Hair & Nails

To improve patient care and outcomes, leading dermatologists offered their recommendations on men’s products. Consideration must be given to:

• bareMinerals SPF 30 Natural Sunscreen
  Bare Escentuals Beauty, Inc
  “I recommend this product to my male patients when they are not wearing a hat. It protects the scalp from UV damage without a heavy greasy finish.”—Shari Lipner, MD, PhD, New York, New York
   
• Ducray Alopexy 5% For Men
  Pierre Fabre Laboratories
  “This dermatologist-dispensed product for men addresses chronic hair loss as well as thinning hair. It contains an optimal level of minoxidil 5% in an elegant unscented formulation and is designed to spray on smoothly and evenly.”—Jeannette Graf, MD, Great Neck, New York
   
• Facial Fuel Energizing Scrub
  Kiehl’s
  “This product is great for oily skin and enlarged pores. The particles in the product allow one to get a deep-clean feeling.”—Gary Goldenberg, MD, New York, New York
   
• Physical Matte UV Defense SPF 50
  SkinCeuticals
  “For men I like to keep things simple. I recommend what I use with the single most important thing being daily sun protection. SkinCeuticals Physical Matte UV Defense SPF 50 is my favorite and I use it after I shave. It goes on smoothly and has a natural tint along with a high SPF.”—Jerome Potozkin, MD, Danville, California
   
• Ultimate Brushless Shave Cream
  Kiehl’s
  “I recommend this product for men with frequent irritation from shaving. This cream-based product helps to provide a close shave without as much irritation from other gel-based products. A small amount goes a long way!”—Anthony M. Rossi, MD, New York, New York

Cutis invites readers to send us their recommendations. Athlete’s foot treatments and cleansing devices will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on men’s products. Consideration must be given to:

• bareMinerals SPF 30 Natural Sunscreen
  Bare Escentuals Beauty, Inc
  “I recommend this product to my male patients when they are not wearing a hat. It protects the scalp from UV damage without a heavy greasy finish.”—Shari Lipner, MD, PhD, New York, New York
   
• Ducray Alopexy 5% For Men
  Pierre Fabre Laboratories
  “This dermatologist-dispensed product for men addresses chronic hair loss as well as thinning hair. It contains an optimal level of minoxidil 5% in an elegant unscented formulation and is designed to spray on smoothly and evenly.”—Jeannette Graf, MD, Great Neck, New York
   
• Facial Fuel Energizing Scrub
  Kiehl’s
  “This product is great for oily skin and enlarged pores. The particles in the product allow one to get a deep-clean feeling.”—Gary Goldenberg, MD, New York, New York
   
• Physical Matte UV Defense SPF 50
  SkinCeuticals
  “For men I like to keep things simple. I recommend what I use with the single most important thing being daily sun protection. SkinCeuticals Physical Matte UV Defense SPF 50 is my favorite and I use it after I shave. It goes on smoothly and has a natural tint along with a high SPF.”—Jerome Potozkin, MD, Danville, California
   
• Ultimate Brushless Shave Cream
  Kiehl’s
  “I recommend this product for men with frequent irritation from shaving. This cream-based product helps to provide a close shave without as much irritation from other gel-based products. A small amount goes a long way!”—Anthony M. Rossi, MD, New York, New York

Cutis invites readers to send us their recommendations. Athlete’s foot treatments and cleansing devices will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on men’s products. Consideration must be given to:

• bareMinerals SPF 30 Natural Sunscreen
  Bare Escentuals Beauty, Inc
  “I recommend this product to my male patients when they are not wearing a hat. It protects the scalp from UV damage without a heavy greasy finish.”—Shari Lipner, MD, PhD, New York, New York
   
• Ducray Alopexy 5% For Men
  Pierre Fabre Laboratories
  “This dermatologist-dispensed product for men addresses chronic hair loss as well as thinning hair. It contains an optimal level of minoxidil 5% in an elegant unscented formulation and is designed to spray on smoothly and evenly.”—Jeannette Graf, MD, Great Neck, New York
   
• Facial Fuel Energizing Scrub
  Kiehl’s
  “This product is great for oily skin and enlarged pores. The particles in the product allow one to get a deep-clean feeling.”—Gary Goldenberg, MD, New York, New York
   
• Physical Matte UV Defense SPF 50
  SkinCeuticals
  “For men I like to keep things simple. I recommend what I use with the single most important thing being daily sun protection. SkinCeuticals Physical Matte UV Defense SPF 50 is my favorite and I use it after I shave. It goes on smoothly and has a natural tint along with a high SPF.”—Jerome Potozkin, MD, Danville, California
   
• Ultimate Brushless Shave Cream
  Kiehl’s
  “I recommend this product for men with frequent irritation from shaving. This cream-based product helps to provide a close shave without as much irritation from other gel-based products. A small amount goes a long way!”—Anthony M. Rossi, MD, New York, New York

Cutis invites readers to send us their recommendations. Athlete’s foot treatments and cleansing devices will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

The Diagnosis: Trichofolliculoma

Microscopic examination revealed a dilated cystic follicle that communicated with the skin surface (Figure). The follicle was lined with squamous epithelium and surrounded by numerous secondary follicles, many of which contained a hair shaft. A diagnosis of trichofolliculoma was made.

Clinically, the differential diagnosis of a flesh-colored papule on the scalp with prominent follicle includes dilated pore of Winer, epidermoid cyst, pilar sheath acanthoma, and trichoepithelioma.^1,2 Multiple hair shafts present in a single follicle may be seen in pili multigemini, tufted folliculitis, trichostasis spinulosa, and trichofolliculoma. On histopathologic examination, a dilated central follicle surrounded with smaller secondary follicles was identified, consistent with trichofolliculoma.

Trichofolliculoma is a rare follicular hamartoma typically occurring on the face, scalp, or trunk as a solitary papule or nodule due to the proliferation of abnormal hair follicle stem cells.^3,4 It may present as a flesh-colored nodule with a central pore that may drain sebum or contain white vellus hairs. Trichofolliculoma is considered a benign entity, despite one case report of malignant transformation.⁵ Biopsy is diagnostic and no further treatment is needed. Recurrence rarely occurs at the primary site after surgical excision, which may be performed for cosmetic purposes or to alleviate functional impairment.

The Diagnosis: Trichofolliculoma

Microscopic examination revealed a dilated cystic follicle that communicated with the skin surface (Figure). The follicle was lined with squamous epithelium and surrounded by numerous secondary follicles, many of which contained a hair shaft. A diagnosis of trichofolliculoma was made.

Clinically, the differential diagnosis of a flesh-colored papule on the scalp with prominent follicle includes dilated pore of Winer, epidermoid cyst, pilar sheath acanthoma, and trichoepithelioma.^1,2 Multiple hair shafts present in a single follicle may be seen in pili multigemini, tufted folliculitis, trichostasis spinulosa, and trichofolliculoma. On histopathologic examination, a dilated central follicle surrounded with smaller secondary follicles was identified, consistent with trichofolliculoma.

Trichofolliculoma is a rare follicular hamartoma typically occurring on the face, scalp, or trunk as a solitary papule or nodule due to the proliferation of abnormal hair follicle stem cells.^3,4 It may present as a flesh-colored nodule with a central pore that may drain sebum or contain white vellus hairs. Trichofolliculoma is considered a benign entity, despite one case report of malignant transformation.⁵ Biopsy is diagnostic and no further treatment is needed. Recurrence rarely occurs at the primary site after surgical excision, which may be performed for cosmetic purposes or to alleviate functional impairment.

The Diagnosis: Trichofolliculoma

Microscopic examination revealed a dilated cystic follicle that communicated with the skin surface (Figure). The follicle was lined with squamous epithelium and surrounded by numerous secondary follicles, many of which contained a hair shaft. A diagnosis of trichofolliculoma was made.

Clinically, the differential diagnosis of a flesh-colored papule on the scalp with prominent follicle includes dilated pore of Winer, epidermoid cyst, pilar sheath acanthoma, and trichoepithelioma.^1,2 Multiple hair shafts present in a single follicle may be seen in pili multigemini, tufted folliculitis, trichostasis spinulosa, and trichofolliculoma. On histopathologic examination, a dilated central follicle surrounded with smaller secondary follicles was identified, consistent with trichofolliculoma.

Trichofolliculoma is a rare follicular hamartoma typically occurring on the face, scalp, or trunk as a solitary papule or nodule due to the proliferation of abnormal hair follicle stem cells.^3,4 It may present as a flesh-colored nodule with a central pore that may drain sebum or contain white vellus hairs. Trichofolliculoma is considered a benign entity, despite one case report of malignant transformation.⁵ Biopsy is diagnostic and no further treatment is needed. Recurrence rarely occurs at the primary site after surgical excision, which may be performed for cosmetic purposes or to alleviate functional impairment.

CHICAGO – Late dermatologic manifestations in children who have received hematopoietic stem cell transplants may be more common than previously thought, according to results of a new study.

Johanna Song, MD, and her collaborators reported that, in their prospective pediatric study, 25% of patients had permanent alopecia and 16% had psoriasis, noting that late nonmalignant skin effects of hematopoietic stem cell transplantation (HSCT) have been studied primarily retrospectively, and in adults. Vitiligo and nail changes were also seen.

In a poster presentation at the World Congress of Dermatology, Dr. Song and her colleagues noted that these figures are higher than the previously reported pediatric rates of 1.7% for vitiligo and 15.6% for permanent alopecia. “Early recognition of these late effects can facilitate prompt and appropriate treatment, if desired,” they said.

The single-center, cross-sectional cohort study tracked pediatric patients over an 18-month period and included patients who were at least 1 year post allogeneic HSCT and had not relapsed. Patients who were not English speaking were excluded.

The median age of the 85 patients enrolled in the study was 13.8 years, and participants were a median of 3.6 years post transplant at the time of enrollment. The study’s analysis attempted to determine which patient, transplant, and disease factors might be associated with the late nonmalignant skin changes, according to Dr. Song, a resident dermatologist at Harvard University, Boston, and her colleagues.

Most – 52– of the patients (61.2%) had hematologic malignancies; 12 patients (14.1%) received their transplant for bone marrow failure, and 11 patients (12.5%) had immunodeficiency. Three patients (3.5%) received HSCT for other malignancies, and seven (8.2%) for nonmalignant diseases.

Diffuse hair thinning was seen in 13 (62%) of the 21 patients who had alopecia, while 11 (52%) of the patients with alopecia had an androgenetic hair loss pattern. Chronic graft versus host disease (GVHD), skin chronic GVHD, a HSCT regimen that included busulfan conditioning, and a family history of early male-pattern alopecia were all significantly associated with post-HSCT permanent alopecia (P less than .05 for all).

The patients with androgenetic alopecia may be experiencing an accelerated time course of a condition to which they are already genetically disposed, noted Dr. Song and her colleagues.

Psoriasis was commonly seen on the scalp, affecting 11 of the 14 patients with psoriasis (79%), and involved the face in five of the patients (36%). Just one patient had psoriasis elsewhere on the body. There was a nonsignificant trend towards human leukocyte antigen mismatch among patients who had psoriasis. Although “psoriasis may be a marker of persistent immune dysregulation,” the investigators said, they did not identify any associated risk factors that would point toward this mechanism in their analysis.

Twelve patients (14%) had vitiligo, with halo nevi seen in four of these patients. Children who were younger than age 10 years and those who received their transplant for primary immunodeficiency were significantly more likely to have vitiligo (P less than .05 for both). Specific possible mechanisms triggering vitiligo could include thymic dysfunction resulting in loss of self-tolerance, and donor alloreactivity against the patient’s host antigens, according to the authors.

