Effective anesthesia facilitates nail unit biopsies, excisions, and other surgical nail procedures. Pain management immediately following the procedure and during the postoperative period are equally important.

Patients who undergo nail surgery may experience anxiety due to fear of a cancer diagnosis, pain during the surgery, or disfigurement from the procedure. This anxiety may lead to increased blood pressure, a decreased pain threshold, and mental and physical discomfort.¹ A detailed explanation of the procedure itself as well as expectations following the surgery are helpful in diminishing these fears. Administration of a fast-acting benzodiazepine also may be helpful in these patients to decrease anxiety prior to the procedure.²

Attaining adequate anesthesia requires an understanding of digital anatomy, particularly innervation. Innervation of the digits is supplied by the volar and dorsal nerves, which divide into 3 branches at the distal interphalangeal joint, innervating the nail bed, the digital tip, and the pulp.³ Pacinian and Ruffini corpuscles and free-ended nociceptors activate nerve fibers that transmit pain impulses.^4,5 Local anesthetics block pain transmission by impeding voltage-gated sodium channels located at free nerve endings. Pain from anesthesia may be due to both needle insertion and fluid infiltration.

Simple measures can maximize patient comfort during digital anesthesia. Both audiovisual distraction and interpersonal interaction can help to put the patient at ease.^6,7 Application of topical anesthetic cream (1–2 hours prior to the procedure under occlusion),⁸ ice (at least 6 minutes),⁹ or an ethyl chloride spray can be applied to the nail folds prior to needle insertion to alleviate injection pain, but these methods do little for infiltration pain. Use of an ethyl chloride spray may be the preferred technique due to the rapidity of the analgesic effects (Figure).¹⁰ A vibrating massager also can be applied in close proximity to the site of needle insertion.¹¹

Proper anesthetic preparation and technique also can minimize pain during injection. Because lidocaine 1% is acidic (pH, 6.09), buffering with sodium bicarbonate 8.4% can result in decreased injection pain and faster onset of action.^6,12 Warming the anesthetic using a water bath, incubator, or autoclave can decrease pain without degradation of lidocaine or epinephrine.¹³ At a minimum, 30-gauge needles are preferred to minimize pain from needle insertion. Use of 33-gauge needles has shown benefit for injecting the face and scalp and may prove to be helpful injecting sensitive areas such as the digits.¹⁴ A slow injection technique is more comfortable for the patient, as rapid injection causes tissue distention.¹¹

The ideal anesthetic for nail surgery would have a fast onset and a long duration of action, which would allow for shorter operation time as well as alleviation of pain postprocedure and some degree of vasoconstriction to help maintain a bloodless field. Lidocaine has the fastest time of onset (<1–3 minutes) but a short duration of action (30–120 minutes) and a vasodilatory effect. Bupivacaine takes 2 to 5 minutes to take effect and has a long duration of action (120–240 minutes) but a risk for cardiotoxicity. Ropivacaine is the preferred anesthetic by some nail surgeons because of its intermediate time of onset (1–15 minutes), long duration of action (120–360 minutes), and the benefit of some vasoconstriction.^5,15 The addition of epinephrine has 2 main advantages: vasoconstriction and prolongation of anesthetic effects; the latter may help to alleviate postoperative pain. If there are no contraindications to its use (ie, severe hypertension, Raynaud phenomenon), it can be used safely in digital anesthesia without risk for ischemia or infarction.¹¹

Digital anesthesia can be achieved by infiltration or using nerve blocks. One major difference between these 2 approaches is the time of onset of anesthesia, with the former being nearly instantaneous and the latter taking up to 15 minutes.¹⁶ There also usually is more prolonged pain at the site of needle insertion with nerve blocks compared to infiltration. The type of nail surgery being performed, the digit involved, and surgeon preference will determine the anesthetic method of choice.¹⁷

Pain management immediately following the procedure and for several days after is essential. Use of a longer-acting anesthetic, such as bupivacaine or ropivacaine, will provide anesthesia for several hours. A well-padded dressing serves to absorb blood and protect the nail and distal digit from trauma, as even minor trauma can exacerbate pain and bleeding. The patient should be instructed to apply ice to the surgical site and keep the ipsilateral extremity elevated for the next 2 days to reduce edema and pain.¹⁵ Written instructions are helpful, as anxiety during and after the procedure may limit the patient’s understanding and recollection of the verbal postoperative instructions. To maximize readability of the information, the National Institutes of Health and American Medical Association recommend that the instructions be written at a fourth- to sixth-grade reading level.^18,19

A single dose of ibuprofen (400 mg) or acetaminophen (500 mg to 1 g) immediately before or after the procedure can reduce opioid use and postoperative pain.²⁰ Gabapentin (300–1200 mg) given 1 to 2 hours before surgery may be considered in patients who are at high risk for postsurgical pain.²¹ Acetaminophen or nonsteroidal anti-inflammatory drugs (eg, ibuprofen [200–400 mg]) administered every 4 to 6 hours provides considerable pain reduction postprocedure. Nonsteroidal anti-inflammatory drugs may be superior to acetaminophen for pain control²² and carry a low risk for postoperative bleeding.²³ Additionally, a combination of acetaminophen with a nonsteroidal anti-inflammatory drug for 3 doses may be more effective than either drug alone.²⁴ Some patients may require an opioid combination, such as codeine plus acetaminophen, for a short time (up to 3 days) for pain relief following surgery. Excessive pain or pain lasting than more than 3 days is not normal or expected; in these cases, patients should return to the office to rule out ischemia or infection.

It is important to implement pain-minimizing strategies for nail surgeries. Because many of these approaches are derived from other surgical specialties, well-controlled clinical trials in patients undergoing nail surgery will be necessary to improve outcomes.

Nail surgery is an important part of dermatologic training and clinical practice, both for diagnosis and treatment of nail disorders as well as benign and malignant nail tumors. Patient comfort is essential prior to the procedure and while administering local anesthetics. Effective anesthesia facilitates nail unit biopsies, excisions, and other surgical nail procedures. Pain management immediately following the procedure and during the postoperative period are equally important.

Patients who undergo nail surgery may experience anxiety due to fear of a cancer diagnosis, pain during the surgery, or disfigurement from the procedure. This anxiety may lead to increased blood pressure, a decreased pain threshold, and mental and physical discomfort.¹ A detailed explanation of the procedure itself as well as expectations following the surgery are helpful in diminishing these fears. Administration of a fast-acting benzodiazepine also may be helpful in these patients to decrease anxiety prior to the procedure.²

Attaining adequate anesthesia requires an understanding of digital anatomy, particularly innervation. Innervation of the digits is supplied by the volar and dorsal nerves, which divide into 3 branches at the distal interphalangeal joint, innervating the nail bed, the digital tip, and the pulp.³ Pacinian and Ruffini corpuscles and free-ended nociceptors activate nerve fibers that transmit pain impulses.^4,5 Local anesthetics block pain transmission by impeding voltage-gated sodium channels located at free nerve endings. Pain from anesthesia may be due to both needle insertion and fluid infiltration.

Simple measures can maximize patient comfort during digital anesthesia. Both audiovisual distraction and interpersonal interaction can help to put the patient at ease.^6,7 Application of topical anesthetic cream (1–2 hours prior to the procedure under occlusion),⁸ ice (at least 6 minutes),⁹ or an ethyl chloride spray can be applied to the nail folds prior to needle insertion to alleviate injection pain, but these methods do little for infiltration pain. Use of an ethyl chloride spray may be the preferred technique due to the rapidity of the analgesic effects (Figure).¹⁰ A vibrating massager also can be applied in close proximity to the site of needle insertion.¹¹

Proper anesthetic preparation and technique also can minimize pain during injection. Because lidocaine 1% is acidic (pH, 6.09), buffering with sodium bicarbonate 8.4% can result in decreased injection pain and faster onset of action.^6,12 Warming the anesthetic using a water bath, incubator, or autoclave can decrease pain without degradation of lidocaine or epinephrine.¹³ At a minimum, 30-gauge needles are preferred to minimize pain from needle insertion. Use of 33-gauge needles has shown benefit for injecting the face and scalp and may prove to be helpful injecting sensitive areas such as the digits.¹⁴ A slow injection technique is more comfortable for the patient, as rapid injection causes tissue distention.¹¹

The ideal anesthetic for nail surgery would have a fast onset and a long duration of action, which would allow for shorter operation time as well as alleviation of pain postprocedure and some degree of vasoconstriction to help maintain a bloodless field. Lidocaine has the fastest time of onset (<1–3 minutes) but a short duration of action (30–120 minutes) and a vasodilatory effect. Bupivacaine takes 2 to 5 minutes to take effect and has a long duration of action (120–240 minutes) but a risk for cardiotoxicity. Ropivacaine is the preferred anesthetic by some nail surgeons because of its intermediate time of onset (1–15 minutes), long duration of action (120–360 minutes), and the benefit of some vasoconstriction.^5,15 The addition of epinephrine has 2 main advantages: vasoconstriction and prolongation of anesthetic effects; the latter may help to alleviate postoperative pain. If there are no contraindications to its use (ie, severe hypertension, Raynaud phenomenon), it can be used safely in digital anesthesia without risk for ischemia or infarction.¹¹

Digital anesthesia can be achieved by infiltration or using nerve blocks. One major difference between these 2 approaches is the time of onset of anesthesia, with the former being nearly instantaneous and the latter taking up to 15 minutes.¹⁶ There also usually is more prolonged pain at the site of needle insertion with nerve blocks compared to infiltration. The type of nail surgery being performed, the digit involved, and surgeon preference will determine the anesthetic method of choice.¹⁷

Pain management immediately following the procedure and for several days after is essential. Use of a longer-acting anesthetic, such as bupivacaine or ropivacaine, will provide anesthesia for several hours. A well-padded dressing serves to absorb blood and protect the nail and distal digit from trauma, as even minor trauma can exacerbate pain and bleeding. The patient should be instructed to apply ice to the surgical site and keep the ipsilateral extremity elevated for the next 2 days to reduce edema and pain.¹⁵ Written instructions are helpful, as anxiety during and after the procedure may limit the patient’s understanding and recollection of the verbal postoperative instructions. To maximize readability of the information, the National Institutes of Health and American Medical Association recommend that the instructions be written at a fourth- to sixth-grade reading level.^18,19

A single dose of ibuprofen (400 mg) or acetaminophen (500 mg to 1 g) immediately before or after the procedure can reduce opioid use and postoperative pain.²⁰ Gabapentin (300–1200 mg) given 1 to 2 hours before surgery may be considered in patients who are at high risk for postsurgical pain.²¹ Acetaminophen or nonsteroidal anti-inflammatory drugs (eg, ibuprofen [200–400 mg]) administered every 4 to 6 hours provides considerable pain reduction postprocedure. Nonsteroidal anti-inflammatory drugs may be superior to acetaminophen for pain control²² and carry a low risk for postoperative bleeding.²³ Additionally, a combination of acetaminophen with a nonsteroidal anti-inflammatory drug for 3 doses may be more effective than either drug alone.²⁴ Some patients may require an opioid combination, such as codeine plus acetaminophen, for a short time (up to 3 days) for pain relief following surgery. Excessive pain or pain lasting than more than 3 days is not normal or expected; in these cases, patients should return to the office to rule out ischemia or infection.

It is important to implement pain-minimizing strategies for nail surgeries. Because many of these approaches are derived from other surgical specialties, well-controlled clinical trials in patients undergoing nail surgery will be necessary to improve outcomes.

Nail surgery is an important part of dermatologic training and clinical practice, both for diagnosis and treatment of nail disorders as well as benign and malignant nail tumors. Patient comfort is essential prior to the procedure and while administering local anesthetics. Effective anesthesia facilitates nail unit biopsies, excisions, and other surgical nail procedures. Pain management immediately following the procedure and during the postoperative period are equally important.

Patients who undergo nail surgery may experience anxiety due to fear of a cancer diagnosis, pain during the surgery, or disfigurement from the procedure. This anxiety may lead to increased blood pressure, a decreased pain threshold, and mental and physical discomfort.¹ A detailed explanation of the procedure itself as well as expectations following the surgery are helpful in diminishing these fears. Administration of a fast-acting benzodiazepine also may be helpful in these patients to decrease anxiety prior to the procedure.²

Attaining adequate anesthesia requires an understanding of digital anatomy, particularly innervation. Innervation of the digits is supplied by the volar and dorsal nerves, which divide into 3 branches at the distal interphalangeal joint, innervating the nail bed, the digital tip, and the pulp.³ Pacinian and Ruffini corpuscles and free-ended nociceptors activate nerve fibers that transmit pain impulses.^4,5 Local anesthetics block pain transmission by impeding voltage-gated sodium channels located at free nerve endings. Pain from anesthesia may be due to both needle insertion and fluid infiltration.