Nail changes such as pterygium and nail pitting, ridging, or thickening were seen in just five patients, all of whom had chronic GVHD of the skin. “Nail changes are likely a result of persistent inflammation and immune dysregulation from chronic GVHD,” said Dr. Song.

These late effects “can significantly impact patients’ quality of life,” according to the authors, who called for larger studies that follow pediatric HSCT patients longitudinally, beginning before the transplant – and for more investigation into the pathogenesis of specific late effects.

Dr. Song reported no relevant conflicts of interest.
 

[email protected]

On Twitter @karioakes

CHICAGO – Late dermatologic manifestations in children who have received hematopoietic stem cell transplants may be more common than previously thought, according to results of a new study.

Johanna Song, MD, and her collaborators reported that, in their prospective pediatric study, 25% of patients had permanent alopecia and 16% had psoriasis, noting that late nonmalignant skin effects of hematopoietic stem cell transplantation (HSCT) have been studied primarily retrospectively, and in adults. Vitiligo and nail changes were also seen.

In a poster presentation at the World Congress of Dermatology, Dr. Song and her colleagues noted that these figures are higher than the previously reported pediatric rates of 1.7% for vitiligo and 15.6% for permanent alopecia. “Early recognition of these late effects can facilitate prompt and appropriate treatment, if desired,” they said.

The single-center, cross-sectional cohort study tracked pediatric patients over an 18-month period and included patients who were at least 1 year post allogeneic HSCT and had not relapsed. Patients who were not English speaking were excluded.

The median age of the 85 patients enrolled in the study was 13.8 years, and participants were a median of 3.6 years post transplant at the time of enrollment. The study’s analysis attempted to determine which patient, transplant, and disease factors might be associated with the late nonmalignant skin changes, according to Dr. Song, a resident dermatologist at Harvard University, Boston, and her colleagues.

Most – 52– of the patients (61.2%) had hematologic malignancies; 12 patients (14.1%) received their transplant for bone marrow failure, and 11 patients (12.5%) had immunodeficiency. Three patients (3.5%) received HSCT for other malignancies, and seven (8.2%) for nonmalignant diseases.

Diffuse hair thinning was seen in 13 (62%) of the 21 patients who had alopecia, while 11 (52%) of the patients with alopecia had an androgenetic hair loss pattern. Chronic graft versus host disease (GVHD), skin chronic GVHD, a HSCT regimen that included busulfan conditioning, and a family history of early male-pattern alopecia were all significantly associated with post-HSCT permanent alopecia (P less than .05 for all).

The patients with androgenetic alopecia may be experiencing an accelerated time course of a condition to which they are already genetically disposed, noted Dr. Song and her colleagues.

Psoriasis was commonly seen on the scalp, affecting 11 of the 14 patients with psoriasis (79%), and involved the face in five of the patients (36%). Just one patient had psoriasis elsewhere on the body. There was a nonsignificant trend towards human leukocyte antigen mismatch among patients who had psoriasis. Although “psoriasis may be a marker of persistent immune dysregulation,” the investigators said, they did not identify any associated risk factors that would point toward this mechanism in their analysis.

Twelve patients (14%) had vitiligo, with halo nevi seen in four of these patients. Children who were younger than age 10 years and those who received their transplant for primary immunodeficiency were significantly more likely to have vitiligo (P less than .05 for both). Specific possible mechanisms triggering vitiligo could include thymic dysfunction resulting in loss of self-tolerance, and donor alloreactivity against the patient’s host antigens, according to the authors.

Nail changes such as pterygium and nail pitting, ridging, or thickening were seen in just five patients, all of whom had chronic GVHD of the skin. “Nail changes are likely a result of persistent inflammation and immune dysregulation from chronic GVHD,” said Dr. Song.

These late effects “can significantly impact patients’ quality of life,” according to the authors, who called for larger studies that follow pediatric HSCT patients longitudinally, beginning before the transplant – and for more investigation into the pathogenesis of specific late effects.

Dr. Song reported no relevant conflicts of interest.
 

[email protected]

On Twitter @karioakes

CHICAGO – Late dermatologic manifestations in children who have received hematopoietic stem cell transplants may be more common than previously thought, according to results of a new study.

Johanna Song, MD, and her collaborators reported that, in their prospective pediatric study, 25% of patients had permanent alopecia and 16% had psoriasis, noting that late nonmalignant skin effects of hematopoietic stem cell transplantation (HSCT) have been studied primarily retrospectively, and in adults. Vitiligo and nail changes were also seen.

In a poster presentation at the World Congress of Dermatology, Dr. Song and her colleagues noted that these figures are higher than the previously reported pediatric rates of 1.7% for vitiligo and 15.6% for permanent alopecia. “Early recognition of these late effects can facilitate prompt and appropriate treatment, if desired,” they said.

The single-center, cross-sectional cohort study tracked pediatric patients over an 18-month period and included patients who were at least 1 year post allogeneic HSCT and had not relapsed. Patients who were not English speaking were excluded.

The median age of the 85 patients enrolled in the study was 13.8 years, and participants were a median of 3.6 years post transplant at the time of enrollment. The study’s analysis attempted to determine which patient, transplant, and disease factors might be associated with the late nonmalignant skin changes, according to Dr. Song, a resident dermatologist at Harvard University, Boston, and her colleagues.

Most – 52– of the patients (61.2%) had hematologic malignancies; 12 patients (14.1%) received their transplant for bone marrow failure, and 11 patients (12.5%) had immunodeficiency. Three patients (3.5%) received HSCT for other malignancies, and seven (8.2%) for nonmalignant diseases.

Diffuse hair thinning was seen in 13 (62%) of the 21 patients who had alopecia, while 11 (52%) of the patients with alopecia had an androgenetic hair loss pattern. Chronic graft versus host disease (GVHD), skin chronic GVHD, a HSCT regimen that included busulfan conditioning, and a family history of early male-pattern alopecia were all significantly associated with post-HSCT permanent alopecia (P less than .05 for all).

The patients with androgenetic alopecia may be experiencing an accelerated time course of a condition to which they are already genetically disposed, noted Dr. Song and her colleagues.

Psoriasis was commonly seen on the scalp, affecting 11 of the 14 patients with psoriasis (79%), and involved the face in five of the patients (36%). Just one patient had psoriasis elsewhere on the body. There was a nonsignificant trend towards human leukocyte antigen mismatch among patients who had psoriasis. Although “psoriasis may be a marker of persistent immune dysregulation,” the investigators said, they did not identify any associated risk factors that would point toward this mechanism in their analysis.

Twelve patients (14%) had vitiligo, with halo nevi seen in four of these patients. Children who were younger than age 10 years and those who received their transplant for primary immunodeficiency were significantly more likely to have vitiligo (P less than .05 for both). Specific possible mechanisms triggering vitiligo could include thymic dysfunction resulting in loss of self-tolerance, and donor alloreactivity against the patient’s host antigens, according to the authors.

Nail changes such as pterygium and nail pitting, ridging, or thickening were seen in just five patients, all of whom had chronic GVHD of the skin. “Nail changes are likely a result of persistent inflammation and immune dysregulation from chronic GVHD,” said Dr. Song.

These late effects “can significantly impact patients’ quality of life,” according to the authors, who called for larger studies that follow pediatric HSCT patients longitudinally, beginning before the transplant – and for more investigation into the pathogenesis of specific late effects.

Dr. Song reported no relevant conflicts of interest.
 

[email protected]

On Twitter @karioakes

The gold standard for diagnosing dermatophytosis is the use of direct microscopic examination together with fungal culture.¹ However, in the last 2 decades, molecular techniques that currently are available worldwide have improved the diagnosis procedure.^2,3 In the practice of dermatology, potassium hydroxide (KOH) testing is a commonly used method for the diagnosis of superficial fungal infections.⁴ The sensitivity and specificity of KOH testing in patients with tinea pedis have been reported as 73.3% and 42.5%, respectively.⁵ Repetition of this test after an initial negative test result is recommended if the clinical picture strongly suggests a fungal infection.^6,7 Alternatively, several repetitions of direct microscopic examinations also have been proposed for detecting other microorganisms. For example, 3 negative sputum smears traditionally are recommended to exclude a diagnosis of pulmonary tuberculosis.⁸ However, after numerous investigations in various regions of the world, the World Health Organization reduced the recommended number of these specimens from 3 to 2 in 2007.⁹

The literature suggests that successive mycological tests, both with direct microscopy and fungal cultures, improve the diagnosis of onychomycosis.^1,10,11 Therefore, if such investigations are increased in number, recommendations for successive mycological tests may be more reliable. In the current study, we aimed to investigate the value of successive KOH testing in the management of patients with clinically suspected tinea pedis.

Methods

Patients and Clinical Evaluation
One hundred thirty-five consecutive patients (63 male; 72 female) with clinical symptoms suggestive of intertriginous, vesiculobullous, and/or moccasin-type tinea pedis were enrolled in this prospective study. The mean age (SD) of patients was 45.9 (14.7) years (range, 11–77 years). Almost exclusively, the clinical symptoms suggestive of tinea pedis were desquamation or maceration in the toe webs, blistering lesions on the soles, and diffuse or patchy scaling or keratosis on the soles. A single dermatologist (B.F.K.) clinically evaluated the patients and found only 1 region showing different patterns suggestive of tinea pedis in 72 patients, 2 regions in 61 patients, and 3 regions in 2 patients. Therefore, 200 lesions from the 135 patients were chosen for the KOH test. The dermatologist recorded her level of suspicion for a fungal infection as low or high for each lesion, depending on the absence or presence of signs (eg, unilateral involvement, a well-defined border). None of the patients had used topical or systemic antifungal therapy for at least 1 month prior to the study.¹²

Clinical Sampling and Direct Microscopic Examination
The dermatologist took 3 samples of skin scrapings from each of the 200 lesions. All 3 samples from a given lesion were obtained from sites with the same clinical symptoms in a single session. Special attention was paid to samples from the active advancing borders of the lesions and the roofs of blisters if they were present.¹³ Upon completion of every 15 samples from every 5 lesions, the dermatologist randomized the order of the samples (https://www.random.org/). She then gave the samples, without the identities of the patients or any clinical information, to an experienced laboratory technician for direct microscopic examination. The technician prepared and examined the samples as described elsewhere^5,7,14 and recorded the results as positive if hyphal elements were present or negative if they were not. The study was reviewed and approved by the Çukurova University Faculty of Medicine Ethics Committee (Adana, Turkey). Informed consent was obtained from each patient or from his/her guardian(s) prior to initiating the study.

Statistical Analysis
Statistical analysis was conducted using the χ² test in the SPSS software version 20.0. McNemar test was used for analysis of the paired data.

Results

Among the 135 patients, lesions were suggestive of the intertriginous type of tinea pedis in 24 patients, moccasin type in 50 patients, and both intertriginous and moccasin type in 58 patients. Among the remaining 3 patients, 1 had lesions suggestive of the vesiculobullous type, and another patient had both the vesiculobullous and intertriginous types; the last patient demonstrated lesions that were inconsistent with any of these 3 subtypes of tinea pedis, and a well-defined eczematous plaque was observed on the dorsal surface of the patient’s left foot.

Among the 200 lesions from which skin scrapings were taken for KOH testing, 83 were in the toe webs, 110 were on the soles, and 7 were on the dorsal surfaces of the feet. Of these 7 dorsal lesions, 6 were extensions from lesions on the toe webs or soles and 1 was inconsistent with the 3 subtypes of tinea pedis. Among the 200 lesions, the main clinical symptom was maceration in 38 lesions, desquamation or scaling in 132 lesions, keratosis in 28 lesions, and blistering in 2 lesions. The dermatologist recorded the level of suspicion for tinea pedis as low in 68 lesions and high in 132.

According to the order in which the dermatologist took the 3 samples from each lesion, the KOH test was positive in 95 of the first set of 200 samples, 94 of the second set, and 86 of the third set; however, from the second set, the incremental yield (ie, the number of lesions in which the first KOH test was negative and the second was positive) was 10. The number of lesions in which the first and the second tests were negative and the third was positive was only 4. Therefore, the number of lesions with a positive KOH test was significantly increased from 95 to 105 by performing the second KOH test (P=.002). This number again increased from 105 to 109 when a third test was performed; however, this increase was not statistically significant (P=.125)(Table 1).

According to an evaluation that was not stratified by the dermatologist’s order of sampling, 72 lesions (36.0%) showed KOH test positivity in all 3 samples, 22 (11.0%) were positive in 2 samples, 15 (7.5%) were positive in only 1 sample, and 91 (45.5%) were positive in none of the samples (Table 2). When the data were subdivided based on the sites of the lesions, the toe web lesions (n=83) showed rates of 41.0%, 9.6%, and 4.8% for 3, 2, and 1 positive KOH tests, respectively. For the sole lesions (n=110), the rates were somewhat different at 31.8%, 11.8%, and 10.0%, respectively, but the difference was not statistically significant (P=.395).

For the subgroups based on the main clinical symptoms, the percentage of lesions having at least 1 positive KOH test from the 3 samples was 35.7% for the keratotic lesions (n=28). This rate was lower than macerated lesions (n=38) and desquamating or scaling lesions (n=132), which were 52.6% and 59.1%, respectively (Table 2). On the other hand, the percentage of lesions that produced only 1 or 2 positive KOH tests from the 3 samples was 25.0% for the keratotic lesions, which was higher than the rates for the macerated lesions and the desquamating or scaling lesions (13.1% and 18.9%, respectively). In particular, the difference between the keratotic lesions and the desquamating or scaling lesions in the distribution of the rates of 0, 1, 2, and 3 positive KOH tests was statistically significant (P=.019). The macerated, desquamating or scaling, keratotic, and blistering lesions are presented in the Figure.

Comment

In the current study, we aimed to investigate if successive KOH tests provide an incremental diagnostic yield in the management of patients with clinically suspected tinea pedis and if these results differ among the subgroups of patients. Both in the evaluation taking into account the order of sampling and in the evaluation disregarding this order, we found that the second sample was necessary for all subgroups, and even the third sample was necessary for patients with keratotic lesions. The main limitation of the study was that we lacked a gold-standard technique (eg, a molecular-based technique); therefore, we are unable to comment on the false-negative and false-positive results of the successive KOH testing.

Summerbell et al¹¹ found in their study that in initial specimens of toenails with apparent lesions taken from 473 patients, the KOH test was 73.8% sensitive for dermatophytes, and this rate was only somewhat higher for cultures (74.6%). Arabatzis et al² investigated 92 skin, nail, and hair specimens from 67 patients with suspected dermatophytosis and found that the KOH test was superior to culture for the detection of dermatophytes (43% vs 33%). Moreover and more importantly, they noted that a real-time polymerase chain reaction (PCR) assay yielded a higher detection rate (51%).² In another study, Wisselink et al³ examined 1437 clinical samples and demonstrated a great increase in the detection of dermatophytes using a real-time PCR assay (48.5%) compared to culture (26.9%). However, PCR may not reflect active disease and could lead to false-positive results.^2,3 Therefore, the aforementioned weakness of our study will be overcome in further studies investigating the benefit of successive KOH testing compared to a molecular-based assay, such as the real-time PCR assay.

In this study, repeating the KOH test provided better results for achieving the diagnosis of tinea pedis in a large number of samples from clinically suspected lesions. Additionally, the distribution of 3, 2, or 1 positive results on the 3 KOH tests was different among the subgroups of lesions. Overall, positivity was less frequent in the keratotic lesions compared to the macerated or desquamating or scaling lesions. Moreover, positivity on all 3 tests also was less frequent in the keratotic lesions. Inversely, the frequency of samples with only 1 or 2 positive results was higher in this subgroup. The necessity for the second, even the third, tests was greater in this subgroup.

Our findings were consistent with the results of the studies performed with successive mycological tests on the nail specimens. Meireles et al¹ repeated 156 mycological nail tests 3 times and found the rate of positivity in the first test to be 19.9%. When the results of the first and second tests were combined, this rate increased to 28.2%, and when the results of all 3 tests were combined, it increased to 37.8%.¹ Gupta¹⁰ demonstrated that even a fourth culture provided an incremental diagnostic yield in the diagnosis of onychomycosis, yet 4 cultures may not be clinically practical. Furthermore, periodic acid–Schiff staining is a more effective measure of positivity in onychomycosis.¹⁵

Although the overall rate of positivity on the 3 tests in our study was unsurprisingly higher in lesions rated highly suspicious for a fungal infection, the rate of only 1 or 2 positive tests was surprisingly somewhat higher in low-suspicion lesions, which suggested that repeating the KOH test would be beneficial, even if the clinical suspicion for tinea pedis was low. The novel contribution of this study includes the finding that mycological information was markedly improved in highly suspicious tinea pedis lesions regardless of the infection site (Table 1) by using 3 successive KOH tests; the percentage of lesions with 1, 2, or 3 positive KOH tests was 5.3%, 12.1%, and 47.0%, respectively (Table 2). A single physician from a single geographical location introduces a limitation to the study for a variety of reasons, including bias in the cases chosen and possible overrepresentation of the causative organism due to region-specific incidence. It is unknown how different causative organisms affect KOH results. The lack of fungal culture results limits the value of this information.

Conclusion

In this study, we investigated the benefit of successive KOH testing in the laboratory diagnosis of tinea pedis and found that the use of second samples in particular provided a substantial increase in diagnostic yield. In other words, the utilization of successive KOH testing remarkably improved the diagnosis of tinea pedis. Therefore, we suggest that at least 2 samples of skin scrapings should be taken for the diagnosis of tinea pedis and that the number of samples should be at least 3 for keratotic lesions. However, further study by using a gold-standard method such as a molecular-based assay as well as taking the samples in daily or weekly intervals is recommended to achieve a more reliable result.

Acknowledgment

The authors would like to thank Gökçen Şahin (Adana, Turkey) for providing technical support in direct microscopic examination.

The gold standard for diagnosing dermatophytosis is the use of direct microscopic examination together with fungal culture.¹ However, in the last 2 decades, molecular techniques that currently are available worldwide have improved the diagnosis procedure.^2,3 In the practice of dermatology, potassium hydroxide (KOH) testing is a commonly used method for the diagnosis of superficial fungal infections.⁴ The sensitivity and specificity of KOH testing in patients with tinea pedis have been reported as 73.3% and 42.5%, respectively.⁵ Repetition of this test after an initial negative test result is recommended if the clinical picture strongly suggests a fungal infection.^6,7 Alternatively, several repetitions of direct microscopic examinations also have been proposed for detecting other microorganisms. For example, 3 negative sputum smears traditionally are recommended to exclude a diagnosis of pulmonary tuberculosis.⁸ However, after numerous investigations in various regions of the world, the World Health Organization reduced the recommended number of these specimens from 3 to 2 in 2007.⁹

The literature suggests that successive mycological tests, both with direct microscopy and fungal cultures, improve the diagnosis of onychomycosis.^1,10,11 Therefore, if such investigations are increased in number, recommendations for successive mycological tests may be more reliable. In the current study, we aimed to investigate the value of successive KOH testing in the management of patients with clinically suspected tinea pedis.

Methods

Patients and Clinical Evaluation
One hundred thirty-five consecutive patients (63 male; 72 female) with clinical symptoms suggestive of intertriginous, vesiculobullous, and/or moccasin-type tinea pedis were enrolled in this prospective study. The mean age (SD) of patients was 45.9 (14.7) years (range, 11–77 years). Almost exclusively, the clinical symptoms suggestive of tinea pedis were desquamation or maceration in the toe webs, blistering lesions on the soles, and diffuse or patchy scaling or keratosis on the soles. A single dermatologist (B.F.K.) clinically evaluated the patients and found only 1 region showing different patterns suggestive of tinea pedis in 72 patients, 2 regions in 61 patients, and 3 regions in 2 patients. Therefore, 200 lesions from the 135 patients were chosen for the KOH test. The dermatologist recorded her level of suspicion for a fungal infection as low or high for each lesion, depending on the absence or presence of signs (eg, unilateral involvement, a well-defined border). None of the patients had used topical or systemic antifungal therapy for at least 1 month prior to the study.¹²

Clinical Sampling and Direct Microscopic Examination
The dermatologist took 3 samples of skin scrapings from each of the 200 lesions. All 3 samples from a given lesion were obtained from sites with the same clinical symptoms in a single session. Special attention was paid to samples from the active advancing borders of the lesions and the roofs of blisters if they were present.¹³ Upon completion of every 15 samples from every 5 lesions, the dermatologist randomized the order of the samples (https://www.random.org/). She then gave the samples, without the identities of the patients or any clinical information, to an experienced laboratory technician for direct microscopic examination. The technician prepared and examined the samples as described elsewhere^5,7,14 and recorded the results as positive if hyphal elements were present or negative if they were not. The study was reviewed and approved by the Çukurova University Faculty of Medicine Ethics Committee (Adana, Turkey). Informed consent was obtained from each patient or from his/her guardian(s) prior to initiating the study.

Statistical Analysis
Statistical analysis was conducted using the χ² test in the SPSS software version 20.0. McNemar test was used for analysis of the paired data.

Results

Among the 135 patients, lesions were suggestive of the intertriginous type of tinea pedis in 24 patients, moccasin type in 50 patients, and both intertriginous and moccasin type in 58 patients. Among the remaining 3 patients, 1 had lesions suggestive of the vesiculobullous type, and another patient had both the vesiculobullous and intertriginous types; the last patient demonstrated lesions that were inconsistent with any of these 3 subtypes of tinea pedis, and a well-defined eczematous plaque was observed on the dorsal surface of the patient’s left foot.

Among the 200 lesions from which skin scrapings were taken for KOH testing, 83 were in the toe webs, 110 were on the soles, and 7 were on the dorsal surfaces of the feet. Of these 7 dorsal lesions, 6 were extensions from lesions on the toe webs or soles and 1 was inconsistent with the 3 subtypes of tinea pedis. Among the 200 lesions, the main clinical symptom was maceration in 38 lesions, desquamation or scaling in 132 lesions, keratosis in 28 lesions, and blistering in 2 lesions. The dermatologist recorded the level of suspicion for tinea pedis as low in 68 lesions and high in 132.

According to the order in which the dermatologist took the 3 samples from each lesion, the KOH test was positive in 95 of the first set of 200 samples, 94 of the second set, and 86 of the third set; however, from the second set, the incremental yield (ie, the number of lesions in which the first KOH test was negative and the second was positive) was 10. The number of lesions in which the first and the second tests were negative and the third was positive was only 4. Therefore, the number of lesions with a positive KOH test was significantly increased from 95 to 105 by performing the second KOH test (P=.002). This number again increased from 105 to 109 when a third test was performed; however, this increase was not statistically significant (P=.125)(Table 1).