Simple measures can maximize patient comfort during digital anesthesia. Both audiovisual distraction and interpersonal interaction can help to put the patient at ease.^6,7 Application of topical anesthetic cream (1–2 hours prior to the procedure under occlusion),⁸ ice (at least 6 minutes),⁹ or an ethyl chloride spray can be applied to the nail folds prior to needle insertion to alleviate injection pain, but these methods do little for infiltration pain. Use of an ethyl chloride spray may be the preferred technique due to the rapidity of the analgesic effects (Figure).¹⁰ A vibrating massager also can be applied in close proximity to the site of needle insertion.¹¹

Proper anesthetic preparation and technique also can minimize pain during injection. Because lidocaine 1% is acidic (pH, 6.09), buffering with sodium bicarbonate 8.4% can result in decreased injection pain and faster onset of action.^6,12 Warming the anesthetic using a water bath, incubator, or autoclave can decrease pain without degradation of lidocaine or epinephrine.¹³ At a minimum, 30-gauge needles are preferred to minimize pain from needle insertion. Use of 33-gauge needles has shown benefit for injecting the face and scalp and may prove to be helpful injecting sensitive areas such as the digits.¹⁴ A slow injection technique is more comfortable for the patient, as rapid injection causes tissue distention.¹¹

The ideal anesthetic for nail surgery would have a fast onset and a long duration of action, which would allow for shorter operation time as well as alleviation of pain postprocedure and some degree of vasoconstriction to help maintain a bloodless field. Lidocaine has the fastest time of onset (<1–3 minutes) but a short duration of action (30–120 minutes) and a vasodilatory effect. Bupivacaine takes 2 to 5 minutes to take effect and has a long duration of action (120–240 minutes) but a risk for cardiotoxicity. Ropivacaine is the preferred anesthetic by some nail surgeons because of its intermediate time of onset (1–15 minutes), long duration of action (120–360 minutes), and the benefit of some vasoconstriction.^5,15 The addition of epinephrine has 2 main advantages: vasoconstriction and prolongation of anesthetic effects; the latter may help to alleviate postoperative pain. If there are no contraindications to its use (ie, severe hypertension, Raynaud phenomenon), it can be used safely in digital anesthesia without risk for ischemia or infarction.¹¹

Digital anesthesia can be achieved by infiltration or using nerve blocks. One major difference between these 2 approaches is the time of onset of anesthesia, with the former being nearly instantaneous and the latter taking up to 15 minutes.¹⁶ There also usually is more prolonged pain at the site of needle insertion with nerve blocks compared to infiltration. The type of nail surgery being performed, the digit involved, and surgeon preference will determine the anesthetic method of choice.¹⁷

Pain management immediately following the procedure and for several days after is essential. Use of a longer-acting anesthetic, such as bupivacaine or ropivacaine, will provide anesthesia for several hours. A well-padded dressing serves to absorb blood and protect the nail and distal digit from trauma, as even minor trauma can exacerbate pain and bleeding. The patient should be instructed to apply ice to the surgical site and keep the ipsilateral extremity elevated for the next 2 days to reduce edema and pain.¹⁵ Written instructions are helpful, as anxiety during and after the procedure may limit the patient’s understanding and recollection of the verbal postoperative instructions. To maximize readability of the information, the National Institutes of Health and American Medical Association recommend that the instructions be written at a fourth- to sixth-grade reading level.^18,19

A single dose of ibuprofen (400 mg) or acetaminophen (500 mg to 1 g) immediately before or after the procedure can reduce opioid use and postoperative pain.²⁰ Gabapentin (300–1200 mg) given 1 to 2 hours before surgery may be considered in patients who are at high risk for postsurgical pain.²¹ Acetaminophen or nonsteroidal anti-inflammatory drugs (eg, ibuprofen [200–400 mg]) administered every 4 to 6 hours provides considerable pain reduction postprocedure. Nonsteroidal anti-inflammatory drugs may be superior to acetaminophen for pain control²² and carry a low risk for postoperative bleeding.²³ Additionally, a combination of acetaminophen with a nonsteroidal anti-inflammatory drug for 3 doses may be more effective than either drug alone.²⁴ Some patients may require an opioid combination, such as codeine plus acetaminophen, for a short time (up to 3 days) for pain relief following surgery. Excessive pain or pain lasting than more than 3 days is not normal or expected; in these cases, patients should return to the office to rule out ischemia or infection.

It is important to implement pain-minimizing strategies for nail surgeries. Because many of these approaches are derived from other surgical specialties, well-controlled clinical trials in patients undergoing nail surgery will be necessary to improve outcomes.

Janus kinase inhibitors look promising in the treatment of severe alopecia areata, particularly in adolescents, said Lucy Yichu Liu, MD, and Brett Andrew King, MD, of Yale University, New Haven, Conn.

Standard medical therapies for alopecia areata – usually topical or injected corticosteroids and allergic contact sensitization – are not very effective for severe disease, particularly alopecia totalis and alopecia universalis. The Janus kinase (JAK) pathway recently has been suggested as a target for treatment.

Dr. Liu and Dr. King reviewed several studies, including a retrospective cohort study of 13 patients aged 12-17 years, in which 7 patients had 100% hair loss and 6 had 20%-70% scalp hair loss. The adolescents were treated with the JAK1/3 inhibitor tofacitinib citrate 5 mg twice daily for 2-16 months (median, 5 months). That led to 93% median improvement in Severity of Alopecia Tool (SALT) score (range, 1%-100%) from baseline. Nine patients experienced hair regrowth. There were mild adverse effects, such as upper respiratory infections and headaches.

Courtesy RegionalDerm.com

SOURCE: Liu LY et al. J Investig Dermatol Symp Proc. 2018 Jan. doi: 10.1016/j.jisp.2017.10.003.

Janus kinase inhibitors look promising in the treatment of severe alopecia areata, particularly in adolescents, said Lucy Yichu Liu, MD, and Brett Andrew King, MD, of Yale University, New Haven, Conn.

Standard medical therapies for alopecia areata – usually topical or injected corticosteroids and allergic contact sensitization – are not very effective for severe disease, particularly alopecia totalis and alopecia universalis. The Janus kinase (JAK) pathway recently has been suggested as a target for treatment.

Dr. Liu and Dr. King reviewed several studies, including a retrospective cohort study of 13 patients aged 12-17 years, in which 7 patients had 100% hair loss and 6 had 20%-70% scalp hair loss. The adolescents were treated with the JAK1/3 inhibitor tofacitinib citrate 5 mg twice daily for 2-16 months (median, 5 months). That led to 93% median improvement in Severity of Alopecia Tool (SALT) score (range, 1%-100%) from baseline. Nine patients experienced hair regrowth. There were mild adverse effects, such as upper respiratory infections and headaches.

Courtesy RegionalDerm.com

SOURCE: Liu LY et al. J Investig Dermatol Symp Proc. 2018 Jan. doi: 10.1016/j.jisp.2017.10.003.

Janus kinase inhibitors look promising in the treatment of severe alopecia areata, particularly in adolescents, said Lucy Yichu Liu, MD, and Brett Andrew King, MD, of Yale University, New Haven, Conn.

Standard medical therapies for alopecia areata – usually topical or injected corticosteroids and allergic contact sensitization – are not very effective for severe disease, particularly alopecia totalis and alopecia universalis. The Janus kinase (JAK) pathway recently has been suggested as a target for treatment.

Dr. Liu and Dr. King reviewed several studies, including a retrospective cohort study of 13 patients aged 12-17 years, in which 7 patients had 100% hair loss and 6 had 20%-70% scalp hair loss. The adolescents were treated with the JAK1/3 inhibitor tofacitinib citrate 5 mg twice daily for 2-16 months (median, 5 months). That led to 93% median improvement in Severity of Alopecia Tool (SALT) score (range, 1%-100%) from baseline. Nine patients experienced hair regrowth. There were mild adverse effects, such as upper respiratory infections and headaches.

Courtesy RegionalDerm.com

SOURCE: Liu LY et al. J Investig Dermatol Symp Proc. 2018 Jan. doi: 10.1016/j.jisp.2017.10.003.

The Diagnosis: Nevus Sebaceous

The patient presented with a typical solitary scalp lesion characteristic of nevus sebaceous (NS). The lesion was present at birth as a flat and smooth hairless plaque; however, over time it became more thickened and noticeable, which prompted the parents to seek medical advice.

Nevus sebaceous, also known as NS of Jadassohn, is a benign congenital hamartoma of the sebaceous gland that usually is present at birth and frequently involves the scalp and/or the face. The classic NS lesion is solitary and appears as a well-circumscribed, waxy, yellow-orange or tan, hairless plaque. Despite the presence of these lesions at birth, they may not be noted until early childhood or rarely until adulthood. Generally, the lesion tends to thicken and become more verrucous and velvety over time, particularly around the time of reaching puberty.¹ Clinically, NS lesions vary in size from 1 cm to several centimeters. Lesions initially tend to grow proportionately with the child until puberty when they become notably thicker, greasier, and verrucous or nodular under hormonal influences. The yellow discoloration of the lesion is due to sebaceous gland secretion, and the characteristic color usually becomes less evident with age.

Nevus sebaceous occurs in approximately 0.3% of newborns and tends to be sporadic in nature; however, rare familial forms have been reported.^2,3 Nevus sebaceous can present as multiple nevi that tend to be extensive and distributed along the Blaschko lines, and they usually are associated with neurologic, ocular, or skeletal defects. Involvement of the central nervous system frequently is associated with large sebaceous nevi located on the face or scalp. This association has been termed NS syndrome.⁴ Neurologic abnormalities associated with NS syndrome include seizures, mental retardation, and hemimegalencephaly.⁵ Ocular findings most communally associated with the syndrome are choristomas and colobomas.^6-8

There are several benign and malignant epithelial neoplasms that may develop within sebaceous nevi. Benign tumors include trichoblastoma, syringocystadenoma papilliferum, trichilemmoma, sebaceoma, nodular hidradenoma, and hidrocystoma.^1,8,9 Malignant neoplasms include basal cell carcinoma (BCC), apocrine carcinoma, sebaceous carcinoma, and squamous cell carcinoma. The lifetime risk of malignancy in NS is unknown. In an extensive literature review by Moody et al¹⁰ of 4923 cases of NS for the development of secondary benign and malignant neoplasms, 16% developed benign tumors while 8% developed malignant tumors such as BCC. However, subsequent studies suggested that the incidence of BCC may have been overestimated due to misinterpretation of trichoblastoma and may be less than 1%.^11-13

Usually the diagnosis of NS is made clinically and rarely a biopsy for histopathologic confirmation may be needed when the diagnosis is uncertain. Typically, these histopathologic findings include immature hair follicles, hyperplastic immature sebaceous glands, dilated apocrine glands, and epidermal hyperplasia.⁹ For patients with suspected NS syndrome, additional neurologic and ophthalmologic evaluations should be performed including neuroimaging studies, skeletal radiography, and analysis of liver and renal function.¹⁴

The current standard of care in treating NS is full-thickness excision. However, the decision should be individualized based on patient age, extension and location of the lesion, concerns about the cosmetic appearance, and the risk for malignancy. 

The 2 main reasons to excise NS include concern about malignancy and undesirable cosmetic appearance. Once a malignant lesion develops within NS, it generally is agreed that the tumor and the entire nevus should be removed; however, recommendations vary for excising NS prophylactically to decrease the risk for malignant growths. Because the risk for malignant transformation seems to be lower than previously thought, observation can be a reasonable choice for lesions that are not associated with cosmetic concern.^12,13

Photodynamic therapy, CO2 laser resurfacing, and dermabrasion have been reported as alternative therapeutic approaches. However, there is a growing concern on how effective these treatment modalities are in completely removing the lesion and whether the risk for recurrence and potential for neoplasm development remains.^1,9

This patient was healthy with normal development and growth and no signs of neurologic or ocular involvement. The parents were counseled about the risk for malignancy and the long-term cosmetic appearance of the lesion. They opted for surgical excision of the lesion at 18 months of age.

The Diagnosis: Nevus Sebaceous

The patient presented with a typical solitary scalp lesion characteristic of nevus sebaceous (NS). The lesion was present at birth as a flat and smooth hairless plaque; however, over time it became more thickened and noticeable, which prompted the parents to seek medical advice.

Nevus sebaceous, also known as NS of Jadassohn, is a benign congenital hamartoma of the sebaceous gland that usually is present at birth and frequently involves the scalp and/or the face. The classic NS lesion is solitary and appears as a well-circumscribed, waxy, yellow-orange or tan, hairless plaque. Despite the presence of these lesions at birth, they may not be noted until early childhood or rarely until adulthood. Generally, the lesion tends to thicken and become more verrucous and velvety over time, particularly around the time of reaching puberty.¹ Clinically, NS lesions vary in size from 1 cm to several centimeters. Lesions initially tend to grow proportionately with the child until puberty when they become notably thicker, greasier, and verrucous or nodular under hormonal influences. The yellow discoloration of the lesion is due to sebaceous gland secretion, and the characteristic color usually becomes less evident with age.

Nevus sebaceous occurs in approximately 0.3% of newborns and tends to be sporadic in nature; however, rare familial forms have been reported.^2,3 Nevus sebaceous can present as multiple nevi that tend to be extensive and distributed along the Blaschko lines, and they usually are associated with neurologic, ocular, or skeletal defects. Involvement of the central nervous system frequently is associated with large sebaceous nevi located on the face or scalp. This association has been termed NS syndrome.⁴ Neurologic abnormalities associated with NS syndrome include seizures, mental retardation, and hemimegalencephaly.⁵ Ocular findings most communally associated with the syndrome are choristomas and colobomas.^6-8

There are several benign and malignant epithelial neoplasms that may develop within sebaceous nevi. Benign tumors include trichoblastoma, syringocystadenoma papilliferum, trichilemmoma, sebaceoma, nodular hidradenoma, and hidrocystoma.^1,8,9 Malignant neoplasms include basal cell carcinoma (BCC), apocrine carcinoma, sebaceous carcinoma, and squamous cell carcinoma. The lifetime risk of malignancy in NS is unknown. In an extensive literature review by Moody et al¹⁰ of 4923 cases of NS for the development of secondary benign and malignant neoplasms, 16% developed benign tumors while 8% developed malignant tumors such as BCC. However, subsequent studies suggested that the incidence of BCC may have been overestimated due to misinterpretation of trichoblastoma and may be less than 1%.^11-13

Usually the diagnosis of NS is made clinically and rarely a biopsy for histopathologic confirmation may be needed when the diagnosis is uncertain. Typically, these histopathologic findings include immature hair follicles, hyperplastic immature sebaceous glands, dilated apocrine glands, and epidermal hyperplasia.⁹ For patients with suspected NS syndrome, additional neurologic and ophthalmologic evaluations should be performed including neuroimaging studies, skeletal radiography, and analysis of liver and renal function.¹⁴

The current standard of care in treating NS is full-thickness excision. However, the decision should be individualized based on patient age, extension and location of the lesion, concerns about the cosmetic appearance, and the risk for malignancy. 

The 2 main reasons to excise NS include concern about malignancy and undesirable cosmetic appearance. Once a malignant lesion develops within NS, it generally is agreed that the tumor and the entire nevus should be removed; however, recommendations vary for excising NS prophylactically to decrease the risk for malignant growths. Because the risk for malignant transformation seems to be lower than previously thought, observation can be a reasonable choice for lesions that are not associated with cosmetic concern.^12,13

Photodynamic therapy, CO2 laser resurfacing, and dermabrasion have been reported as alternative therapeutic approaches. However, there is a growing concern on how effective these treatment modalities are in completely removing the lesion and whether the risk for recurrence and potential for neoplasm development remains.^1,9

This patient was healthy with normal development and growth and no signs of neurologic or ocular involvement. The parents were counseled about the risk for malignancy and the long-term cosmetic appearance of the lesion. They opted for surgical excision of the lesion at 18 months of age.

The Diagnosis: Nevus Sebaceous

The patient presented with a typical solitary scalp lesion characteristic of nevus sebaceous (NS). The lesion was present at birth as a flat and smooth hairless plaque; however, over time it became more thickened and noticeable, which prompted the parents to seek medical advice.

Nevus sebaceous, also known as NS of Jadassohn, is a benign congenital hamartoma of the sebaceous gland that usually is present at birth and frequently involves the scalp and/or the face. The classic NS lesion is solitary and appears as a well-circumscribed, waxy, yellow-orange or tan, hairless plaque. Despite the presence of these lesions at birth, they may not be noted until early childhood or rarely until adulthood. Generally, the lesion tends to thicken and become more verrucous and velvety over time, particularly around the time of reaching puberty.¹ Clinically, NS lesions vary in size from 1 cm to several centimeters. Lesions initially tend to grow proportionately with the child until puberty when they become notably thicker, greasier, and verrucous or nodular under hormonal influences. The yellow discoloration of the lesion is due to sebaceous gland secretion, and the characteristic color usually becomes less evident with age.

Nevus sebaceous occurs in approximately 0.3% of newborns and tends to be sporadic in nature; however, rare familial forms have been reported.^2,3 Nevus sebaceous can present as multiple nevi that tend to be extensive and distributed along the Blaschko lines, and they usually are associated with neurologic, ocular, or skeletal defects. Involvement of the central nervous system frequently is associated with large sebaceous nevi located on the face or scalp. This association has been termed NS syndrome.⁴ Neurologic abnormalities associated with NS syndrome include seizures, mental retardation, and hemimegalencephaly.⁵ Ocular findings most communally associated with the syndrome are choristomas and colobomas.^6-8

There are several benign and malignant epithelial neoplasms that may develop within sebaceous nevi. Benign tumors include trichoblastoma, syringocystadenoma papilliferum, trichilemmoma, sebaceoma, nodular hidradenoma, and hidrocystoma.^1,8,9 Malignant neoplasms include basal cell carcinoma (BCC), apocrine carcinoma, sebaceous carcinoma, and squamous cell carcinoma. The lifetime risk of malignancy in NS is unknown. In an extensive literature review by Moody et al¹⁰ of 4923 cases of NS for the development of secondary benign and malignant neoplasms, 16% developed benign tumors while 8% developed malignant tumors such as BCC. However, subsequent studies suggested that the incidence of BCC may have been overestimated due to misinterpretation of trichoblastoma and may be less than 1%.^11-13

Usually the diagnosis of NS is made clinically and rarely a biopsy for histopathologic confirmation may be needed when the diagnosis is uncertain. Typically, these histopathologic findings include immature hair follicles, hyperplastic immature sebaceous glands, dilated apocrine glands, and epidermal hyperplasia.⁹ For patients with suspected NS syndrome, additional neurologic and ophthalmologic evaluations should be performed including neuroimaging studies, skeletal radiography, and analysis of liver and renal function.¹⁴

The current standard of care in treating NS is full-thickness excision. However, the decision should be individualized based on patient age, extension and location of the lesion, concerns about the cosmetic appearance, and the risk for malignancy. 

The 2 main reasons to excise NS include concern about malignancy and undesirable cosmetic appearance. Once a malignant lesion develops within NS, it generally is agreed that the tumor and the entire nevus should be removed; however, recommendations vary for excising NS prophylactically to decrease the risk for malignant growths. Because the risk for malignant transformation seems to be lower than previously thought, observation can be a reasonable choice for lesions that are not associated with cosmetic concern.^12,13

Photodynamic therapy, CO2 laser resurfacing, and dermabrasion have been reported as alternative therapeutic approaches. However, there is a growing concern on how effective these treatment modalities are in completely removing the lesion and whether the risk for recurrence and potential for neoplasm development remains.^1,9

This patient was healthy with normal development and growth and no signs of neurologic or ocular involvement. The parents were counseled about the risk for malignancy and the long-term cosmetic appearance of the lesion. They opted for surgical excision of the lesion at 18 months of age.

African American women with alopecia have significantly higher odds of developing fibroids, based on data from more than 400,000 women.

In a study published in JAMA Dermatology, researchers reviewed data from 487,104 black women seen at a single center between Aug. 1, 2013, and Aug. 1, 2017. Overall, 14% of women with central centrifugal cicatricial alopecia (CCCA) also had a history of uterine fibroids, compared with 3% percent of black women without CCCA.

“Alopecia is more than just a cosmetic problem. … It could signal an increased risk of developing other conditions,” corresponding author Crystal Aguh, MD, of Johns Hopkins University in Baltimore said in an interview. “To our knowledge, this is the first time that an association has been noted between these two conditions. We believe that the fact that both are related to excess scarring and fibrous tissue deposition may reflect similarities in how both [conditions] develop, but this is still unknown.” 

[email protected]

SOURCE: Dina Y et al. JAMA Dermatol. 2017 Dec 27. doi: 10.1001/jamadermatol.2017.5163

African American women with alopecia have significantly higher odds of developing fibroids, based on data from more than 400,000 women.

In a study published in JAMA Dermatology, researchers reviewed data from 487,104 black women seen at a single center between Aug. 1, 2013, and Aug. 1, 2017. Overall, 14% of women with central centrifugal cicatricial alopecia (CCCA) also had a history of uterine fibroids, compared with 3% percent of black women without CCCA.

“Alopecia is more than just a cosmetic problem. … It could signal an increased risk of developing other conditions,” corresponding author Crystal Aguh, MD, of Johns Hopkins University in Baltimore said in an interview. “To our knowledge, this is the first time that an association has been noted between these two conditions. We believe that the fact that both are related to excess scarring and fibrous tissue deposition may reflect similarities in how both [conditions] develop, but this is still unknown.” 

[email protected]

SOURCE: Dina Y et al. JAMA Dermatol. 2017 Dec 27. doi: 10.1001/jamadermatol.2017.5163

African American women with alopecia have significantly higher odds of developing fibroids, based on data from more than 400,000 women.

In a study published in JAMA Dermatology, researchers reviewed data from 487,104 black women seen at a single center between Aug. 1, 2013, and Aug. 1, 2017. Overall, 14% of women with central centrifugal cicatricial alopecia (CCCA) also had a history of uterine fibroids, compared with 3% percent of black women without CCCA.

“Alopecia is more than just a cosmetic problem. … It could signal an increased risk of developing other conditions,” corresponding author Crystal Aguh, MD, of Johns Hopkins University in Baltimore said in an interview. “To our knowledge, this is the first time that an association has been noted between these two conditions. We believe that the fact that both are related to excess scarring and fibrous tissue deposition may reflect similarities in how both [conditions] develop, but this is still unknown.” 

[email protected]

SOURCE: Dina Y et al. JAMA Dermatol. 2017 Dec 27. doi: 10.1001/jamadermatol.2017.5163

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Case Report

A 58-year-old man presented for evaluation of a pruritic rash involving the pubic area of 30 years’ duration. Multiple primary care physicians and dermatologists had evaluated the patient during this period, but he noted a specific diagnosis had not been rendered and multiple treatments had been unsuccessful. The patient described a rash, which was absent at the time of evaluation, as a self-remitting and exacerbating irritation typically induced by sweating and physical activity. The patient also stated that the irritation was associated with a strong, distinct, musty odor that severely interrupted his sex life and decreased his quality of life. Prior treatments included various topical corticosteroids, topical and oral antibiotics, and various homeopathic treatments that were minimally efficacious or nonefficacious. He was unsure if antifungals had previously been prescribed.

The patient’s medical history was notable for pulmonary interstitial fibrosis, anxiety, posttraumatic stress disorder, and mild glucose intolerance. The patient had no pertinent surgical history and no known drug allergies. Current medications included a bronchodilating inhaler, escitalopram, trazodone, buspirone, clonazepam, prazosin, gabapentin, and azithromycin for current upper respiratory tract infection. The patient was a former smoker and a social drinker.

On physical evaluation the pubic area displayed slight patchy erythema without a papular component and was otherwise unremarkable to the unaided eye. Upon palpation of the skin, there were no remarkable findings. Under dermoscopic evaluation, small white-yellow concretions along the hair shaft were noticed. Evaluation with a Wood lamp is shown in Figure 1.

The patient was treated empirically with ketoconazole cream 2% applied to the affected area once daily until follow-up 3 weeks later. The patient also was advised to shave the pubic area to remove potentially infected hairs, as white piedra (WP) was suspected. A diagnosis of WP was confirmed on histologic evaluation of pubic hair samples approximately 1 to 2 weeks later (Figure 2).

At 3-week follow-up, Wood lamp evaluation did not identify concretions along the pubic hair shafts. The patient was symptom free and extremely pleased. Of note, the patient did not shave the pubic area and was counseled on recurrence.

Comment

Piedra (meaning stone in Spanish) describes a group of fungal infections that present with gritty concretions on the hair shaft.^1,2 In 1911, Horta³ classified piedra into 2 subtypes: black piedra, caused by Piedraia hortae, and WP, caused by Trichosporon species. Black piedra occurs more frequently in tropical countries and commonly affects hair shafts on the scalp.⁴ White piedra most commonly affects the pubic area, with rare cases in scalp and facial hair.^1,5-7

Epidemiology
White piedra is seen worldwide, including Europe, South America, India, Southeast Asia, Africa, South America, and southern parts of the United States. The majority of cases occur in tropical and temperate regions.¹ White piedra likely is underdiagnosed; for example, in a study of 166 young men with genital concerns in Houston, Texas, Trichosporon was isolated in 40% of cultured scrotal hairs.⁸

Species Identification
There are several species of WP; special techniques must be used to differentiate them, which is beyond the scope of this case. The known species include Trichosporon asahii, Trichosporon asteroides, Trichosporon cutaneum, Trichosporon inkin, Trichosporon mucoides, and Trichosporon ovoides.¹Trichosporon asahii and T mucoides have been known to cause systemic infections in immunocompromised hosts known as trichosporonosis.^1,9 As an example of a special technique used for species recognition, Sugita et al¹⁰ used sequence analysis of the ribosomal DNA intergenic spacer 1 regions to distinguish T asahii isolates. Identification of species may be warranted in the proper clinical scenario; however, histologic evaluation by an experienced dermatopathologist frequently is sufficient to identify the Trichosporon genus.

Transmission
The 2 most common causative organisms of WP are T inkin and T ovoides. Furthermore, T inkin causes the vast majority of WP in the pubic region.⁸Trichosporon species may be found in air, soil, water, and sewage,⁷ and have been isolated in hair samples from horses, dogs, and monkeys.¹¹ The mode of transmission in humans remains elusive but has been reported from poor personal hygiene and bathing in stagnant water as well as sexual transmission in the case of pubic infestation.^5,8,11-13

Diagnosis and Differential
White piedra is characterized by the presence of adherent tan to white nodules along the hair shafts. The concretions tend to be softer than black piedra and, unlike trichomycosis, normally do not fluoresce.¹ They do not encircle the hair shaft as hair casts do and can be readily distinguished from Trichomycosis axillaris, black piedra, pediculosis, and trichorrhexis nodosa on microscopic examination.¹⁴ The hair shaft concretions of WP are difficult to visualize with the unaided eye. As a result, it is easily misdiagnosed.¹⁵ Upon palpation of the infected hair shafts, a grainy sensation is evident. Dermoscopy improves visualization, and fluorescence was useful in our case. Microscopic evaluation will identify the adherent organism and is readily cultured on Sabouraud agar.¹⁶ Although Trichosporon species typically do not fluoresce,¹ Wood lamp examination occasionally may reveal the organism, such as in our case. A possible explanation for this finding is the synergistic relationship with Corynebacterium,¹⁷ some producing fluorescent chemicals. Growth of Trichosporon species may be enhanced by or even dependent on Corynebacterium; therefore, WP is likely a coinfection of fungus and bacteria.^17,18 Studies also name a novel species of Brevibacterium in relationship with genital WP.¹⁹ This species was described as producing a foul odor, as in our patient.

Treatment
The American Academy of Dermatology’s Guidelines Committee recommends complete removal of the infected hairs.¹ The recommendation traditionally is hair removal in conjunction with topical or oral medications,¹ such as topical imidazoles, ciclopirox olamine, selenium sulfide 2%, chlorhexidine solution, zinc pyrithione, amphotericin B lotion, and oral itraconazole. Recurrence rates are high and spontaneous remission sometimes occurs.^9,20 Triazole antifungals currently are preferred for treatment of Trichosporon infections.⁵ Patients should be counseled to dispose of undergarments, as the organism has been recovered from cotton fibers and are a source of reinfection.^1,21

Conclusion

White piedra, though relatively uncommon, is likely underdiagnosed in the United States and should be suspected in any patient presenting with irritation and a foul odor in the genital area or multiple failed therapies for a nonspecific genital dermatitis. This clinical scenario warrants dermoscopic and Wood lamp examination of the affected skin and hair shafts in addition to microscopic examination of pubic hair shafts by a dermatopathologist. Fluorescence under Wood lamp may aid in diagnosis, and conflicting findings may be attributed to its synergistic relationship with Corynebacterium and Brevibacterium coinfection. Proper treatment includes shaving of the affected hair, oral or topical antifungal treatment, and disposal of affected clothing.