According to an evaluation that was not stratified by the dermatologist’s order of sampling, 72 lesions (36.0%) showed KOH test positivity in all 3 samples, 22 (11.0%) were positive in 2 samples, 15 (7.5%) were positive in only 1 sample, and 91 (45.5%) were positive in none of the samples (Table 2). When the data were subdivided based on the sites of the lesions, the toe web lesions (n=83) showed rates of 41.0%, 9.6%, and 4.8% for 3, 2, and 1 positive KOH tests, respectively. For the sole lesions (n=110), the rates were somewhat different at 31.8%, 11.8%, and 10.0%, respectively, but the difference was not statistically significant (P=.395).

For the subgroups based on the main clinical symptoms, the percentage of lesions having at least 1 positive KOH test from the 3 samples was 35.7% for the keratotic lesions (n=28). This rate was lower than macerated lesions (n=38) and desquamating or scaling lesions (n=132), which were 52.6% and 59.1%, respectively (Table 2). On the other hand, the percentage of lesions that produced only 1 or 2 positive KOH tests from the 3 samples was 25.0% for the keratotic lesions, which was higher than the rates for the macerated lesions and the desquamating or scaling lesions (13.1% and 18.9%, respectively). In particular, the difference between the keratotic lesions and the desquamating or scaling lesions in the distribution of the rates of 0, 1, 2, and 3 positive KOH tests was statistically significant (P=.019). The macerated, desquamating or scaling, keratotic, and blistering lesions are presented in the Figure.

Comment

In the current study, we aimed to investigate if successive KOH tests provide an incremental diagnostic yield in the management of patients with clinically suspected tinea pedis and if these results differ among the subgroups of patients. Both in the evaluation taking into account the order of sampling and in the evaluation disregarding this order, we found that the second sample was necessary for all subgroups, and even the third sample was necessary for patients with keratotic lesions. The main limitation of the study was that we lacked a gold-standard technique (eg, a molecular-based technique); therefore, we are unable to comment on the false-negative and false-positive results of the successive KOH testing.

Summerbell et al¹¹ found in their study that in initial specimens of toenails with apparent lesions taken from 473 patients, the KOH test was 73.8% sensitive for dermatophytes, and this rate was only somewhat higher for cultures (74.6%). Arabatzis et al² investigated 92 skin, nail, and hair specimens from 67 patients with suspected dermatophytosis and found that the KOH test was superior to culture for the detection of dermatophytes (43% vs 33%). Moreover and more importantly, they noted that a real-time polymerase chain reaction (PCR) assay yielded a higher detection rate (51%).² In another study, Wisselink et al³ examined 1437 clinical samples and demonstrated a great increase in the detection of dermatophytes using a real-time PCR assay (48.5%) compared to culture (26.9%). However, PCR may not reflect active disease and could lead to false-positive results.^2,3 Therefore, the aforementioned weakness of our study will be overcome in further studies investigating the benefit of successive KOH testing compared to a molecular-based assay, such as the real-time PCR assay.

In this study, repeating the KOH test provided better results for achieving the diagnosis of tinea pedis in a large number of samples from clinically suspected lesions. Additionally, the distribution of 3, 2, or 1 positive results on the 3 KOH tests was different among the subgroups of lesions. Overall, positivity was less frequent in the keratotic lesions compared to the macerated or desquamating or scaling lesions. Moreover, positivity on all 3 tests also was less frequent in the keratotic lesions. Inversely, the frequency of samples with only 1 or 2 positive results was higher in this subgroup. The necessity for the second, even the third, tests was greater in this subgroup.

Our findings were consistent with the results of the studies performed with successive mycological tests on the nail specimens. Meireles et al¹ repeated 156 mycological nail tests 3 times and found the rate of positivity in the first test to be 19.9%. When the results of the first and second tests were combined, this rate increased to 28.2%, and when the results of all 3 tests were combined, it increased to 37.8%.¹ Gupta¹⁰ demonstrated that even a fourth culture provided an incremental diagnostic yield in the diagnosis of onychomycosis, yet 4 cultures may not be clinically practical. Furthermore, periodic acid–Schiff staining is a more effective measure of positivity in onychomycosis.¹⁵

Although the overall rate of positivity on the 3 tests in our study was unsurprisingly higher in lesions rated highly suspicious for a fungal infection, the rate of only 1 or 2 positive tests was surprisingly somewhat higher in low-suspicion lesions, which suggested that repeating the KOH test would be beneficial, even if the clinical suspicion for tinea pedis was low. The novel contribution of this study includes the finding that mycological information was markedly improved in highly suspicious tinea pedis lesions regardless of the infection site (Table 1) by using 3 successive KOH tests; the percentage of lesions with 1, 2, or 3 positive KOH tests was 5.3%, 12.1%, and 47.0%, respectively (Table 2). A single physician from a single geographical location introduces a limitation to the study for a variety of reasons, including bias in the cases chosen and possible overrepresentation of the causative organism due to region-specific incidence. It is unknown how different causative organisms affect KOH results. The lack of fungal culture results limits the value of this information.

Conclusion

In this study, we investigated the benefit of successive KOH testing in the laboratory diagnosis of tinea pedis and found that the use of second samples in particular provided a substantial increase in diagnostic yield. In other words, the utilization of successive KOH testing remarkably improved the diagnosis of tinea pedis. Therefore, we suggest that at least 2 samples of skin scrapings should be taken for the diagnosis of tinea pedis and that the number of samples should be at least 3 for keratotic lesions. However, further study by using a gold-standard method such as a molecular-based assay as well as taking the samples in daily or weekly intervals is recommended to achieve a more reliable result.

Acknowledgment

The authors would like to thank Gökçen Şahin (Adana, Turkey) for providing technical support in direct microscopic examination.

The gold standard for diagnosing dermatophytosis is the use of direct microscopic examination together with fungal culture.¹ However, in the last 2 decades, molecular techniques that currently are available worldwide have improved the diagnosis procedure.^2,3 In the practice of dermatology, potassium hydroxide (KOH) testing is a commonly used method for the diagnosis of superficial fungal infections.⁴ The sensitivity and specificity of KOH testing in patients with tinea pedis have been reported as 73.3% and 42.5%, respectively.⁵ Repetition of this test after an initial negative test result is recommended if the clinical picture strongly suggests a fungal infection.^6,7 Alternatively, several repetitions of direct microscopic examinations also have been proposed for detecting other microorganisms. For example, 3 negative sputum smears traditionally are recommended to exclude a diagnosis of pulmonary tuberculosis.⁸ However, after numerous investigations in various regions of the world, the World Health Organization reduced the recommended number of these specimens from 3 to 2 in 2007.⁹

The literature suggests that successive mycological tests, both with direct microscopy and fungal cultures, improve the diagnosis of onychomycosis.^1,10,11 Therefore, if such investigations are increased in number, recommendations for successive mycological tests may be more reliable. In the current study, we aimed to investigate the value of successive KOH testing in the management of patients with clinically suspected tinea pedis.

Methods

Patients and Clinical Evaluation
One hundred thirty-five consecutive patients (63 male; 72 female) with clinical symptoms suggestive of intertriginous, vesiculobullous, and/or moccasin-type tinea pedis were enrolled in this prospective study. The mean age (SD) of patients was 45.9 (14.7) years (range, 11–77 years). Almost exclusively, the clinical symptoms suggestive of tinea pedis were desquamation or maceration in the toe webs, blistering lesions on the soles, and diffuse or patchy scaling or keratosis on the soles. A single dermatologist (B.F.K.) clinically evaluated the patients and found only 1 region showing different patterns suggestive of tinea pedis in 72 patients, 2 regions in 61 patients, and 3 regions in 2 patients. Therefore, 200 lesions from the 135 patients were chosen for the KOH test. The dermatologist recorded her level of suspicion for a fungal infection as low or high for each lesion, depending on the absence or presence of signs (eg, unilateral involvement, a well-defined border). None of the patients had used topical or systemic antifungal therapy for at least 1 month prior to the study.¹²

Clinical Sampling and Direct Microscopic Examination
The dermatologist took 3 samples of skin scrapings from each of the 200 lesions. All 3 samples from a given lesion were obtained from sites with the same clinical symptoms in a single session. Special attention was paid to samples from the active advancing borders of the lesions and the roofs of blisters if they were present.¹³ Upon completion of every 15 samples from every 5 lesions, the dermatologist randomized the order of the samples (https://www.random.org/). She then gave the samples, without the identities of the patients or any clinical information, to an experienced laboratory technician for direct microscopic examination. The technician prepared and examined the samples as described elsewhere^5,7,14 and recorded the results as positive if hyphal elements were present or negative if they were not. The study was reviewed and approved by the Çukurova University Faculty of Medicine Ethics Committee (Adana, Turkey). Informed consent was obtained from each patient or from his/her guardian(s) prior to initiating the study.

Statistical Analysis
Statistical analysis was conducted using the χ² test in the SPSS software version 20.0. McNemar test was used for analysis of the paired data.

Results

Among the 135 patients, lesions were suggestive of the intertriginous type of tinea pedis in 24 patients, moccasin type in 50 patients, and both intertriginous and moccasin type in 58 patients. Among the remaining 3 patients, 1 had lesions suggestive of the vesiculobullous type, and another patient had both the vesiculobullous and intertriginous types; the last patient demonstrated lesions that were inconsistent with any of these 3 subtypes of tinea pedis, and a well-defined eczematous plaque was observed on the dorsal surface of the patient’s left foot.

Among the 200 lesions from which skin scrapings were taken for KOH testing, 83 were in the toe webs, 110 were on the soles, and 7 were on the dorsal surfaces of the feet. Of these 7 dorsal lesions, 6 were extensions from lesions on the toe webs or soles and 1 was inconsistent with the 3 subtypes of tinea pedis. Among the 200 lesions, the main clinical symptom was maceration in 38 lesions, desquamation or scaling in 132 lesions, keratosis in 28 lesions, and blistering in 2 lesions. The dermatologist recorded the level of suspicion for tinea pedis as low in 68 lesions and high in 132.

According to the order in which the dermatologist took the 3 samples from each lesion, the KOH test was positive in 95 of the first set of 200 samples, 94 of the second set, and 86 of the third set; however, from the second set, the incremental yield (ie, the number of lesions in which the first KOH test was negative and the second was positive) was 10. The number of lesions in which the first and the second tests were negative and the third was positive was only 4. Therefore, the number of lesions with a positive KOH test was significantly increased from 95 to 105 by performing the second KOH test (P=.002). This number again increased from 105 to 109 when a third test was performed; however, this increase was not statistically significant (P=.125)(Table 1).

According to an evaluation that was not stratified by the dermatologist’s order of sampling, 72 lesions (36.0%) showed KOH test positivity in all 3 samples, 22 (11.0%) were positive in 2 samples, 15 (7.5%) were positive in only 1 sample, and 91 (45.5%) were positive in none of the samples (Table 2). When the data were subdivided based on the sites of the lesions, the toe web lesions (n=83) showed rates of 41.0%, 9.6%, and 4.8% for 3, 2, and 1 positive KOH tests, respectively. For the sole lesions (n=110), the rates were somewhat different at 31.8%, 11.8%, and 10.0%, respectively, but the difference was not statistically significant (P=.395).

For the subgroups based on the main clinical symptoms, the percentage of lesions having at least 1 positive KOH test from the 3 samples was 35.7% for the keratotic lesions (n=28). This rate was lower than macerated lesions (n=38) and desquamating or scaling lesions (n=132), which were 52.6% and 59.1%, respectively (Table 2). On the other hand, the percentage of lesions that produced only 1 or 2 positive KOH tests from the 3 samples was 25.0% for the keratotic lesions, which was higher than the rates for the macerated lesions and the desquamating or scaling lesions (13.1% and 18.9%, respectively). In particular, the difference between the keratotic lesions and the desquamating or scaling lesions in the distribution of the rates of 0, 1, 2, and 3 positive KOH tests was statistically significant (P=.019). The macerated, desquamating or scaling, keratotic, and blistering lesions are presented in the Figure.