Case Report

A 58-year-old man presented for evaluation of a pruritic rash involving the pubic area of 30 years’ duration. Multiple primary care physicians and dermatologists had evaluated the patient during this period, but he noted a specific diagnosis had not been rendered and multiple treatments had been unsuccessful. The patient described a rash, which was absent at the time of evaluation, as a self-remitting and exacerbating irritation typically induced by sweating and physical activity. The patient also stated that the irritation was associated with a strong, distinct, musty odor that severely interrupted his sex life and decreased his quality of life. Prior treatments included various topical corticosteroids, topical and oral antibiotics, and various homeopathic treatments that were minimally efficacious or nonefficacious. He was unsure if antifungals had previously been prescribed.

The patient’s medical history was notable for pulmonary interstitial fibrosis, anxiety, posttraumatic stress disorder, and mild glucose intolerance. The patient had no pertinent surgical history and no known drug allergies. Current medications included a bronchodilating inhaler, escitalopram, trazodone, buspirone, clonazepam, prazosin, gabapentin, and azithromycin for current upper respiratory tract infection. The patient was a former smoker and a social drinker.

On physical evaluation the pubic area displayed slight patchy erythema without a papular component and was otherwise unremarkable to the unaided eye. Upon palpation of the skin, there were no remarkable findings. Under dermoscopic evaluation, small white-yellow concretions along the hair shaft were noticed. Evaluation with a Wood lamp is shown in Figure 1.

The patient was treated empirically with ketoconazole cream 2% applied to the affected area once daily until follow-up 3 weeks later. The patient also was advised to shave the pubic area to remove potentially infected hairs, as white piedra (WP) was suspected. A diagnosis of WP was confirmed on histologic evaluation of pubic hair samples approximately 1 to 2 weeks later (Figure 2).

At 3-week follow-up, Wood lamp evaluation did not identify concretions along the pubic hair shafts. The patient was symptom free and extremely pleased. Of note, the patient did not shave the pubic area and was counseled on recurrence.

Comment

Piedra (meaning stone in Spanish) describes a group of fungal infections that present with gritty concretions on the hair shaft.^1,2 In 1911, Horta³ classified piedra into 2 subtypes: black piedra, caused by Piedraia hortae, and WP, caused by Trichosporon species. Black piedra occurs more frequently in tropical countries and commonly affects hair shafts on the scalp.⁴ White piedra most commonly affects the pubic area, with rare cases in scalp and facial hair.^1,5-7

Epidemiology
White piedra is seen worldwide, including Europe, South America, India, Southeast Asia, Africa, South America, and southern parts of the United States. The majority of cases occur in tropical and temperate regions.¹ White piedra likely is underdiagnosed; for example, in a study of 166 young men with genital concerns in Houston, Texas, Trichosporon was isolated in 40% of cultured scrotal hairs.⁸

Species Identification
There are several species of WP; special techniques must be used to differentiate them, which is beyond the scope of this case. The known species include Trichosporon asahii, Trichosporon asteroides, Trichosporon cutaneum, Trichosporon inkin, Trichosporon mucoides, and Trichosporon ovoides.¹Trichosporon asahii and T mucoides have been known to cause systemic infections in immunocompromised hosts known as trichosporonosis.^1,9 As an example of a special technique used for species recognition, Sugita et al¹⁰ used sequence analysis of the ribosomal DNA intergenic spacer 1 regions to distinguish T asahii isolates. Identification of species may be warranted in the proper clinical scenario; however, histologic evaluation by an experienced dermatopathologist frequently is sufficient to identify the Trichosporon genus.

Transmission
The 2 most common causative organisms of WP are T inkin and T ovoides. Furthermore, T inkin causes the vast majority of WP in the pubic region.⁸Trichosporon species may be found in air, soil, water, and sewage,⁷ and have been isolated in hair samples from horses, dogs, and monkeys.¹¹ The mode of transmission in humans remains elusive but has been reported from poor personal hygiene and bathing in stagnant water as well as sexual transmission in the case of pubic infestation.^5,8,11-13

Diagnosis and Differential
White piedra is characterized by the presence of adherent tan to white nodules along the hair shafts. The concretions tend to be softer than black piedra and, unlike trichomycosis, normally do not fluoresce.¹ They do not encircle the hair shaft as hair casts do and can be readily distinguished from Trichomycosis axillaris, black piedra, pediculosis, and trichorrhexis nodosa on microscopic examination.¹⁴ The hair shaft concretions of WP are difficult to visualize with the unaided eye. As a result, it is easily misdiagnosed.¹⁵ Upon palpation of the infected hair shafts, a grainy sensation is evident. Dermoscopy improves visualization, and fluorescence was useful in our case. Microscopic evaluation will identify the adherent organism and is readily cultured on Sabouraud agar.¹⁶ Although Trichosporon species typically do not fluoresce,¹ Wood lamp examination occasionally may reveal the organism, such as in our case. A possible explanation for this finding is the synergistic relationship with Corynebacterium,¹⁷ some producing fluorescent chemicals. Growth of Trichosporon species may be enhanced by or even dependent on Corynebacterium; therefore, WP is likely a coinfection of fungus and bacteria.^17,18 Studies also name a novel species of Brevibacterium in relationship with genital WP.¹⁹ This species was described as producing a foul odor, as in our patient.

Treatment
The American Academy of Dermatology’s Guidelines Committee recommends complete removal of the infected hairs.¹ The recommendation traditionally is hair removal in conjunction with topical or oral medications,¹ such as topical imidazoles, ciclopirox olamine, selenium sulfide 2%, chlorhexidine solution, zinc pyrithione, amphotericin B lotion, and oral itraconazole. Recurrence rates are high and spontaneous remission sometimes occurs.^9,20 Triazole antifungals currently are preferred for treatment of Trichosporon infections.⁵ Patients should be counseled to dispose of undergarments, as the organism has been recovered from cotton fibers and are a source of reinfection.^1,21

Conclusion

White piedra, though relatively uncommon, is likely underdiagnosed in the United States and should be suspected in any patient presenting with irritation and a foul odor in the genital area or multiple failed therapies for a nonspecific genital dermatitis. This clinical scenario warrants dermoscopic and Wood lamp examination of the affected skin and hair shafts in addition to microscopic examination of pubic hair shafts by a dermatopathologist. Fluorescence under Wood lamp may aid in diagnosis, and conflicting findings may be attributed to its synergistic relationship with Corynebacterium and Brevibacterium coinfection. Proper treatment includes shaving of the affected hair, oral or topical antifungal treatment, and disposal of affected clothing.

Case Report

A 58-year-old man presented for evaluation of a pruritic rash involving the pubic area of 30 years’ duration. Multiple primary care physicians and dermatologists had evaluated the patient during this period, but he noted a specific diagnosis had not been rendered and multiple treatments had been unsuccessful. The patient described a rash, which was absent at the time of evaluation, as a self-remitting and exacerbating irritation typically induced by sweating and physical activity. The patient also stated that the irritation was associated with a strong, distinct, musty odor that severely interrupted his sex life and decreased his quality of life. Prior treatments included various topical corticosteroids, topical and oral antibiotics, and various homeopathic treatments that were minimally efficacious or nonefficacious. He was unsure if antifungals had previously been prescribed.

The patient’s medical history was notable for pulmonary interstitial fibrosis, anxiety, posttraumatic stress disorder, and mild glucose intolerance. The patient had no pertinent surgical history and no known drug allergies. Current medications included a bronchodilating inhaler, escitalopram, trazodone, buspirone, clonazepam, prazosin, gabapentin, and azithromycin for current upper respiratory tract infection. The patient was a former smoker and a social drinker.

On physical evaluation the pubic area displayed slight patchy erythema without a papular component and was otherwise unremarkable to the unaided eye. Upon palpation of the skin, there were no remarkable findings. Under dermoscopic evaluation, small white-yellow concretions along the hair shaft were noticed. Evaluation with a Wood lamp is shown in Figure 1.

The patient was treated empirically with ketoconazole cream 2% applied to the affected area once daily until follow-up 3 weeks later. The patient also was advised to shave the pubic area to remove potentially infected hairs, as white piedra (WP) was suspected. A diagnosis of WP was confirmed on histologic evaluation of pubic hair samples approximately 1 to 2 weeks later (Figure 2).

At 3-week follow-up, Wood lamp evaluation did not identify concretions along the pubic hair shafts. The patient was symptom free and extremely pleased. Of note, the patient did not shave the pubic area and was counseled on recurrence.

Comment

Piedra (meaning stone in Spanish) describes a group of fungal infections that present with gritty concretions on the hair shaft.^1,2 In 1911, Horta³ classified piedra into 2 subtypes: black piedra, caused by Piedraia hortae, and WP, caused by Trichosporon species. Black piedra occurs more frequently in tropical countries and commonly affects hair shafts on the scalp.⁴ White piedra most commonly affects the pubic area, with rare cases in scalp and facial hair.^1,5-7

Epidemiology
White piedra is seen worldwide, including Europe, South America, India, Southeast Asia, Africa, South America, and southern parts of the United States. The majority of cases occur in tropical and temperate regions.¹ White piedra likely is underdiagnosed; for example, in a study of 166 young men with genital concerns in Houston, Texas, Trichosporon was isolated in 40% of cultured scrotal hairs.⁸

Species Identification
There are several species of WP; special techniques must be used to differentiate them, which is beyond the scope of this case. The known species include Trichosporon asahii, Trichosporon asteroides, Trichosporon cutaneum, Trichosporon inkin, Trichosporon mucoides, and Trichosporon ovoides.¹Trichosporon asahii and T mucoides have been known to cause systemic infections in immunocompromised hosts known as trichosporonosis.^1,9 As an example of a special technique used for species recognition, Sugita et al¹⁰ used sequence analysis of the ribosomal DNA intergenic spacer 1 regions to distinguish T asahii isolates. Identification of species may be warranted in the proper clinical scenario; however, histologic evaluation by an experienced dermatopathologist frequently is sufficient to identify the Trichosporon genus.

Transmission
The 2 most common causative organisms of WP are T inkin and T ovoides. Furthermore, T inkin causes the vast majority of WP in the pubic region.⁸Trichosporon species may be found in air, soil, water, and sewage,⁷ and have been isolated in hair samples from horses, dogs, and monkeys.¹¹ The mode of transmission in humans remains elusive but has been reported from poor personal hygiene and bathing in stagnant water as well as sexual transmission in the case of pubic infestation.^5,8,11-13

Diagnosis and Differential
White piedra is characterized by the presence of adherent tan to white nodules along the hair shafts. The concretions tend to be softer than black piedra and, unlike trichomycosis, normally do not fluoresce.¹ They do not encircle the hair shaft as hair casts do and can be readily distinguished from Trichomycosis axillaris, black piedra, pediculosis, and trichorrhexis nodosa on microscopic examination.¹⁴ The hair shaft concretions of WP are difficult to visualize with the unaided eye. As a result, it is easily misdiagnosed.¹⁵ Upon palpation of the infected hair shafts, a grainy sensation is evident. Dermoscopy improves visualization, and fluorescence was useful in our case. Microscopic evaluation will identify the adherent organism and is readily cultured on Sabouraud agar.¹⁶ Although Trichosporon species typically do not fluoresce,¹ Wood lamp examination occasionally may reveal the organism, such as in our case. A possible explanation for this finding is the synergistic relationship with Corynebacterium,¹⁷ some producing fluorescent chemicals. Growth of Trichosporon species may be enhanced by or even dependent on Corynebacterium; therefore, WP is likely a coinfection of fungus and bacteria.^17,18 Studies also name a novel species of Brevibacterium in relationship with genital WP.¹⁹ This species was described as producing a foul odor, as in our patient.

Treatment
The American Academy of Dermatology’s Guidelines Committee recommends complete removal of the infected hairs.¹ The recommendation traditionally is hair removal in conjunction with topical or oral medications,¹ such as topical imidazoles, ciclopirox olamine, selenium sulfide 2%, chlorhexidine solution, zinc pyrithione, amphotericin B lotion, and oral itraconazole. Recurrence rates are high and spontaneous remission sometimes occurs.^9,20 Triazole antifungals currently are preferred for treatment of Trichosporon infections.⁵ Patients should be counseled to dispose of undergarments, as the organism has been recovered from cotton fibers and are a source of reinfection.^1,21

Conclusion

White piedra, though relatively uncommon, is likely underdiagnosed in the United States and should be suspected in any patient presenting with irritation and a foul odor in the genital area or multiple failed therapies for a nonspecific genital dermatitis. This clinical scenario warrants dermoscopic and Wood lamp examination of the affected skin and hair shafts in addition to microscopic examination of pubic hair shafts by a dermatopathologist. Fluorescence under Wood lamp may aid in diagnosis, and conflicting findings may be attributed to its synergistic relationship with Corynebacterium and Brevibacterium coinfection. Proper treatment includes shaving of the affected hair, oral or topical antifungal treatment, and disposal of affected clothing.

The head louse (Pediculus humanus capitis) is a blood-sucking arthropod of the suborder Anoplura. Lice are obligate human parasites that have infested humans since antiquity. Pediculosis capitis is an infestation of the scalp by head lice. It is estimated that 6 to 12 million individuals in the United States are affected with head lice per year.¹ Resistance to topical chemical pediculicides is widespread, and new agents have been developed to address this gap in care.

Characteristics of Head Lice

The head louse is a tan-gray–colored, wingless insect measuring approximately 2- to 3-mm long with 3 body segments. It has 6 legs with claws used to grasp individual hairs, and it moves by crawling; it does not fly or jump.^2,3 The head louse has an elongated abdomen and a small head with short antennae and anterior piercing mouthparts (Figure 1).⁴ Nits are transparent, flask-shaped, 0.5- to 0.8-mm egg cases found firmly cemented to the hair shafts approximately 1 to 4 mm above the level of the scalp (Figure 2).⁵ The head louse resides on scalp hair and feeds off the scalp itself. Both lice and nits can be present throughout the scalp but are most commonly found in the postauricular and occipital scalp.^3,4

Female lice live approximately 30 days and lay 5 to 10 eggs per day. Eggs incubate individually in nits laid close to the scalp for 8 to 10 days before hatching.^1,6 The newly hatched nymphs (also called instars) have multiple exoskeletons that are shed as they grow.⁷ Nymphs mature into adults in approximately 2 weeks, and the life cycle begins again.⁸ Head lice are obligate human parasites, feeding approximately every 4 to 6 hours on the blood of the host; however, they can survive up to 4 days without a blood meal on fomites if the climate and conditions are favorable.^5,9

Epidemiology and Transmission

Head lice infestations commonly occur in children aged 3 to 11 years and are more prevalent in girls and women.^1,10 Infestation rates are not reliably recorded, and few population-based studies have been performed; however, it is estimated that 6 to 12 million individuals are infested annually in the United States.¹ Prevalence in some European populations has been estimated to range from 1% to 20%.¹¹ A 2008 literature review found that worldwide prevalence varied across populations from 0.7% to 59%.¹⁰

Transmission occurs most frequently from direct head-to-head contact. One study found that transmission is most likely to occur when hairs are arranged in a parallel alignment and move slowly in relation to one another.¹² Although controversial and probably less notable, transmission also may occur indirectly via fomites or the sharing of hairbrushes, hats, or other headgear.^13,14 Classrooms are a common place for transmission.¹ A 2009 study in Germany found an increase in health department consultations for head lice when schools reopened after vacations. The investigators also found that pediculicide sales peaked from mid-September through October, subsequent to schools reopening after the summer holiday.¹⁵ There is some evidence that overcrowded housing also can lead to increased incidence and transmission.^16,17 There is no consistent correlation of infestation with socioeconomic status.^1,17,18

Clinical Manifestations and Diagnosis

Clinically, patients with head lice present with scalp pruritus and sometimes posterior cervical or occipital lymphadenopathy. Pediculosis also can be asymptomatic. With the first exposure, symptoms may not develop for up to 4 to 6 weeks as the immune system develops sensitivity to the louse saliva.⁶ Bite reactions consisting of papules or wheals are related to immune sensitization.⁵ Louse feces and excoriations from scratching to relieve itch also may be present on examination. Secondary infection of excoriations also is possible.¹

Diagnosis of an active infestation is made by identifying living lice. Because lice move quickly and can be difficult to detect, tightly attached nits on the hair shaft within 4 mm of the scalp are at least indicative of a historic infestation and can be suggestive of active infestation.^1,19 Dermoscopy is a helpful tool in differentiating eggs containing nymphs from the empty cases of hatched lice and also from amorphous pseudonits (hair casts)(Figure 3).^19,20 Wet combing improves the accuracy of diagnosing an active infection.²¹

Treatment

Effective treatment of head lice requires eradication of all living lice as well as louse eggs. Topically applied pyrethroids, including pyrethrin shampoos and mousses and permethrin lotion 1%, are considered the first-line therapy.⁸ Pyrethroids are over-the-counter treatments that act by interfering with sodium transport in the louse, causing depolarization of the neuromembranes and respiratory paralysis.²² Pyrethrins are natural compounds derived from the chrysanthemum plant; permethrin is a synthetic compound. Pyrethrins often are combined with piperonyl butoxide, an insecticide synergist that improves efficacy by inhibiting pyrethrin catabolism.²³ Resistance to pyrethroids has become an increasingly important problem in the United States and worldwide.

Malathion lotion 0.5% is another therapeutic option for head lice. Malathion is a prescription organophosphate cholinesterase inhibitor that also causes respiratory paralysis of the louse and is one of the few treatments that is ovicidal.²² It was withdrawn from the market in 1995 due to its flammability and a theoretical risk of respiratory depression if ingested; however, it was reintroduced in 1999 and remains an effective treatment option with little resistance in the United States.²⁴

Lindane 1% (shampoo and lotion), an organochloride compound that acts by causing neuronal hyperstimulation and eventual paralysis of lice, is no longer recommended due to its serious side effects, including central nervous system toxicity and increased risk of seizure.^8,24

New US Food and Drug Administration–Approved Therapies
Newer topical treatments include benzyl alcohol lotion 5%, spinosad topical suspension 0.9%, ivermectin lotion 0.5%, and dimethicone-based products. Benzyl alcohol was approved by the US Food and Drug Administration (FDA) in 2009 and is available in the United States by prescription.²⁵ Benzyl alcohol kills lice by asphyxiation. Phase 2 and 3 clinical trials showed significant treatment success 1 day posttreatment (fewer live lice than the vehicle alone; P=.004) and 2 weeks posttreatment (absence of live lice compared to the vehicle alone; P=.001).²⁶

Spinosad was approved by the FDA in 2011 and is available in the United States by prescription.²⁵ It contains the compounds spinosyn A and spinosyn D, which are naturally derived through fermentation by the soil bacterium Saccharopolyspora spinosa. It also contains benzyl alcohol. Spinosad paralyzes lice by disrupting neuronal activity and is at least partially ovicidal.²⁷ Phase 3 clinical trials published in 2009 showed that spinosad was significantly more effective than permethrin in eradicating head lice (P<.001).²⁸

Topical ivermectin was approved by the FDA in 2012 for prescription use.²⁵ It acts on chloride ion channels, causing hyperpolarization of the muscle cells of lice and resulting in paralysis and death. Oral ivermectin (200 μg/kg) given once and repeated in 10 days is not FDA approved for the treatment of head lice but has shown some effectiveness and is sometimes used.⁸ A comparison study of topical versus oral ivermectin published in 2014 found that eradication was achieved in 88% (n=27) of topical ivermectin users after 1 treatment and 100% (n=31) after 2 treatments. Oral ivermectin produced cure rates of 45% (n=14) after 1 treatment and 97% (n=30) after 2 treatments. Both topical and oral ivermectin treatments are well tolerated.²⁹

Physically Acting Preparations
Products with a physical mode of action are a new attractive option for treatment of pediculosis because the development of resistance is less likely. Studies of silicone-based fluids that physically occlude the respiratory system of the louse, such as dimethicone liquid gel 4%, have shown superiority over treatment with pyrethroids.^30,31 Although the safety of dimethicone has been demonstrated, silicone-based treatments have not yet been widely adopted in the United States and are not currently used as a first-line treatment.³² However, use of such physically acting pediculicides may in time surpass traditional neurotoxic treatments due to their low susceptibility to resistance and good safety profile.^33,34

Alternative Therapies
Nonchemical treatments for head lice that have shown variable success include wet combing, hot air treatments, and varying occlusive treatments. Physical removal via wet combing requires persistent repeated treatments over several weeks; for example, wet combing may be performed every 3 days for at least 2 weeks or until no head lice are detected on 4 consecutive occasions.³⁵ Cure rates range from 38% to 75% with wet combing as a sole treatment of head lice.³⁶ Because this treatment has minimal risks and no adverse side effects, it can be considered as an alternative treatment for some patients.

Hot air treatments also have been studied. A 2006 study showed that a hot air treatment device had the potential to eradicate head lice, most likely by desiccation. Specifically, 30 minutes of exposure to hot air (at 58.9°F, slightly cooler than a standard hair dryer) using the custom-built device resulted in 98% mortality of eggs and 80% mortality of hatched lice.³⁷ Large randomized controlled trials of hot air treatments have not been performed.

Other alternative treatments include plant-derived oils. A laboratory study of essential oils found that spearmint, cassia, and clove showed pediculicidal activity similar to malathion with improved ovicidal activity.³⁸ However, there is a potential for development of contact dermatitis from essential oils.

Complete Eradication of Head Lice
Removal of nits is an important component of effective lice eradication. Biochemical analysis has revealed that the nit sheath of the head louse is similar in composition to amyloid, rendering it difficult to design products that will unravel the nit sheath while leaving human hair undamaged.³⁹ Because pediculicides are not necessarily ovicidal and complete physical nit removal is difficult to achieve, re-treatment in 7 to 10 days often is advisable to ensure that lice in all stages of the life cycle have been killed.⁴ Treatment of any secondary bacterial infection also is important. Although transmission of lice via fomites is less likely than from head-to-head contact, the cleaning of hats, hairbrushes, and linens is prudent. Diagnosing and treating infested close contacts also is essential to achieving eradication.⁴ Coordinated surveillance, education, and treatment efforts in high-risk communities can help detect asymptomatic cases and control local epidemics in a cost-effective manner.⁴⁰ However, “no nit” policies at schools likely cause a net harm, as nit removal is difficult and children with nonviable nits are then excluded from the classroom.⁵

Treatment Resistance
Resistance to topical neurotoxic treatments is becoming increasingly common.^41-43 Therefore, it is important to identify local patterns of resistance, if possible, when selecting a therapy for head lice. Improper usage, changes in pediculicide formulations and packaging, decreased product efficacy, and natural selection have all contributed to this rise in resistance.⁷ Additionally, due to protection from multiple exoskeletons and the natural molting process as they mature into adults, nymphs may only receive a sublethal dose when exposed to pediculicides, contributing further to resistance.⁷ Resistance to synthetic pyrethroids is most predominant, likely due to selection pressure because permethrin historically has been the most widely used insecticide for pediculosis. A 2014 study found that the frequency of sodium-channel insensitivity to pyrethroids, also known as knockdown resistance (or kdr), in US head louse populations collected over a 10-year period was 84.4% and approached 100% in some communities in recent years.⁴⁴ This evidence strongly supports the use of alternative therapeutic categories to effectively eradicate head lice infestations.

Conclusion

Head lice infestation is common in children, and although it is not harmful to the host, it can be an irritating and symptomatic problem and can lead to notable distress, missed days of school, and secondary infections. Identifying active adult lice is the gold standard for diagnosis. Current recommended treatments include pyrethroids as the first-line therapy; however, resistance to these neurotoxic agents is becoming increasingly common. Alternative therapies such as newer neurotoxic agents or pediculicides with physical mechanisms of action (eg, dimethicone-based products) should be considered, particularly in regions where resistance is known to be high. Education about head lice, proper use of treatment, and coordinated diagnosis are necessary for effective management of this problem.

The head louse (Pediculus humanus capitis) is a blood-sucking arthropod of the suborder Anoplura. Lice are obligate human parasites that have infested humans since antiquity. Pediculosis capitis is an infestation of the scalp by head lice. It is estimated that 6 to 12 million individuals in the United States are affected with head lice per year.¹ Resistance to topical chemical pediculicides is widespread, and new agents have been developed to address this gap in care.

Characteristics of Head Lice

The head louse is a tan-gray–colored, wingless insect measuring approximately 2- to 3-mm long with 3 body segments. It has 6 legs with claws used to grasp individual hairs, and it moves by crawling; it does not fly or jump.^2,3 The head louse has an elongated abdomen and a small head with short antennae and anterior piercing mouthparts (Figure 1).⁴ Nits are transparent, flask-shaped, 0.5- to 0.8-mm egg cases found firmly cemented to the hair shafts approximately 1 to 4 mm above the level of the scalp (Figure 2).⁵ The head louse resides on scalp hair and feeds off the scalp itself. Both lice and nits can be present throughout the scalp but are most commonly found in the postauricular and occipital scalp.^3,4

Female lice live approximately 30 days and lay 5 to 10 eggs per day. Eggs incubate individually in nits laid close to the scalp for 8 to 10 days before hatching.^1,6 The newly hatched nymphs (also called instars) have multiple exoskeletons that are shed as they grow.⁷ Nymphs mature into adults in approximately 2 weeks, and the life cycle begins again.⁸ Head lice are obligate human parasites, feeding approximately every 4 to 6 hours on the blood of the host; however, they can survive up to 4 days without a blood meal on fomites if the climate and conditions are favorable.^5,9

Epidemiology and Transmission

Head lice infestations commonly occur in children aged 3 to 11 years and are more prevalent in girls and women.^1,10 Infestation rates are not reliably recorded, and few population-based studies have been performed; however, it is estimated that 6 to 12 million individuals are infested annually in the United States.¹ Prevalence in some European populations has been estimated to range from 1% to 20%.¹¹ A 2008 literature review found that worldwide prevalence varied across populations from 0.7% to 59%.¹⁰

Transmission occurs most frequently from direct head-to-head contact. One study found that transmission is most likely to occur when hairs are arranged in a parallel alignment and move slowly in relation to one another.¹² Although controversial and probably less notable, transmission also may occur indirectly via fomites or the sharing of hairbrushes, hats, or other headgear.^13,14 Classrooms are a common place for transmission.¹ A 2009 study in Germany found an increase in health department consultations for head lice when schools reopened after vacations. The investigators also found that pediculicide sales peaked from mid-September through October, subsequent to schools reopening after the summer holiday.¹⁵ There is some evidence that overcrowded housing also can lead to increased incidence and transmission.^16,17 There is no consistent correlation of infestation with socioeconomic status.^1,17,18

Clinical Manifestations and Diagnosis

Clinically, patients with head lice present with scalp pruritus and sometimes posterior cervical or occipital lymphadenopathy. Pediculosis also can be asymptomatic. With the first exposure, symptoms may not develop for up to 4 to 6 weeks as the immune system develops sensitivity to the louse saliva.⁶ Bite reactions consisting of papules or wheals are related to immune sensitization.⁵ Louse feces and excoriations from scratching to relieve itch also may be present on examination. Secondary infection of excoriations also is possible.¹

Diagnosis of an active infestation is made by identifying living lice. Because lice move quickly and can be difficult to detect, tightly attached nits on the hair shaft within 4 mm of the scalp are at least indicative of a historic infestation and can be suggestive of active infestation.^1,19 Dermoscopy is a helpful tool in differentiating eggs containing nymphs from the empty cases of hatched lice and also from amorphous pseudonits (hair casts)(Figure 3).^19,20 Wet combing improves the accuracy of diagnosing an active infection.²¹

Treatment

Effective treatment of head lice requires eradication of all living lice as well as louse eggs. Topically applied pyrethroids, including pyrethrin shampoos and mousses and permethrin lotion 1%, are considered the first-line therapy.⁸ Pyrethroids are over-the-counter treatments that act by interfering with sodium transport in the louse, causing depolarization of the neuromembranes and respiratory paralysis.²² Pyrethrins are natural compounds derived from the chrysanthemum plant; permethrin is a synthetic compound. Pyrethrins often are combined with piperonyl butoxide, an insecticide synergist that improves efficacy by inhibiting pyrethrin catabolism.²³ Resistance to pyrethroids has become an increasingly important problem in the United States and worldwide.