Comment

In the current study, we aimed to investigate if successive KOH tests provide an incremental diagnostic yield in the management of patients with clinically suspected tinea pedis and if these results differ among the subgroups of patients. Both in the evaluation taking into account the order of sampling and in the evaluation disregarding this order, we found that the second sample was necessary for all subgroups, and even the third sample was necessary for patients with keratotic lesions. The main limitation of the study was that we lacked a gold-standard technique (eg, a molecular-based technique); therefore, we are unable to comment on the false-negative and false-positive results of the successive KOH testing.

Summerbell et al¹¹ found in their study that in initial specimens of toenails with apparent lesions taken from 473 patients, the KOH test was 73.8% sensitive for dermatophytes, and this rate was only somewhat higher for cultures (74.6%). Arabatzis et al² investigated 92 skin, nail, and hair specimens from 67 patients with suspected dermatophytosis and found that the KOH test was superior to culture for the detection of dermatophytes (43% vs 33%). Moreover and more importantly, they noted that a real-time polymerase chain reaction (PCR) assay yielded a higher detection rate (51%).² In another study, Wisselink et al³ examined 1437 clinical samples and demonstrated a great increase in the detection of dermatophytes using a real-time PCR assay (48.5%) compared to culture (26.9%). However, PCR may not reflect active disease and could lead to false-positive results.^2,3 Therefore, the aforementioned weakness of our study will be overcome in further studies investigating the benefit of successive KOH testing compared to a molecular-based assay, such as the real-time PCR assay.

In this study, repeating the KOH test provided better results for achieving the diagnosis of tinea pedis in a large number of samples from clinically suspected lesions. Additionally, the distribution of 3, 2, or 1 positive results on the 3 KOH tests was different among the subgroups of lesions. Overall, positivity was less frequent in the keratotic lesions compared to the macerated or desquamating or scaling lesions. Moreover, positivity on all 3 tests also was less frequent in the keratotic lesions. Inversely, the frequency of samples with only 1 or 2 positive results was higher in this subgroup. The necessity for the second, even the third, tests was greater in this subgroup.

Our findings were consistent with the results of the studies performed with successive mycological tests on the nail specimens. Meireles et al¹ repeated 156 mycological nail tests 3 times and found the rate of positivity in the first test to be 19.9%. When the results of the first and second tests were combined, this rate increased to 28.2%, and when the results of all 3 tests were combined, it increased to 37.8%.¹ Gupta¹⁰ demonstrated that even a fourth culture provided an incremental diagnostic yield in the diagnosis of onychomycosis, yet 4 cultures may not be clinically practical. Furthermore, periodic acid–Schiff staining is a more effective measure of positivity in onychomycosis.¹⁵

Although the overall rate of positivity on the 3 tests in our study was unsurprisingly higher in lesions rated highly suspicious for a fungal infection, the rate of only 1 or 2 positive tests was surprisingly somewhat higher in low-suspicion lesions, which suggested that repeating the KOH test would be beneficial, even if the clinical suspicion for tinea pedis was low. The novel contribution of this study includes the finding that mycological information was markedly improved in highly suspicious tinea pedis lesions regardless of the infection site (Table 1) by using 3 successive KOH tests; the percentage of lesions with 1, 2, or 3 positive KOH tests was 5.3%, 12.1%, and 47.0%, respectively (Table 2). A single physician from a single geographical location introduces a limitation to the study for a variety of reasons, including bias in the cases chosen and possible overrepresentation of the causative organism due to region-specific incidence. It is unknown how different causative organisms affect KOH results. The lack of fungal culture results limits the value of this information.

Conclusion

In this study, we investigated the benefit of successive KOH testing in the laboratory diagnosis of tinea pedis and found that the use of second samples in particular provided a substantial increase in diagnostic yield. In other words, the utilization of successive KOH testing remarkably improved the diagnosis of tinea pedis. Therefore, we suggest that at least 2 samples of skin scrapings should be taken for the diagnosis of tinea pedis and that the number of samples should be at least 3 for keratotic lesions. However, further study by using a gold-standard method such as a molecular-based assay as well as taking the samples in daily or weekly intervals is recommended to achieve a more reliable result.

Acknowledgment

The authors would like to thank Gökçen Şahin (Adana, Turkey) for providing technical support in direct microscopic examination.

To the Editor:

Hereditary hypotrichosis simplex (HHS)(Online Mendelian Inheritance in Man [OMIM] 146520) is a rare form of hypotrichosis that typically presents in school-aged children as worsening hair loss localized to the scalp.¹ Most patients are unaffected at birth and otherwise healthy without abnormalities of the nails, teeth, or perspiration. Examination of the scalp reveals normal follicular ostia and absence of scale and erythema; however, decreased follicular density may be noted.¹ The histopathologic findings of HHS reveal velluslike hair follicles without associated fibrosis or inflammation.² Examination of hair follicles with light microscopy is unremarkable.^3,4 Historically, this condition has been largely regarded as autosomal dominant, with variable severity also described within families. Herein, we report a case of this rare disease in a child, with 2 family members displaying a less severe phenotype.

A 7-year-old girl presented with gradual thinning of the scalp hair of 3 to 4 years’ duration. Her mother reported the patient had normal hair density at birth. Over the next several years, she was noted to have an inability to grow lengthy hair. At approximately 3 years of age, thinning of scalp hair was identified. There was no prior history of increased shedding, hypohidrosis, or tooth or nail abnormalities. Family history revealed fine hair in her older sister and fine thin hair at the frontal scalp in her mother. Her mother reported similar inability to grow lengthy hair. Physical examination of the patient demonstrated short blonde hair with diffuse thinning of the crown (Figure 1). The longest hair was approximately 10 cm in length. Follicular ostia were without erythema or scale but notably fewer in number on the crown. Eyebrows, eyelashes, teeth, and fingernails were without abnormalities. A hair pull test was negative and hair mount revealed normal bulb and shaft. Microscopy of hair shafts under polarized light was unremarkable.

Two punch biopsies were obtained and submitted for vertical and horizontal sectioning. Sections demonstrated an intact epidermis, decreased follicle number, and small follicles with hypoplastic velluslike appearance (Figure 2). Fibrosis and inflammation were not seen; there was no increase in catagen or telogen hairs. Clinical and histopathological findings were consistent with HHS.

Hereditary hypotrichosis localized to the scalp was first described by Toribio and Quinones⁵ in 1974 in a large Spanish family presenting with normal scalp hair at birth followed by gradual diffuse hair loss. Hair loss that usually began in school-aged children with subsequent few fine hairs remaining on the scalp by the third decade of life was identified in these individuals.Eyelashes, eyebrows, pubic, axillary, and other truncal hairs were normal.⁵ Several similar cases of HHS localized to the scalp have since been reported.^2,6 Hereditary hypotrichosis simplex is inherited in an autosomal-dominant fashion, with the exception of 1 reported sporadic case.³

Research on HHS has primarily focused on genetic analyses of several affected families. Betz et al⁷ mapped the gene for HHS to band 6p21.3 in 2 families of Danish origin and in the Spanish family initially described by Toribio and Quinones.⁵ Three years later, a nonsense mutation in the CDSN gene encoding corneodesmosin was described.⁸ Despite these genetic advances, the pathogenesis of HHS and the role that corneodesmosin may play remain unclear.

Generalized forms of hypotrichosis (OMIM #605389) have long been reported and described as loss of scalp hair with involvement of eyebrows, eyelashes, and other body hair.⁹ Genetic studies have allowed for genome-wide linkage analysis, linking 3 families with this more generalized HHS phenotype to chromosome 18; specifically, an Italian family with sparse scalp and body hair but normal eyelashes and eyebrows,⁴ and 2 Pakistani families with thinning scalp hair and sparse truncal hair.¹⁰ A mutation in the APC downregulated 1 gene, APCDD1, also has been identified in these families.¹⁰ These genetic findings indicate that the generalized form of HHS is a distinct syndrome.

The differential diagnosis of HHS includes Marie-Unna hereditary hypotrichosis, loose anagen hair syndrome, trichothiodystrophy, and androgenetic alopecia. Marie-Unna hereditary hypotrichosis usually presents as near-complete absence of scalp hair at birth, development of wiry twisted hair in childhood, and progressive alopecia.³ Loose anagen hair syndrome usually demonstrates a ruffled cuticle on hair pull test and remits in late childhood. Polarization of the hair shaft can identify patients with trichothiodystrophy. Follicular miniaturization may lead one to consider early-onset androgenetic alopecia in some patients.

There is no effective treatment of HHS. Due to potential phenotypic variation, patients should be counseled that they may experience progressive or possible total loss of scalp hair by the third decade of life.^2,3,5 As with other hair loss disorders, wigs or additional over-the-counter cosmetic options may be considered.³ Currently, there are no known patient resources specific for HHS. Therefore, our patient’s family was referred to the National Alopecia Areata Foundation website (https://naaf.org/) for resources on discussing alopecia with school-aged children. The psychological impact of alopecia should not be overlooked and psychiatric referral should be provided, if needed. Examination of family members along with clinical monitoring are recommended. Genetic counseling also may be offered.³

To the Editor:

Hereditary hypotrichosis simplex (HHS)(Online Mendelian Inheritance in Man [OMIM] 146520) is a rare form of hypotrichosis that typically presents in school-aged children as worsening hair loss localized to the scalp.¹ Most patients are unaffected at birth and otherwise healthy without abnormalities of the nails, teeth, or perspiration. Examination of the scalp reveals normal follicular ostia and absence of scale and erythema; however, decreased follicular density may be noted.¹ The histopathologic findings of HHS reveal velluslike hair follicles without associated fibrosis or inflammation.² Examination of hair follicles with light microscopy is unremarkable.^3,4 Historically, this condition has been largely regarded as autosomal dominant, with variable severity also described within families. Herein, we report a case of this rare disease in a child, with 2 family members displaying a less severe phenotype.

A 7-year-old girl presented with gradual thinning of the scalp hair of 3 to 4 years’ duration. Her mother reported the patient had normal hair density at birth. Over the next several years, she was noted to have an inability to grow lengthy hair. At approximately 3 years of age, thinning of scalp hair was identified. There was no prior history of increased shedding, hypohidrosis, or tooth or nail abnormalities. Family history revealed fine hair in her older sister and fine thin hair at the frontal scalp in her mother. Her mother reported similar inability to grow lengthy hair. Physical examination of the patient demonstrated short blonde hair with diffuse thinning of the crown (Figure 1). The longest hair was approximately 10 cm in length. Follicular ostia were without erythema or scale but notably fewer in number on the crown. Eyebrows, eyelashes, teeth, and fingernails were without abnormalities. A hair pull test was negative and hair mount revealed normal bulb and shaft. Microscopy of hair shafts under polarized light was unremarkable.

Two punch biopsies were obtained and submitted for vertical and horizontal sectioning. Sections demonstrated an intact epidermis, decreased follicle number, and small follicles with hypoplastic velluslike appearance (Figure 2). Fibrosis and inflammation were not seen; there was no increase in catagen or telogen hairs. Clinical and histopathological findings were consistent with HHS.

Hereditary hypotrichosis localized to the scalp was first described by Toribio and Quinones⁵ in 1974 in a large Spanish family presenting with normal scalp hair at birth followed by gradual diffuse hair loss. Hair loss that usually began in school-aged children with subsequent few fine hairs remaining on the scalp by the third decade of life was identified in these individuals.Eyelashes, eyebrows, pubic, axillary, and other truncal hairs were normal.⁵ Several similar cases of HHS localized to the scalp have since been reported.^2,6 Hereditary hypotrichosis simplex is inherited in an autosomal-dominant fashion, with the exception of 1 reported sporadic case.³

Research on HHS has primarily focused on genetic analyses of several affected families. Betz et al⁷ mapped the gene for HHS to band 6p21.3 in 2 families of Danish origin and in the Spanish family initially described by Toribio and Quinones.⁵ Three years later, a nonsense mutation in the CDSN gene encoding corneodesmosin was described.⁸ Despite these genetic advances, the pathogenesis of HHS and the role that corneodesmosin may play remain unclear.

Generalized forms of hypotrichosis (OMIM #605389) have long been reported and described as loss of scalp hair with involvement of eyebrows, eyelashes, and other body hair.⁹ Genetic studies have allowed for genome-wide linkage analysis, linking 3 families with this more generalized HHS phenotype to chromosome 18; specifically, an Italian family with sparse scalp and body hair but normal eyelashes and eyebrows,⁴ and 2 Pakistani families with thinning scalp hair and sparse truncal hair.¹⁰ A mutation in the APC downregulated 1 gene, APCDD1, also has been identified in these families.¹⁰ These genetic findings indicate that the generalized form of HHS is a distinct syndrome.

The differential diagnosis of HHS includes Marie-Unna hereditary hypotrichosis, loose anagen hair syndrome, trichothiodystrophy, and androgenetic alopecia. Marie-Unna hereditary hypotrichosis usually presents as near-complete absence of scalp hair at birth, development of wiry twisted hair in childhood, and progressive alopecia.³ Loose anagen hair syndrome usually demonstrates a ruffled cuticle on hair pull test and remits in late childhood. Polarization of the hair shaft can identify patients with trichothiodystrophy. Follicular miniaturization may lead one to consider early-onset androgenetic alopecia in some patients.

There is no effective treatment of HHS. Due to potential phenotypic variation, patients should be counseled that they may experience progressive or possible total loss of scalp hair by the third decade of life.^2,3,5 As with other hair loss disorders, wigs or additional over-the-counter cosmetic options may be considered.³ Currently, there are no known patient resources specific for HHS. Therefore, our patient’s family was referred to the National Alopecia Areata Foundation website (https://naaf.org/) for resources on discussing alopecia with school-aged children. The psychological impact of alopecia should not be overlooked and psychiatric referral should be provided, if needed. Examination of family members along with clinical monitoring are recommended. Genetic counseling also may be offered.³

To the Editor:

Hereditary hypotrichosis simplex (HHS)(Online Mendelian Inheritance in Man [OMIM] 146520) is a rare form of hypotrichosis that typically presents in school-aged children as worsening hair loss localized to the scalp.¹ Most patients are unaffected at birth and otherwise healthy without abnormalities of the nails, teeth, or perspiration. Examination of the scalp reveals normal follicular ostia and absence of scale and erythema; however, decreased follicular density may be noted.¹ The histopathologic findings of HHS reveal velluslike hair follicles without associated fibrosis or inflammation.² Examination of hair follicles with light microscopy is unremarkable.^3,4 Historically, this condition has been largely regarded as autosomal dominant, with variable severity also described within families. Herein, we report a case of this rare disease in a child, with 2 family members displaying a less severe phenotype.

A 7-year-old girl presented with gradual thinning of the scalp hair of 3 to 4 years’ duration. Her mother reported the patient had normal hair density at birth. Over the next several years, she was noted to have an inability to grow lengthy hair. At approximately 3 years of age, thinning of scalp hair was identified. There was no prior history of increased shedding, hypohidrosis, or tooth or nail abnormalities. Family history revealed fine hair in her older sister and fine thin hair at the frontal scalp in her mother. Her mother reported similar inability to grow lengthy hair. Physical examination of the patient demonstrated short blonde hair with diffuse thinning of the crown (Figure 1). The longest hair was approximately 10 cm in length. Follicular ostia were without erythema or scale but notably fewer in number on the crown. Eyebrows, eyelashes, teeth, and fingernails were without abnormalities. A hair pull test was negative and hair mount revealed normal bulb and shaft. Microscopy of hair shafts under polarized light was unremarkable.

Two punch biopsies were obtained and submitted for vertical and horizontal sectioning. Sections demonstrated an intact epidermis, decreased follicle number, and small follicles with hypoplastic velluslike appearance (Figure 2). Fibrosis and inflammation were not seen; there was no increase in catagen or telogen hairs. Clinical and histopathological findings were consistent with HHS.

Hereditary hypotrichosis localized to the scalp was first described by Toribio and Quinones⁵ in 1974 in a large Spanish family presenting with normal scalp hair at birth followed by gradual diffuse hair loss. Hair loss that usually began in school-aged children with subsequent few fine hairs remaining on the scalp by the third decade of life was identified in these individuals.Eyelashes, eyebrows, pubic, axillary, and other truncal hairs were normal.⁵ Several similar cases of HHS localized to the scalp have since been reported.^2,6 Hereditary hypotrichosis simplex is inherited in an autosomal-dominant fashion, with the exception of 1 reported sporadic case.³

Research on HHS has primarily focused on genetic analyses of several affected families. Betz et al⁷ mapped the gene for HHS to band 6p21.3 in 2 families of Danish origin and in the Spanish family initially described by Toribio and Quinones.⁵ Three years later, a nonsense mutation in the CDSN gene encoding corneodesmosin was described.⁸ Despite these genetic advances, the pathogenesis of HHS and the role that corneodesmosin may play remain unclear.

Generalized forms of hypotrichosis (OMIM #605389) have long been reported and described as loss of scalp hair with involvement of eyebrows, eyelashes, and other body hair.⁹ Genetic studies have allowed for genome-wide linkage analysis, linking 3 families with this more generalized HHS phenotype to chromosome 18; specifically, an Italian family with sparse scalp and body hair but normal eyelashes and eyebrows,⁴ and 2 Pakistani families with thinning scalp hair and sparse truncal hair.¹⁰ A mutation in the APC downregulated 1 gene, APCDD1, also has been identified in these families.¹⁰ These genetic findings indicate that the generalized form of HHS is a distinct syndrome.

The differential diagnosis of HHS includes Marie-Unna hereditary hypotrichosis, loose anagen hair syndrome, trichothiodystrophy, and androgenetic alopecia. Marie-Unna hereditary hypotrichosis usually presents as near-complete absence of scalp hair at birth, development of wiry twisted hair in childhood, and progressive alopecia.³ Loose anagen hair syndrome usually demonstrates a ruffled cuticle on hair pull test and remits in late childhood. Polarization of the hair shaft can identify patients with trichothiodystrophy. Follicular miniaturization may lead one to consider early-onset androgenetic alopecia in some patients.

There is no effective treatment of HHS. Due to potential phenotypic variation, patients should be counseled that they may experience progressive or possible total loss of scalp hair by the third decade of life.^2,3,5 As with other hair loss disorders, wigs or additional over-the-counter cosmetic options may be considered.³ Currently, there are no known patient resources specific for HHS. Therefore, our patient’s family was referred to the National Alopecia Areata Foundation website (https://naaf.org/) for resources on discussing alopecia with school-aged children. The psychological impact of alopecia should not be overlooked and psychiatric referral should be provided, if needed. Examination of family members along with clinical monitoring are recommended. Genetic counseling also may be offered.³

Patients on immunotherapy treatments for lung cancer have experienced repigmentation of their formerly gray hair, according to a new report. Moreover, researchers say, all but one of the patients experiencing this effect also responded well to the therapy, suggesting that hair repigmentation could potentially serve as a marker of treatment response.

In a case series published online July 12 in JAMA Dermatology (2017. doi: 10.1001/jamadermatol.2017.2106), Noelia Rivera, MD, of the Universitat Autònoma de Barcelona and her colleagues report findings from 14 patients (13 male, mean age 65) receiving anti–programmed cell death 1 (anti–PD-1) and anti–programmed cell death ligand 1 (anti–PD-L1) therapies to treat squamous cell lung cancer or lung adenocarcinoma, with most (11) receiving nivolumab (Opdivo). All but one patient experienced a diffuse darkening of the hair to resemble its previous color, while the remaining patient’s repigmentation occurred in patches.

XiXinXing/Thinkstock

Patients on immunotherapy treatments for lung cancer have experienced repigmentation of their formerly gray hair, according to a new report. Moreover, researchers say, all but one of the patients experiencing this effect also responded well to the therapy, suggesting that hair repigmentation could potentially serve as a marker of treatment response.

In a case series published online July 12 in JAMA Dermatology (2017. doi: 10.1001/jamadermatol.2017.2106), Noelia Rivera, MD, of the Universitat Autònoma de Barcelona and her colleagues report findings from 14 patients (13 male, mean age 65) receiving anti–programmed cell death 1 (anti–PD-1) and anti–programmed cell death ligand 1 (anti–PD-L1) therapies to treat squamous cell lung cancer or lung adenocarcinoma, with most (11) receiving nivolumab (Opdivo). All but one patient experienced a diffuse darkening of the hair to resemble its previous color, while the remaining patient’s repigmentation occurred in patches.

XiXinXing/Thinkstock

Patients on immunotherapy treatments for lung cancer have experienced repigmentation of their formerly gray hair, according to a new report. Moreover, researchers say, all but one of the patients experiencing this effect also responded well to the therapy, suggesting that hair repigmentation could potentially serve as a marker of treatment response.

In a case series published online July 12 in JAMA Dermatology (2017. doi: 10.1001/jamadermatol.2017.2106), Noelia Rivera, MD, of the Universitat Autònoma de Barcelona and her colleagues report findings from 14 patients (13 male, mean age 65) receiving anti–programmed cell death 1 (anti–PD-1) and anti–programmed cell death ligand 1 (anti–PD-L1) therapies to treat squamous cell lung cancer or lung adenocarcinoma, with most (11) receiving nivolumab (Opdivo). All but one patient experienced a diffuse darkening of the hair to resemble its previous color, while the remaining patient’s repigmentation occurred in patches.

XiXinXing/Thinkstock

To the Editor:

Temporal triangular alopecia (TTA), a condition first described by Sabouraud¹ in 1905, is a circumscribed nonscarring form of alopecia. Also referred to as congenital triangular alopecia, TTA presents as a triangular or lancet-shaped area of hair loss involving the frontotemporal hairline. Temporal triangular alopecia is characterized histologically by a normal number of miniaturized hair follicles without notable inflammation.² Although the majority of cases arise between birth and 9 years of age,^3,4 rare cases of adult-onset TTA also have been reported.^5,6 Adult-onset cases can cause notable diagnostic confusion and inappropriate treatment, as reported in our patient.

A 25-year-old woman with a history of Hashimoto thyroiditis presented with hair loss affecting the right temporal scalp of 3 years' duration that was first noticed by her husband. The lesion was an asymptomatic, 6×8-cm, roughly lancet-shaped patch of alopecia located on the right temporal scalp, bordering on the frontal hairline (Figure 1). Centrally, the patch appeared almost hairless with a few retained terminal hairs. The frontal hairline was thinned but still present. There was no scaling or erythema, and fine vellus hairs and a few isolated terminal hairs covered the area. The corresponding skin on the contralateral temporal scalp showed normal hair density. The patient insisted that she had normal hair at the affected area until 22 years of age, and she denied a history of trauma or tight hairstyles. Initially diagnosed with alopecia areata by her primary care provider, the patient was treated with topical corticosteroids for 6 months without benefit. She was subsequently referred to a dermatologist who again offered a diagnosis of alopecia areata and treated the lesions with 2 intralesional corticosteroid injections without benefit. No biopsies of the affected area were performed, and the patient was given a trial of topical minoxidil.