Malathion lotion 0.5% is another therapeutic option for head lice. Malathion is a prescription organophosphate cholinesterase inhibitor that also causes respiratory paralysis of the louse and is one of the few treatments that is ovicidal.²² It was withdrawn from the market in 1995 due to its flammability and a theoretical risk of respiratory depression if ingested; however, it was reintroduced in 1999 and remains an effective treatment option with little resistance in the United States.²⁴

Lindane 1% (shampoo and lotion), an organochloride compound that acts by causing neuronal hyperstimulation and eventual paralysis of lice, is no longer recommended due to its serious side effects, including central nervous system toxicity and increased risk of seizure.^8,24

New US Food and Drug Administration–Approved Therapies
Newer topical treatments include benzyl alcohol lotion 5%, spinosad topical suspension 0.9%, ivermectin lotion 0.5%, and dimethicone-based products. Benzyl alcohol was approved by the US Food and Drug Administration (FDA) in 2009 and is available in the United States by prescription.²⁵ Benzyl alcohol kills lice by asphyxiation. Phase 2 and 3 clinical trials showed significant treatment success 1 day posttreatment (fewer live lice than the vehicle alone; P=.004) and 2 weeks posttreatment (absence of live lice compared to the vehicle alone; P=.001).²⁶

Spinosad was approved by the FDA in 2011 and is available in the United States by prescription.²⁵ It contains the compounds spinosyn A and spinosyn D, which are naturally derived through fermentation by the soil bacterium Saccharopolyspora spinosa. It also contains benzyl alcohol. Spinosad paralyzes lice by disrupting neuronal activity and is at least partially ovicidal.²⁷ Phase 3 clinical trials published in 2009 showed that spinosad was significantly more effective than permethrin in eradicating head lice (P<.001).²⁸

Topical ivermectin was approved by the FDA in 2012 for prescription use.²⁵ It acts on chloride ion channels, causing hyperpolarization of the muscle cells of lice and resulting in paralysis and death. Oral ivermectin (200 μg/kg) given once and repeated in 10 days is not FDA approved for the treatment of head lice but has shown some effectiveness and is sometimes used.⁸ A comparison study of topical versus oral ivermectin published in 2014 found that eradication was achieved in 88% (n=27) of topical ivermectin users after 1 treatment and 100% (n=31) after 2 treatments. Oral ivermectin produced cure rates of 45% (n=14) after 1 treatment and 97% (n=30) after 2 treatments. Both topical and oral ivermectin treatments are well tolerated.²⁹

Physically Acting Preparations
Products with a physical mode of action are a new attractive option for treatment of pediculosis because the development of resistance is less likely. Studies of silicone-based fluids that physically occlude the respiratory system of the louse, such as dimethicone liquid gel 4%, have shown superiority over treatment with pyrethroids.^30,31 Although the safety of dimethicone has been demonstrated, silicone-based treatments have not yet been widely adopted in the United States and are not currently used as a first-line treatment.³² However, use of such physically acting pediculicides may in time surpass traditional neurotoxic treatments due to their low susceptibility to resistance and good safety profile.^33,34

Alternative Therapies
Nonchemical treatments for head lice that have shown variable success include wet combing, hot air treatments, and varying occlusive treatments. Physical removal via wet combing requires persistent repeated treatments over several weeks; for example, wet combing may be performed every 3 days for at least 2 weeks or until no head lice are detected on 4 consecutive occasions.³⁵ Cure rates range from 38% to 75% with wet combing as a sole treatment of head lice.³⁶ Because this treatment has minimal risks and no adverse side effects, it can be considered as an alternative treatment for some patients.

Hot air treatments also have been studied. A 2006 study showed that a hot air treatment device had the potential to eradicate head lice, most likely by desiccation. Specifically, 30 minutes of exposure to hot air (at 58.9°F, slightly cooler than a standard hair dryer) using the custom-built device resulted in 98% mortality of eggs and 80% mortality of hatched lice.³⁷ Large randomized controlled trials of hot air treatments have not been performed.

Other alternative treatments include plant-derived oils. A laboratory study of essential oils found that spearmint, cassia, and clove showed pediculicidal activity similar to malathion with improved ovicidal activity.³⁸ However, there is a potential for development of contact dermatitis from essential oils.

Complete Eradication of Head Lice
Removal of nits is an important component of effective lice eradication. Biochemical analysis has revealed that the nit sheath of the head louse is similar in composition to amyloid, rendering it difficult to design products that will unravel the nit sheath while leaving human hair undamaged.³⁹ Because pediculicides are not necessarily ovicidal and complete physical nit removal is difficult to achieve, re-treatment in 7 to 10 days often is advisable to ensure that lice in all stages of the life cycle have been killed.⁴ Treatment of any secondary bacterial infection also is important. Although transmission of lice via fomites is less likely than from head-to-head contact, the cleaning of hats, hairbrushes, and linens is prudent. Diagnosing and treating infested close contacts also is essential to achieving eradication.⁴ Coordinated surveillance, education, and treatment efforts in high-risk communities can help detect asymptomatic cases and control local epidemics in a cost-effective manner.⁴⁰ However, “no nit” policies at schools likely cause a net harm, as nit removal is difficult and children with nonviable nits are then excluded from the classroom.⁵

Treatment Resistance
Resistance to topical neurotoxic treatments is becoming increasingly common.^41-43 Therefore, it is important to identify local patterns of resistance, if possible, when selecting a therapy for head lice. Improper usage, changes in pediculicide formulations and packaging, decreased product efficacy, and natural selection have all contributed to this rise in resistance.⁷ Additionally, due to protection from multiple exoskeletons and the natural molting process as they mature into adults, nymphs may only receive a sublethal dose when exposed to pediculicides, contributing further to resistance.⁷ Resistance to synthetic pyrethroids is most predominant, likely due to selection pressure because permethrin historically has been the most widely used insecticide for pediculosis. A 2014 study found that the frequency of sodium-channel insensitivity to pyrethroids, also known as knockdown resistance (or kdr), in US head louse populations collected over a 10-year period was 84.4% and approached 100% in some communities in recent years.⁴⁴ This evidence strongly supports the use of alternative therapeutic categories to effectively eradicate head lice infestations.

Conclusion

Head lice infestation is common in children, and although it is not harmful to the host, it can be an irritating and symptomatic problem and can lead to notable distress, missed days of school, and secondary infections. Identifying active adult lice is the gold standard for diagnosis. Current recommended treatments include pyrethroids as the first-line therapy; however, resistance to these neurotoxic agents is becoming increasingly common. Alternative therapies such as newer neurotoxic agents or pediculicides with physical mechanisms of action (eg, dimethicone-based products) should be considered, particularly in regions where resistance is known to be high. Education about head lice, proper use of treatment, and coordinated diagnosis are necessary for effective management of this problem.

The head louse (Pediculus humanus capitis) is a blood-sucking arthropod of the suborder Anoplura. Lice are obligate human parasites that have infested humans since antiquity. Pediculosis capitis is an infestation of the scalp by head lice. It is estimated that 6 to 12 million individuals in the United States are affected with head lice per year.¹ Resistance to topical chemical pediculicides is widespread, and new agents have been developed to address this gap in care.

Characteristics of Head Lice

The head louse is a tan-gray–colored, wingless insect measuring approximately 2- to 3-mm long with 3 body segments. It has 6 legs with claws used to grasp individual hairs, and it moves by crawling; it does not fly or jump.^2,3 The head louse has an elongated abdomen and a small head with short antennae and anterior piercing mouthparts (Figure 1).⁴ Nits are transparent, flask-shaped, 0.5- to 0.8-mm egg cases found firmly cemented to the hair shafts approximately 1 to 4 mm above the level of the scalp (Figure 2).⁵ The head louse resides on scalp hair and feeds off the scalp itself. Both lice and nits can be present throughout the scalp but are most commonly found in the postauricular and occipital scalp.^3,4

Female lice live approximately 30 days and lay 5 to 10 eggs per day. Eggs incubate individually in nits laid close to the scalp for 8 to 10 days before hatching.^1,6 The newly hatched nymphs (also called instars) have multiple exoskeletons that are shed as they grow.⁷ Nymphs mature into adults in approximately 2 weeks, and the life cycle begins again.⁸ Head lice are obligate human parasites, feeding approximately every 4 to 6 hours on the blood of the host; however, they can survive up to 4 days without a blood meal on fomites if the climate and conditions are favorable.^5,9

Epidemiology and Transmission

Head lice infestations commonly occur in children aged 3 to 11 years and are more prevalent in girls and women.^1,10 Infestation rates are not reliably recorded, and few population-based studies have been performed; however, it is estimated that 6 to 12 million individuals are infested annually in the United States.¹ Prevalence in some European populations has been estimated to range from 1% to 20%.¹¹ A 2008 literature review found that worldwide prevalence varied across populations from 0.7% to 59%.¹⁰

Transmission occurs most frequently from direct head-to-head contact. One study found that transmission is most likely to occur when hairs are arranged in a parallel alignment and move slowly in relation to one another.¹² Although controversial and probably less notable, transmission also may occur indirectly via fomites or the sharing of hairbrushes, hats, or other headgear.^13,14 Classrooms are a common place for transmission.¹ A 2009 study in Germany found an increase in health department consultations for head lice when schools reopened after vacations. The investigators also found that pediculicide sales peaked from mid-September through October, subsequent to schools reopening after the summer holiday.¹⁵ There is some evidence that overcrowded housing also can lead to increased incidence and transmission.^16,17 There is no consistent correlation of infestation with socioeconomic status.^1,17,18

Clinical Manifestations and Diagnosis

Clinically, patients with head lice present with scalp pruritus and sometimes posterior cervical or occipital lymphadenopathy. Pediculosis also can be asymptomatic. With the first exposure, symptoms may not develop for up to 4 to 6 weeks as the immune system develops sensitivity to the louse saliva.⁶ Bite reactions consisting of papules or wheals are related to immune sensitization.⁵ Louse feces and excoriations from scratching to relieve itch also may be present on examination. Secondary infection of excoriations also is possible.¹

Diagnosis of an active infestation is made by identifying living lice. Because lice move quickly and can be difficult to detect, tightly attached nits on the hair shaft within 4 mm of the scalp are at least indicative of a historic infestation and can be suggestive of active infestation.^1,19 Dermoscopy is a helpful tool in differentiating eggs containing nymphs from the empty cases of hatched lice and also from amorphous pseudonits (hair casts)(Figure 3).^19,20 Wet combing improves the accuracy of diagnosing an active infection.²¹

Treatment

Effective treatment of head lice requires eradication of all living lice as well as louse eggs. Topically applied pyrethroids, including pyrethrin shampoos and mousses and permethrin lotion 1%, are considered the first-line therapy.⁸ Pyrethroids are over-the-counter treatments that act by interfering with sodium transport in the louse, causing depolarization of the neuromembranes and respiratory paralysis.²² Pyrethrins are natural compounds derived from the chrysanthemum plant; permethrin is a synthetic compound. Pyrethrins often are combined with piperonyl butoxide, an insecticide synergist that improves efficacy by inhibiting pyrethrin catabolism.²³ Resistance to pyrethroids has become an increasingly important problem in the United States and worldwide.