The patient consulted a new primary care provider and was diagnosed with scarring alopecia. She was referred to our dermatology department for further treatment. An initial biopsy at the edge of the affected area was interpreted as normal, but after failing additional intralesional corticosteroid injections, she was referred to our hair clinic where another biopsy was performed in the central portion of the lesion. A 4-mm diameter punch biopsy specimen revealed a normal epidermis and dermis; however, in the lower dermis only a single terminal follicle was seen (Figure 2). Sections through the upper dermis (Figure 3) showed that the total number of hairs was normal or nearly normal with at least 22 follicles, but most were vellus and indeterminate hairs with only a single terminal hair. The dermal architecture was otherwise normal. Given the clinical and histologic findings, a diagnosis of TTA was made. Subsequent to the diagnosis, the patient did not pursue any additional treatment options and preferred to style her hair so that the area of TTA remained covered.

The differential diagnosis in adults presenting with a patch of localized alopecia includes alopecia areata, trichotillomania, pressure-induced alopecia, traction alopecia, lichen planopilaris, discoid lupus erythematosus, and rarely TTA. Temporal triangular alopecia is a fairly common, if underreported, nonscarring form of alopecia that mainly affects young children. A PubMed search of articles indexed for MEDLINE using the terms temporal triangular alopecia or congenital triangular alopecia or triangular alopecia documented only 76 cases of TTA including our own, with the majority of patients diagnosed before 9 years of age. Only 2 cases of adult-onset TTA have been reported,^5,6 possibly leading to misdiagnosis of adult patients who present with similar areas of hair loss. As with some prior cases of TTA,^5,7 our patient was misdiagnosed with alopecia areata and scarring alopecia, both treated unsuccessfully before a diagnosis of TTA was considered. Clues to the diagnosis included the location, the lack of change in size and shape, the lack of response to intralesional corticosteroids, and the presence of numerous vellus hairs on the surface. A biopsy of the visibly hairless zone was confirmatory. The normal or nearly normal number of miniaturized hairs in specimens of TTA suggest that topical minoxidil therapy (eg, 5% solution twice daily for at least 6 months) might be useful, but the authors have tried it on a few other patients with clinically typical TTA without discernible benefit. When lesions are small, excision provides a fast and permanent solution to the problem, albeit with the usual risks of minor surgery.

To the Editor:

Temporal triangular alopecia (TTA), a condition first described by Sabouraud¹ in 1905, is a circumscribed nonscarring form of alopecia. Also referred to as congenital triangular alopecia, TTA presents as a triangular or lancet-shaped area of hair loss involving the frontotemporal hairline. Temporal triangular alopecia is characterized histologically by a normal number of miniaturized hair follicles without notable inflammation.² Although the majority of cases arise between birth and 9 years of age,^3,4 rare cases of adult-onset TTA also have been reported.^5,6 Adult-onset cases can cause notable diagnostic confusion and inappropriate treatment, as reported in our patient.

A 25-year-old woman with a history of Hashimoto thyroiditis presented with hair loss affecting the right temporal scalp of 3 years' duration that was first noticed by her husband. The lesion was an asymptomatic, 6×8-cm, roughly lancet-shaped patch of alopecia located on the right temporal scalp, bordering on the frontal hairline (Figure 1). Centrally, the patch appeared almost hairless with a few retained terminal hairs. The frontal hairline was thinned but still present. There was no scaling or erythema, and fine vellus hairs and a few isolated terminal hairs covered the area. The corresponding skin on the contralateral temporal scalp showed normal hair density. The patient insisted that she had normal hair at the affected area until 22 years of age, and she denied a history of trauma or tight hairstyles. Initially diagnosed with alopecia areata by her primary care provider, the patient was treated with topical corticosteroids for 6 months without benefit. She was subsequently referred to a dermatologist who again offered a diagnosis of alopecia areata and treated the lesions with 2 intralesional corticosteroid injections without benefit. No biopsies of the affected area were performed, and the patient was given a trial of topical minoxidil.

The patient consulted a new primary care provider and was diagnosed with scarring alopecia. She was referred to our dermatology department for further treatment. An initial biopsy at the edge of the affected area was interpreted as normal, but after failing additional intralesional corticosteroid injections, she was referred to our hair clinic where another biopsy was performed in the central portion of the lesion. A 4-mm diameter punch biopsy specimen revealed a normal epidermis and dermis; however, in the lower dermis only a single terminal follicle was seen (Figure 2). Sections through the upper dermis (Figure 3) showed that the total number of hairs was normal or nearly normal with at least 22 follicles, but most were vellus and indeterminate hairs with only a single terminal hair. The dermal architecture was otherwise normal. Given the clinical and histologic findings, a diagnosis of TTA was made. Subsequent to the diagnosis, the patient did not pursue any additional treatment options and preferred to style her hair so that the area of TTA remained covered.

The differential diagnosis in adults presenting with a patch of localized alopecia includes alopecia areata, trichotillomania, pressure-induced alopecia, traction alopecia, lichen planopilaris, discoid lupus erythematosus, and rarely TTA. Temporal triangular alopecia is a fairly common, if underreported, nonscarring form of alopecia that mainly affects young children. A PubMed search of articles indexed for MEDLINE using the terms temporal triangular alopecia or congenital triangular alopecia or triangular alopecia documented only 76 cases of TTA including our own, with the majority of patients diagnosed before 9 years of age. Only 2 cases of adult-onset TTA have been reported,^5,6 possibly leading to misdiagnosis of adult patients who present with similar areas of hair loss. As with some prior cases of TTA,^5,7 our patient was misdiagnosed with alopecia areata and scarring alopecia, both treated unsuccessfully before a diagnosis of TTA was considered. Clues to the diagnosis included the location, the lack of change in size and shape, the lack of response to intralesional corticosteroids, and the presence of numerous vellus hairs on the surface. A biopsy of the visibly hairless zone was confirmatory. The normal or nearly normal number of miniaturized hairs in specimens of TTA suggest that topical minoxidil therapy (eg, 5% solution twice daily for at least 6 months) might be useful, but the authors have tried it on a few other patients with clinically typical TTA without discernible benefit. When lesions are small, excision provides a fast and permanent solution to the problem, albeit with the usual risks of minor surgery.

To the Editor:

Temporal triangular alopecia (TTA), a condition first described by Sabouraud¹ in 1905, is a circumscribed nonscarring form of alopecia. Also referred to as congenital triangular alopecia, TTA presents as a triangular or lancet-shaped area of hair loss involving the frontotemporal hairline. Temporal triangular alopecia is characterized histologically by a normal number of miniaturized hair follicles without notable inflammation.² Although the majority of cases arise between birth and 9 years of age,^3,4 rare cases of adult-onset TTA also have been reported.^5,6 Adult-onset cases can cause notable diagnostic confusion and inappropriate treatment, as reported in our patient.

A 25-year-old woman with a history of Hashimoto thyroiditis presented with hair loss affecting the right temporal scalp of 3 years' duration that was first noticed by her husband. The lesion was an asymptomatic, 6×8-cm, roughly lancet-shaped patch of alopecia located on the right temporal scalp, bordering on the frontal hairline (Figure 1). Centrally, the patch appeared almost hairless with a few retained terminal hairs. The frontal hairline was thinned but still present. There was no scaling or erythema, and fine vellus hairs and a few isolated terminal hairs covered the area. The corresponding skin on the contralateral temporal scalp showed normal hair density. The patient insisted that she had normal hair at the affected area until 22 years of age, and she denied a history of trauma or tight hairstyles. Initially diagnosed with alopecia areata by her primary care provider, the patient was treated with topical corticosteroids for 6 months without benefit. She was subsequently referred to a dermatologist who again offered a diagnosis of alopecia areata and treated the lesions with 2 intralesional corticosteroid injections without benefit. No biopsies of the affected area were performed, and the patient was given a trial of topical minoxidil.

The patient consulted a new primary care provider and was diagnosed with scarring alopecia. She was referred to our dermatology department for further treatment. An initial biopsy at the edge of the affected area was interpreted as normal, but after failing additional intralesional corticosteroid injections, she was referred to our hair clinic where another biopsy was performed in the central portion of the lesion. A 4-mm diameter punch biopsy specimen revealed a normal epidermis and dermis; however, in the lower dermis only a single terminal follicle was seen (Figure 2). Sections through the upper dermis (Figure 3) showed that the total number of hairs was normal or nearly normal with at least 22 follicles, but most were vellus and indeterminate hairs with only a single terminal hair. The dermal architecture was otherwise normal. Given the clinical and histologic findings, a diagnosis of TTA was made. Subsequent to the diagnosis, the patient did not pursue any additional treatment options and preferred to style her hair so that the area of TTA remained covered.

The differential diagnosis in adults presenting with a patch of localized alopecia includes alopecia areata, trichotillomania, pressure-induced alopecia, traction alopecia, lichen planopilaris, discoid lupus erythematosus, and rarely TTA. Temporal triangular alopecia is a fairly common, if underreported, nonscarring form of alopecia that mainly affects young children. A PubMed search of articles indexed for MEDLINE using the terms temporal triangular alopecia or congenital triangular alopecia or triangular alopecia documented only 76 cases of TTA including our own, with the majority of patients diagnosed before 9 years of age. Only 2 cases of adult-onset TTA have been reported,^5,6 possibly leading to misdiagnosis of adult patients who present with similar areas of hair loss. As with some prior cases of TTA,^5,7 our patient was misdiagnosed with alopecia areata and scarring alopecia, both treated unsuccessfully before a diagnosis of TTA was considered. Clues to the diagnosis included the location, the lack of change in size and shape, the lack of response to intralesional corticosteroids, and the presence of numerous vellus hairs on the surface. A biopsy of the visibly hairless zone was confirmatory. The normal or nearly normal number of miniaturized hairs in specimens of TTA suggest that topical minoxidil therapy (eg, 5% solution twice daily for at least 6 months) might be useful, but the authors have tried it on a few other patients with clinically typical TTA without discernible benefit. When lesions are small, excision provides a fast and permanent solution to the problem, albeit with the usual risks of minor surgery.

CHICAGO – How do you talk to your alopecia areata patients and their families about hair loss? If you can’t set the temptation to hurry aside and take the time to listen, things may not go well, said Neil Prose, MD.

With the caveat that Janus kinase inhibitors show promise, Dr. Prose said that “most children who are destined to lose their hair will probably do so despite all of our best efforts.” Figuring out how to engage children and parents and frame a positive conversation about alopecia can present a real challenge, especially in the context of a busy practice, said Dr. Prose, professor of dermatology and medical director of Patterson Place Pediatric Dermatology at Duke University, Durham, N.C.

Abbassyma/Wikimedia Commons/Public Domain

[email protected]

On Twitter @karioakes

CHICAGO – How do you talk to your alopecia areata patients and their families about hair loss? If you can’t set the temptation to hurry aside and take the time to listen, things may not go well, said Neil Prose, MD.

With the caveat that Janus kinase inhibitors show promise, Dr. Prose said that “most children who are destined to lose their hair will probably do so despite all of our best efforts.” Figuring out how to engage children and parents and frame a positive conversation about alopecia can present a real challenge, especially in the context of a busy practice, said Dr. Prose, professor of dermatology and medical director of Patterson Place Pediatric Dermatology at Duke University, Durham, N.C.