Malathion lotion 0.5% is another therapeutic option for head lice. Malathion is a prescription organophosphate cholinesterase inhibitor that also causes respiratory paralysis of the louse and is one of the few treatments that is ovicidal.²² It was withdrawn from the market in 1995 due to its flammability and a theoretical risk of respiratory depression if ingested; however, it was reintroduced in 1999 and remains an effective treatment option with little resistance in the United States.²⁴

Lindane 1% (shampoo and lotion), an organochloride compound that acts by causing neuronal hyperstimulation and eventual paralysis of lice, is no longer recommended due to its serious side effects, including central nervous system toxicity and increased risk of seizure.^8,24

New US Food and Drug Administration–Approved Therapies
Newer topical treatments include benzyl alcohol lotion 5%, spinosad topical suspension 0.9%, ivermectin lotion 0.5%, and dimethicone-based products. Benzyl alcohol was approved by the US Food and Drug Administration (FDA) in 2009 and is available in the United States by prescription.²⁵ Benzyl alcohol kills lice by asphyxiation. Phase 2 and 3 clinical trials showed significant treatment success 1 day posttreatment (fewer live lice than the vehicle alone; P=.004) and 2 weeks posttreatment (absence of live lice compared to the vehicle alone; P=.001).²⁶

Spinosad was approved by the FDA in 2011 and is available in the United States by prescription.²⁵ It contains the compounds spinosyn A and spinosyn D, which are naturally derived through fermentation by the soil bacterium Saccharopolyspora spinosa. It also contains benzyl alcohol. Spinosad paralyzes lice by disrupting neuronal activity and is at least partially ovicidal.²⁷ Phase 3 clinical trials published in 2009 showed that spinosad was significantly more effective than permethrin in eradicating head lice (P<.001).²⁸

Topical ivermectin was approved by the FDA in 2012 for prescription use.²⁵ It acts on chloride ion channels, causing hyperpolarization of the muscle cells of lice and resulting in paralysis and death. Oral ivermectin (200 μg/kg) given once and repeated in 10 days is not FDA approved for the treatment of head lice but has shown some effectiveness and is sometimes used.⁸ A comparison study of topical versus oral ivermectin published in 2014 found that eradication was achieved in 88% (n=27) of topical ivermectin users after 1 treatment and 100% (n=31) after 2 treatments. Oral ivermectin produced cure rates of 45% (n=14) after 1 treatment and 97% (n=30) after 2 treatments. Both topical and oral ivermectin treatments are well tolerated.²⁹

Physically Acting Preparations
Products with a physical mode of action are a new attractive option for treatment of pediculosis because the development of resistance is less likely. Studies of silicone-based fluids that physically occlude the respiratory system of the louse, such as dimethicone liquid gel 4%, have shown superiority over treatment with pyrethroids.^30,31 Although the safety of dimethicone has been demonstrated, silicone-based treatments have not yet been widely adopted in the United States and are not currently used as a first-line treatment.³² However, use of such physically acting pediculicides may in time surpass traditional neurotoxic treatments due to their low susceptibility to resistance and good safety profile.^33,34

Alternative Therapies
Nonchemical treatments for head lice that have shown variable success include wet combing, hot air treatments, and varying occlusive treatments. Physical removal via wet combing requires persistent repeated treatments over several weeks; for example, wet combing may be performed every 3 days for at least 2 weeks or until no head lice are detected on 4 consecutive occasions.³⁵ Cure rates range from 38% to 75% with wet combing as a sole treatment of head lice.³⁶ Because this treatment has minimal risks and no adverse side effects, it can be considered as an alternative treatment for some patients.

Hot air treatments also have been studied. A 2006 study showed that a hot air treatment device had the potential to eradicate head lice, most likely by desiccation. Specifically, 30 minutes of exposure to hot air (at 58.9°F, slightly cooler than a standard hair dryer) using the custom-built device resulted in 98% mortality of eggs and 80% mortality of hatched lice.³⁷ Large randomized controlled trials of hot air treatments have not been performed.

Other alternative treatments include plant-derived oils. A laboratory study of essential oils found that spearmint, cassia, and clove showed pediculicidal activity similar to malathion with improved ovicidal activity.³⁸ However, there is a potential for development of contact dermatitis from essential oils.

Complete Eradication of Head Lice
Removal of nits is an important component of effective lice eradication. Biochemical analysis has revealed that the nit sheath of the head louse is similar in composition to amyloid, rendering it difficult to design products that will unravel the nit sheath while leaving human hair undamaged.³⁹ Because pediculicides are not necessarily ovicidal and complete physical nit removal is difficult to achieve, re-treatment in 7 to 10 days often is advisable to ensure that lice in all stages of the life cycle have been killed.⁴ Treatment of any secondary bacterial infection also is important. Although transmission of lice via fomites is less likely than from head-to-head contact, the cleaning of hats, hairbrushes, and linens is prudent. Diagnosing and treating infested close contacts also is essential to achieving eradication.⁴ Coordinated surveillance, education, and treatment efforts in high-risk communities can help detect asymptomatic cases and control local epidemics in a cost-effective manner.⁴⁰ However, “no nit” policies at schools likely cause a net harm, as nit removal is difficult and children with nonviable nits are then excluded from the classroom.⁵

Treatment Resistance
Resistance to topical neurotoxic treatments is becoming increasingly common.^41-43 Therefore, it is important to identify local patterns of resistance, if possible, when selecting a therapy for head lice. Improper usage, changes in pediculicide formulations and packaging, decreased product efficacy, and natural selection have all contributed to this rise in resistance.⁷ Additionally, due to protection from multiple exoskeletons and the natural molting process as they mature into adults, nymphs may only receive a sublethal dose when exposed to pediculicides, contributing further to resistance.⁷ Resistance to synthetic pyrethroids is most predominant, likely due to selection pressure because permethrin historically has been the most widely used insecticide for pediculosis. A 2014 study found that the frequency of sodium-channel insensitivity to pyrethroids, also known as knockdown resistance (or kdr), in US head louse populations collected over a 10-year period was 84.4% and approached 100% in some communities in recent years.⁴⁴ This evidence strongly supports the use of alternative therapeutic categories to effectively eradicate head lice infestations.

Conclusion

Head lice infestation is common in children, and although it is not harmful to the host, it can be an irritating and symptomatic problem and can lead to notable distress, missed days of school, and secondary infections. Identifying active adult lice is the gold standard for diagnosis. Current recommended treatments include pyrethroids as the first-line therapy; however, resistance to these neurotoxic agents is becoming increasingly common. Alternative therapies such as newer neurotoxic agents or pediculicides with physical mechanisms of action (eg, dimethicone-based products) should be considered, particularly in regions where resistance is known to be high. Education about head lice, proper use of treatment, and coordinated diagnosis are necessary for effective management of this problem.

The use of JAK inhibitors is not the only notable development in the treatment of hair loss; light-based options show potential as well, according to Maria Hordinsky, MD.

“Although the precise mechanism remains unclear, it has been postulated that photobiomodulation acts through oxidative metabolism and transcription factor stimulation,” Dr. Hordinsky said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

The use of JAK inhibitors is not the only notable development in the treatment of hair loss; light-based options show potential as well, according to Maria Hordinsky, MD.

“Although the precise mechanism remains unclear, it has been postulated that photobiomodulation acts through oxidative metabolism and transcription factor stimulation,” Dr. Hordinsky said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

The use of JAK inhibitors is not the only notable development in the treatment of hair loss; light-based options show potential as well, according to Maria Hordinsky, MD.

“Although the precise mechanism remains unclear, it has been postulated that photobiomodulation acts through oxidative metabolism and transcription factor stimulation,” Dr. Hordinsky said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Categorizing hair loss in children depends on many factors, but it is important to rule out an infectious etiology as early as possible, according to Sheila Fallon Friedlander, MD.

“What can Tinea capitis look like? Anything,” she said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Although T. capitis most often presents in children aged 3-7 years as a pattern of localized hair loss, often with scaling, sometimes with nodules, other possibilities include pustules, boggy masses, and diffuse hair loss, said Dr. Friedlander, professor of pediatrics and dermatology at the University of California, San Diego.

Sometimes the hair loss may be so subtle that families come in complaining of “dandruff” rather than hair loss, she noted. Evaluating the patient for the presence of cervical or occipital lymph nodes is crucial; big nodes are usually a tip-off that infection is present.

The optimal treatment plan for T. capitis depends on the source, Dr. Friedlander explained. If M. canis is the cause, “griseofulvin is the drug of choice,” along with a twice-weekly sporicidal shampoo, she said.

Other treatment options include terbinafine, itraconazole, and fluconazole, and each have their pros and cons, she said. Terbinafine – which persists for months in the skin, nails, and hair – is the least expensive, and is her first choice for infections caused by T. tonsurans.

Itraconazole is available as a liquid, but costs more, causes diarrhea, and comes with a boxed warning about the potential for cardiac complications; fluconazole is the most expensive, but may be used in infants, she added.

Other high-risk groups for T. capitis include female caretakers of high-risk individuals, such as “grandma”; wrestlers; and Buddhist monks, she said. “Short hair, sharing combs, and unclean barbers” contributed to a documented increased risk of T. capitis according to a recently published study of 60 Buddhist monks whose average age was 11.6 years, she added. (Pediatr Dermatol. 2017 May;34[3]:371-3).

Dr. Friedlander had no relevant financial conflicts to disclose.

SDEF and this news organization are owned by Frontline Medical Communications.

Categorizing hair loss in children depends on many factors, but it is important to rule out an infectious etiology as early as possible, according to Sheila Fallon Friedlander, MD.

“What can Tinea capitis look like? Anything,” she said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Although T. capitis most often presents in children aged 3-7 years as a pattern of localized hair loss, often with scaling, sometimes with nodules, other possibilities include pustules, boggy masses, and diffuse hair loss, said Dr. Friedlander, professor of pediatrics and dermatology at the University of California, San Diego.

Sometimes the hair loss may be so subtle that families come in complaining of “dandruff” rather than hair loss, she noted. Evaluating the patient for the presence of cervical or occipital lymph nodes is crucial; big nodes are usually a tip-off that infection is present.

The optimal treatment plan for T. capitis depends on the source, Dr. Friedlander explained. If M. canis is the cause, “griseofulvin is the drug of choice,” along with a twice-weekly sporicidal shampoo, she said.

Other treatment options include terbinafine, itraconazole, and fluconazole, and each have their pros and cons, she said. Terbinafine – which persists for months in the skin, nails, and hair – is the least expensive, and is her first choice for infections caused by T. tonsurans.

Itraconazole is available as a liquid, but costs more, causes diarrhea, and comes with a boxed warning about the potential for cardiac complications; fluconazole is the most expensive, but may be used in infants, she added.

Other high-risk groups for T. capitis include female caretakers of high-risk individuals, such as “grandma”; wrestlers; and Buddhist monks, she said. “Short hair, sharing combs, and unclean barbers” contributed to a documented increased risk of T. capitis according to a recently published study of 60 Buddhist monks whose average age was 11.6 years, she added. (Pediatr Dermatol. 2017 May;34[3]:371-3).

Dr. Friedlander had no relevant financial conflicts to disclose.

SDEF and this news organization are owned by Frontline Medical Communications.

Categorizing hair loss in children depends on many factors, but it is important to rule out an infectious etiology as early as possible, according to Sheila Fallon Friedlander, MD.

“What can Tinea capitis look like? Anything,” she said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Although T. capitis most often presents in children aged 3-7 years as a pattern of localized hair loss, often with scaling, sometimes with nodules, other possibilities include pustules, boggy masses, and diffuse hair loss, said Dr. Friedlander, professor of pediatrics and dermatology at the University of California, San Diego.

Sometimes the hair loss may be so subtle that families come in complaining of “dandruff” rather than hair loss, she noted. Evaluating the patient for the presence of cervical or occipital lymph nodes is crucial; big nodes are usually a tip-off that infection is present.

The optimal treatment plan for T. capitis depends on the source, Dr. Friedlander explained. If M. canis is the cause, “griseofulvin is the drug of choice,” along with a twice-weekly sporicidal shampoo, she said.

Other treatment options include terbinafine, itraconazole, and fluconazole, and each have their pros and cons, she said. Terbinafine – which persists for months in the skin, nails, and hair – is the least expensive, and is her first choice for infections caused by T. tonsurans.

Itraconazole is available as a liquid, but costs more, causes diarrhea, and comes with a boxed warning about the potential for cardiac complications; fluconazole is the most expensive, but may be used in infants, she added.

Other high-risk groups for T. capitis include female caretakers of high-risk individuals, such as “grandma”; wrestlers; and Buddhist monks, she said. “Short hair, sharing combs, and unclean barbers” contributed to a documented increased risk of T. capitis according to a recently published study of 60 Buddhist monks whose average age was 11.6 years, she added. (Pediatr Dermatol. 2017 May;34[3]:371-3).

Dr. Friedlander had no relevant financial conflicts to disclose.

SDEF and this news organization are owned by Frontline Medical Communications.

CHICAGO – Maral Skelsey, MD, doesn’t get flowers from her patients very often. But, she said, a big bouquet recently landed on her desk after she had performed a nail biopsy on a patient. The note from the patient read, “That wasn’t as bad as I thought it would be!”

The patient’s relief after the procedure highlights the apprehension that both patients and dermatologists can feel when a nail biopsy becomes necessary, said Dr. Skelsey, director of dermatologic surgery at Georgetown University, Washington, D.C.

Speaking at the summer meeting of the American Academy of Dermatology, Dr. Skelsey said that the most important advice she can give about the nail biopsy is, “Do it early and often.”

Dr. Skelsey reminded the audience that the musician Bob Marley died of malignant melanoma; the first sign of his cancer was a longitudinal melanonychia that went unbiopsied. “The biggest mistake we make is not doing it,” she said.

In performing a nail biopsy, said Dr. Skelsey, the goals are, first and foremost, to optimize the pathologic diagnosis. Correct technique can help avoid complications such as bleeding, infection, and nail dystrophy; the right approach can minimize pain and anxiety, she added.

In preparing for a biopsy for melanonychia, “dermoscopy can be very helpful” in assessing the location of the pigment and fine-tuning planning for the biopsy, said Dr. Skelsey. Also, if the streak of melanonychia has reached the distal nail, sending the clipping for pathology can be useful as well.

For dorsal pigmentation, the proximal nail matrix should be biopsied.

“Do not use a punch biopsy on the nail fold to diagnose melanoma – you will get a false negative,” Dr. Skelsey said. It’s not possible to get an accurate diagnosis going through the nail plate to the nail bed, she said.

The preoperative assessment is usually straightforward. Pertinent items in the patient’s history include any medication allergies, current anticoagulation, and any history of prior trauma to the digit to be biopsied. Occasionally, imaging may be helpful, and patients should always be assessed for vascular insufficiency, she noted.

Preoperatively, she asks her patients to remove nail polish and pretreat the area with povidone iodine for 2 days prior to the procedure. Patients need to have a ride home after the procedure, and should be prepared to elevate the affected extremity for 48 hours post procedure. If a toenail is biopsied, they’re advised to come with a postop shoe.

Her patients receive a 5-minute isopropyl alcohol wash of the area to be biopsied just before the procedure, followed by air drying and a 5-minute scrub with 7.5% povidone iodine, which then is wiped off preprocedure.

For hemostasis, a tourniquet can be improvised with a sterile glove finger and a hemostat; there are also dedicated finger cots available that work well for this purpose, she said. In addition to nail nippers and a nail elevator, an English nail splitter can be helpful, said Dr. Skelsey.

For anesthesia, she said she ordinarily uses a 30 gauge needle with buffered lidocaine and epinephrine at room temperature to deliver a wing block. Beginning about 1 cm proximal and lateral to the junction of the proximal and lateral nail fold, the dermatologist can slowly inject about 1.5 cc per side. As the block takes effect, the lateral nail fold will blanch distally in a wing-shaped pattern. This technique, she said, also has the benefit of acting as a volumetric tourniquet.

“To avulse or not to avulse?” asked Dr. Skelsey. “I used to avulse almost everything,” she said, but noted that a complete avulsion is a “pretty traumatic” procedure. Now, unless a full avulsion is required for complete and accurate pathology, she will usually perform a partial nail plate avulsion.

A partial avulsion can reduce pain and morbidity, and can be done by two different methods: the partial proximal avulsion, and the “trap door” avulsion. In a trap door avulsion, she said, the distal matrix is primarily visualized, so this may be a good option for a longitudinal melanonychia arising from the distal matrix. A Freer elevator is used to detach the nail plate from the bed and the matrix, after which the nail plate can be lifted with a hemostat.

In a partial proximal avulsion, the proximal nail fold is reflected, so it’s a better option when the proximal nail matrix needs evaluation, she said.

After the avulsion has been done, “the matrix has been exposed. Now what? Punch or shave?” asked Dr. Skelsey. She noted that she used to perform punch biopsies on “everything,” and that it’s a good option if the pigmented area spans 3 mm or less. One issue, though, is that the specimen can get stuck in the puncher, and extraction can make it difficult to deliver an intact specimen.

Shave biopsies, Dr. Skelsey said, are effective in dealing with nail matrix lesions. They can yield an accurate pathologic diagnosis, and the biopsied digits healed without nail dystrophy in about three quarters of the cases in one study, she said. Potential recurrence of pigmentation is one drawback of the shave technique, she said.

With a shave biopsy, she performs tangential incisions of the proximal and lateral nail folds, and scores and reflects the nail. Then, the band of pigment is shaved tangentially. She cauterizes the area, and sometimes will use a bit of an absorbable gelatin sponge (Gelfoam) as well. Then the proximal nail fold and nail plate are sutured.

Replacing the nail plate results in better cosmesis and is much more comfortable for the patient, she said. An 18-gauge needle can be used to bore a hole through the avulsed nail plate, which may be held in an antiseptic solution soak during the biopsy. The sutures should then be placed from skin to nail plate, so nail fragments aren’t driven into the skin during the suturing process. Finally, specimen margins should be inked, and separate labeled formalin jars are needed for the nail plate, nail bed, and the matrix.

Dr. Skelsey reported that she had no conflicts of interest.
 

[email protected]

On Twitter @karioakes

CHICAGO – Maral Skelsey, MD, doesn’t get flowers from her patients very often. But, she said, a big bouquet recently landed on her desk after she had performed a nail biopsy on a patient. The note from the patient read, “That wasn’t as bad as I thought it would be!”

The patient’s relief after the procedure highlights the apprehension that both patients and dermatologists can feel when a nail biopsy becomes necessary, said Dr. Skelsey, director of dermatologic surgery at Georgetown University, Washington, D.C.

Speaking at the summer meeting of the American Academy of Dermatology, Dr. Skelsey said that the most important advice she can give about the nail biopsy is, “Do it early and often.”

Dr. Skelsey reminded the audience that the musician Bob Marley died of malignant melanoma; the first sign of his cancer was a longitudinal melanonychia that went unbiopsied. “The biggest mistake we make is not doing it,” she said.

In performing a nail biopsy, said Dr. Skelsey, the goals are, first and foremost, to optimize the pathologic diagnosis. Correct technique can help avoid complications such as bleeding, infection, and nail dystrophy; the right approach can minimize pain and anxiety, she added.

In preparing for a biopsy for melanonychia, “dermoscopy can be very helpful” in assessing the location of the pigment and fine-tuning planning for the biopsy, said Dr. Skelsey. Also, if the streak of melanonychia has reached the distal nail, sending the clipping for pathology can be useful as well.

For dorsal pigmentation, the proximal nail matrix should be biopsied.

“Do not use a punch biopsy on the nail fold to diagnose melanoma – you will get a false negative,” Dr. Skelsey said. It’s not possible to get an accurate diagnosis going through the nail plate to the nail bed, she said.

The preoperative assessment is usually straightforward. Pertinent items in the patient’s history include any medication allergies, current anticoagulation, and any history of prior trauma to the digit to be biopsied. Occasionally, imaging may be helpful, and patients should always be assessed for vascular insufficiency, she noted.

Preoperatively, she asks her patients to remove nail polish and pretreat the area with povidone iodine for 2 days prior to the procedure. Patients need to have a ride home after the procedure, and should be prepared to elevate the affected extremity for 48 hours post procedure. If a toenail is biopsied, they’re advised to come with a postop shoe.

Her patients receive a 5-minute isopropyl alcohol wash of the area to be biopsied just before the procedure, followed by air drying and a 5-minute scrub with 7.5% povidone iodine, which then is wiped off preprocedure.

For hemostasis, a tourniquet can be improvised with a sterile glove finger and a hemostat; there are also dedicated finger cots available that work well for this purpose, she said. In addition to nail nippers and a nail elevator, an English nail splitter can be helpful, said Dr. Skelsey.

For anesthesia, she said she ordinarily uses a 30 gauge needle with buffered lidocaine and epinephrine at room temperature to deliver a wing block. Beginning about 1 cm proximal and lateral to the junction of the proximal and lateral nail fold, the dermatologist can slowly inject about 1.5 cc per side. As the block takes effect, the lateral nail fold will blanch distally in a wing-shaped pattern. This technique, she said, also has the benefit of acting as a volumetric tourniquet.

“To avulse or not to avulse?” asked Dr. Skelsey. “I used to avulse almost everything,” she said, but noted that a complete avulsion is a “pretty traumatic” procedure. Now, unless a full avulsion is required for complete and accurate pathology, she will usually perform a partial nail plate avulsion.

A partial avulsion can reduce pain and morbidity, and can be done by two different methods: the partial proximal avulsion, and the “trap door” avulsion. In a trap door avulsion, she said, the distal matrix is primarily visualized, so this may be a good option for a longitudinal melanonychia arising from the distal matrix. A Freer elevator is used to detach the nail plate from the bed and the matrix, after which the nail plate can be lifted with a hemostat.

In a partial proximal avulsion, the proximal nail fold is reflected, so it’s a better option when the proximal nail matrix needs evaluation, she said.

After the avulsion has been done, “the matrix has been exposed. Now what? Punch or shave?” asked Dr. Skelsey. She noted that she used to perform punch biopsies on “everything,” and that it’s a good option if the pigmented area spans 3 mm or less. One issue, though, is that the specimen can get stuck in the puncher, and extraction can make it difficult to deliver an intact specimen.

Shave biopsies, Dr. Skelsey said, are effective in dealing with nail matrix lesions. They can yield an accurate pathologic diagnosis, and the biopsied digits healed without nail dystrophy in about three quarters of the cases in one study, she said. Potential recurrence of pigmentation is one drawback of the shave technique, she said.

With a shave biopsy, she performs tangential incisions of the proximal and lateral nail folds, and scores and reflects the nail. Then, the band of pigment is shaved tangentially. She cauterizes the area, and sometimes will use a bit of an absorbable gelatin sponge (Gelfoam) as well. Then the proximal nail fold and nail plate are sutured.

Replacing the nail plate results in better cosmesis and is much more comfortable for the patient, she said. An 18-gauge needle can be used to bore a hole through the avulsed nail plate, which may be held in an antiseptic solution soak during the biopsy. The sutures should then be placed from skin to nail plate, so nail fragments aren’t driven into the skin during the suturing process. Finally, specimen margins should be inked, and separate labeled formalin jars are needed for the nail plate, nail bed, and the matrix.

Dr. Skelsey reported that she had no conflicts of interest.
 

[email protected]

On Twitter @karioakes

CHICAGO – Maral Skelsey, MD, doesn’t get flowers from her patients very often. But, she said, a big bouquet recently landed on her desk after she had performed a nail biopsy on a patient. The note from the patient read, “That wasn’t as bad as I thought it would be!”

The patient’s relief after the procedure highlights the apprehension that both patients and dermatologists can feel when a nail biopsy becomes necessary, said Dr. Skelsey, director of dermatologic surgery at Georgetown University, Washington, D.C.

Speaking at the summer meeting of the American Academy of Dermatology, Dr. Skelsey said that the most important advice she can give about the nail biopsy is, “Do it early and often.”

Dr. Skelsey reminded the audience that the musician Bob Marley died of malignant melanoma; the first sign of his cancer was a longitudinal melanonychia that went unbiopsied. “The biggest mistake we make is not doing it,” she said.

In performing a nail biopsy, said Dr. Skelsey, the goals are, first and foremost, to optimize the pathologic diagnosis. Correct technique can help avoid complications such as bleeding, infection, and nail dystrophy; the right approach can minimize pain and anxiety, she added.

In preparing for a biopsy for melanonychia, “dermoscopy can be very helpful” in assessing the location of the pigment and fine-tuning planning for the biopsy, said Dr. Skelsey. Also, if the streak of melanonychia has reached the distal nail, sending the clipping for pathology can be useful as well.

For dorsal pigmentation, the proximal nail matrix should be biopsied.

“Do not use a punch biopsy on the nail fold to diagnose melanoma – you will get a false negative,” Dr. Skelsey said. It’s not possible to get an accurate diagnosis going through the nail plate to the nail bed, she said.

The preoperative assessment is usually straightforward. Pertinent items in the patient’s history include any medication allergies, current anticoagulation, and any history of prior trauma to the digit to be biopsied. Occasionally, imaging may be helpful, and patients should always be assessed for vascular insufficiency, she noted.

Preoperatively, she asks her patients to remove nail polish and pretreat the area with povidone iodine for 2 days prior to the procedure. Patients need to have a ride home after the procedure, and should be prepared to elevate the affected extremity for 48 hours post procedure. If a toenail is biopsied, they’re advised to come with a postop shoe.

Her patients receive a 5-minute isopropyl alcohol wash of the area to be biopsied just before the procedure, followed by air drying and a 5-minute scrub with 7.5% povidone iodine, which then is wiped off preprocedure.

For hemostasis, a tourniquet can be improvised with a sterile glove finger and a hemostat; there are also dedicated finger cots available that work well for this purpose, she said. In addition to nail nippers and a nail elevator, an English nail splitter can be helpful, said Dr. Skelsey.

For anesthesia, she said she ordinarily uses a 30 gauge needle with buffered lidocaine and epinephrine at room temperature to deliver a wing block. Beginning about 1 cm proximal and lateral to the junction of the proximal and lateral nail fold, the dermatologist can slowly inject about 1.5 cc per side. As the block takes effect, the lateral nail fold will blanch distally in a wing-shaped pattern. This technique, she said, also has the benefit of acting as a volumetric tourniquet.

“To avulse or not to avulse?” asked Dr. Skelsey. “I used to avulse almost everything,” she said, but noted that a complete avulsion is a “pretty traumatic” procedure. Now, unless a full avulsion is required for complete and accurate pathology, she will usually perform a partial nail plate avulsion.

A partial avulsion can reduce pain and morbidity, and can be done by two different methods: the partial proximal avulsion, and the “trap door” avulsion. In a trap door avulsion, she said, the distal matrix is primarily visualized, so this may be a good option for a longitudinal melanonychia arising from the distal matrix. A Freer elevator is used to detach the nail plate from the bed and the matrix, after which the nail plate can be lifted with a hemostat.

In a partial proximal avulsion, the proximal nail fold is reflected, so it’s a better option when the proximal nail matrix needs evaluation, she said.

After the avulsion has been done, “the matrix has been exposed. Now what? Punch or shave?” asked Dr. Skelsey. She noted that she used to perform punch biopsies on “everything,” and that it’s a good option if the pigmented area spans 3 mm or less. One issue, though, is that the specimen can get stuck in the puncher, and extraction can make it difficult to deliver an intact specimen.

Shave biopsies, Dr. Skelsey said, are effective in dealing with nail matrix lesions. They can yield an accurate pathologic diagnosis, and the biopsied digits healed without nail dystrophy in about three quarters of the cases in one study, she said. Potential recurrence of pigmentation is one drawback of the shave technique, she said.

With a shave biopsy, she performs tangential incisions of the proximal and lateral nail folds, and scores and reflects the nail. Then, the band of pigment is shaved tangentially. She cauterizes the area, and sometimes will use a bit of an absorbable gelatin sponge (Gelfoam) as well. Then the proximal nail fold and nail plate are sutured.

Replacing the nail plate results in better cosmesis and is much more comfortable for the patient, she said. An 18-gauge needle can be used to bore a hole through the avulsed nail plate, which may be held in an antiseptic solution soak during the biopsy. The sutures should then be placed from skin to nail plate, so nail fragments aren’t driven into the skin during the suturing process. Finally, specimen margins should be inked, and separate labeled formalin jars are needed for the nail plate, nail bed, and the matrix.

Dr. Skelsey reported that she had no conflicts of interest.
 

[email protected]

On Twitter @karioakes