Abbassyma/Wikimedia Commons/Public Domain

[email protected]

On Twitter @karioakes

CHICAGO – How do you talk to your alopecia areata patients and their families about hair loss? If you can’t set the temptation to hurry aside and take the time to listen, things may not go well, said Neil Prose, MD.

With the caveat that Janus kinase inhibitors show promise, Dr. Prose said that “most children who are destined to lose their hair will probably do so despite all of our best efforts.” Figuring out how to engage children and parents and frame a positive conversation about alopecia can present a real challenge, especially in the context of a busy practice, said Dr. Prose, professor of dermatology and medical director of Patterson Place Pediatric Dermatology at Duke University, Durham, N.C.

Abbassyma/Wikimedia Commons/Public Domain

[email protected]

On Twitter @karioakes

CHICAGO – A novel one-time topical treatment for head lice, abametapir, was well tolerated in children as young as 6 months, according to pooled results from 11 clinical trials.

The pooled safety data included results from 11 clinical trials including 1,372 patients. Of these, 700 were aged 6 months to 17 years, and patients were exposed to the novel metalloproteinase inhibitor for 10-20 minutes.

In examining safety data from the pooled trials, Lydie Hazan, MD, of Axis Clinical Trials and her collaborators found that for pediatric patients, most treatment-emergent adverse events (AEs) were skin and subcutaneous tissue-related. The most common AEs were erythema, rash, a burning sensation on the skin, and contact dermatitis.

Data for the three phase II pharmacokinetic trials, the phase II ovicidal efficacy trial, and the two phase III trials were reported separately by Dr. Hazan and her coauthors in a poster presentation at the World Congress of Pediatric Dermatology. The overall incidence of treatment-emergent AEs in the studies ranged from 20% to 29% for patients in the active arms of the trials. For patients who received the vehicle lotion only, the incidence of AEs ranged from 16% to 57%.

©CDC/Reed & Carnrick Pharmaceuticals

*Correction, 8/7/17: An earlier version of this article had an incorrect citation.

[email protected]

On Twitter @karioakes

CHICAGO – A novel one-time topical treatment for head lice, abametapir, was well tolerated in children as young as 6 months, according to pooled results from 11 clinical trials.

The pooled safety data included results from 11 clinical trials including 1,372 patients. Of these, 700 were aged 6 months to 17 years, and patients were exposed to the novel metalloproteinase inhibitor for 10-20 minutes.

In examining safety data from the pooled trials, Lydie Hazan, MD, of Axis Clinical Trials and her collaborators found that for pediatric patients, most treatment-emergent adverse events (AEs) were skin and subcutaneous tissue-related. The most common AEs were erythema, rash, a burning sensation on the skin, and contact dermatitis.

Data for the three phase II pharmacokinetic trials, the phase II ovicidal efficacy trial, and the two phase III trials were reported separately by Dr. Hazan and her coauthors in a poster presentation at the World Congress of Pediatric Dermatology. The overall incidence of treatment-emergent AEs in the studies ranged from 20% to 29% for patients in the active arms of the trials. For patients who received the vehicle lotion only, the incidence of AEs ranged from 16% to 57%.

©CDC/Reed & Carnrick Pharmaceuticals

*Correction, 8/7/17: An earlier version of this article had an incorrect citation.

[email protected]

On Twitter @karioakes

CHICAGO – A novel one-time topical treatment for head lice, abametapir, was well tolerated in children as young as 6 months, according to pooled results from 11 clinical trials.

The pooled safety data included results from 11 clinical trials including 1,372 patients. Of these, 700 were aged 6 months to 17 years, and patients were exposed to the novel metalloproteinase inhibitor for 10-20 minutes.

In examining safety data from the pooled trials, Lydie Hazan, MD, of Axis Clinical Trials and her collaborators found that for pediatric patients, most treatment-emergent adverse events (AEs) were skin and subcutaneous tissue-related. The most common AEs were erythema, rash, a burning sensation on the skin, and contact dermatitis.

Data for the three phase II pharmacokinetic trials, the phase II ovicidal efficacy trial, and the two phase III trials were reported separately by Dr. Hazan and her coauthors in a poster presentation at the World Congress of Pediatric Dermatology. The overall incidence of treatment-emergent AEs in the studies ranged from 20% to 29% for patients in the active arms of the trials. For patients who received the vehicle lotion only, the incidence of AEs ranged from 16% to 57%.

©CDC/Reed & Carnrick Pharmaceuticals

*Correction, 8/7/17: An earlier version of this article had an incorrect citation.

[email protected]

On Twitter @karioakes

The Diagnosis: Piedra

Microscopic examination of the hair shafts revealed brown to black, firmly adherent concretions (Figure 1). Scanning electron microscopy of the nodules was performed, which allowed for greater definition of the constituent hyphae and arthrospores (Figure 2). 

Photograph courtesy of Eric Hossler, MD (Danville, Pennsylvania).

Photograph courtesy of Fred E. Hossler, PhD (Johnson City, Tennesse).

Fungal cultures grew Trichosporon inkin along with other dematiaceous molds. The patient initially was treated with a combination of ketoconazole shampoo and weekly application of topical terbinafine. She trimmed 15.2 cm of the hair of her own volition. At 2-month follow-up the nodules were still present, though smaller and less numerous. Repeat cultures were obtained, which again grew T inkin. She then began taking oral terbinafine 250 mg daily for 6 weeks.

This case of piedra is unique in that our patient presented with black nodules clinically, but cultures grew only the causative agent of white piedra, T inkin. A search of PubMed articles indexed for MEDLINE using the terms black piedra, white piedra, or piedra, and mixed infection or coinfection yielded one other similar case.¹ Kanitakis et al¹ speculated that perhaps there was coinfection of black and white piedra and that Piedraia hortae, the causative agent of black piedra, was unable to flourish in culture facing competition from other fungi. This scenario also could apply to our patient. However, the original culture taken from our patient also grew other dematiaceous molds including Cladosporium and Exophiala species. It also is possible that these other fungi could have contributed pigment to the nodules, giving it the appearance of black piedra when only T inkin was present as the true pathogen.

White piedra is a rare fungal infection of the hair shaft caused by organisms of the genus Trichosporon, with Trichosporon ovoides most likely to infect the scalp.² Black piedra is a similar fungal infection caused by P hortae. Piedra means stone in Spanish, reflecting the appearance of these organisms on the hair shaft. It is common in tropical regions of the world such as Southeast Asia and South America, flourishing in the high temperatures and humidity.² Both infectious agents are found in the soil or in standing water.³ White piedra most commonly is found in facial, axilla, or pubic hair, while black piedra most often is found in the hair of the scalp.^2,4 Local cultural practices may contribute to transfer of Trichosporon or P hortae to the scalp, including the use of Brazilian plant oils in the hair or tying a veil or hijab to wet hair. Interestingly, some groups intentionally introduce the fungus to their hair for cosmetic reasons in endemic areas.^2,3,5

Patients with white or black piedra generally are asymptomatic.⁴ Some may notice a rough texture to the hair or hear a characteristic metallic rattling sound as the nodules make contact with brush bristles.^2,3 On inspection of the scalp, white piedra will appear to be white to light brown nodules, while black piedra presents as brown to black in color. The nodules are often firm on palpation.^2,3 The nodules of white piedra generally are easy to remove in contrast to black piedra, which involves nodules that securely attach to the hair shaft but can be removed with pressure.^3,5 Piedra has natural keratolytic activities and with prolonged infection can penetrate the hair cuticle, causing weakness and eventual breakage of the hair. This invasion into the hair cortex also can complicate treatment regimens, contributing to the chronic course of these infections.⁶ 

Diagnosis is based on clinical and microscopic findings. Nodules on hair shafts can be prepared with potassium hydroxide and placed on glass slides for examination.⁴ Dyes such as toluidine blue or chlorazol black E stain can be used to assist in identifying fungal structures.² Sabouraud agar with cycloheximide may be the best choice for culture medium.² Black piedra slowly grows into small dome-shaped colonies. White piedra will grow more quickly into cream-colored colonies with wrinkles and sometimes mucinous characteristics.³

The best treatment of black or white piedra is to cut the hair, thereby eliminating the fungi,⁷ which is not an easy option for many patients, such as ours, because of the aesthetic implications. Alternative treatments include azole shampoos such as ketoconazole.^2,4 Treatment with oral terbinafine 250 mg daily for 6 weeks has been successfully used for black piedra.⁷ Patients must be careful to thoroughly clean or discard hairbrushes, as they can serve as reservoirs of fungi to reinfect patients or spread to others.^5,7

The Diagnosis: Piedra

Microscopic examination of the hair shafts revealed brown to black, firmly adherent concretions (Figure 1). Scanning electron microscopy of the nodules was performed, which allowed for greater definition of the constituent hyphae and arthrospores (Figure 2). 

Photograph courtesy of Eric Hossler, MD (Danville, Pennsylvania).

Photograph courtesy of Fred E. Hossler, PhD (Johnson City, Tennesse).

Fungal cultures grew Trichosporon inkin along with other dematiaceous molds. The patient initially was treated with a combination of ketoconazole shampoo and weekly application of topical terbinafine. She trimmed 15.2 cm of the hair of her own volition. At 2-month follow-up the nodules were still present, though smaller and less numerous. Repeat cultures were obtained, which again grew T inkin. She then began taking oral terbinafine 250 mg daily for 6 weeks.

This case of piedra is unique in that our patient presented with black nodules clinically, but cultures grew only the causative agent of white piedra, T inkin. A search of PubMed articles indexed for MEDLINE using the terms black piedra, white piedra, or piedra, and mixed infection or coinfection yielded one other similar case.¹ Kanitakis et al¹ speculated that perhaps there was coinfection of black and white piedra and that Piedraia hortae, the causative agent of black piedra, was unable to flourish in culture facing competition from other fungi. This scenario also could apply to our patient. However, the original culture taken from our patient also grew other dematiaceous molds including Cladosporium and Exophiala species. It also is possible that these other fungi could have contributed pigment to the nodules, giving it the appearance of black piedra when only T inkin was present as the true pathogen.

White piedra is a rare fungal infection of the hair shaft caused by organisms of the genus Trichosporon, with Trichosporon ovoides most likely to infect the scalp.² Black piedra is a similar fungal infection caused by P hortae. Piedra means stone in Spanish, reflecting the appearance of these organisms on the hair shaft. It is common in tropical regions of the world such as Southeast Asia and South America, flourishing in the high temperatures and humidity.² Both infectious agents are found in the soil or in standing water.³ White piedra most commonly is found in facial, axilla, or pubic hair, while black piedra most often is found in the hair of the scalp.^2,4 Local cultural practices may contribute to transfer of Trichosporon or P hortae to the scalp, including the use of Brazilian plant oils in the hair or tying a veil or hijab to wet hair. Interestingly, some groups intentionally introduce the fungus to their hair for cosmetic reasons in endemic areas.^2,3,5

Patients with white or black piedra generally are asymptomatic.⁴ Some may notice a rough texture to the hair or hear a characteristic metallic rattling sound as the nodules make contact with brush bristles.^2,3 On inspection of the scalp, white piedra will appear to be white to light brown nodules, while black piedra presents as brown to black in color. The nodules are often firm on palpation.^2,3 The nodules of white piedra generally are easy to remove in contrast to black piedra, which involves nodules that securely attach to the hair shaft but can be removed with pressure.^3,5 Piedra has natural keratolytic activities and with prolonged infection can penetrate the hair cuticle, causing weakness and eventual breakage of the hair. This invasion into the hair cortex also can complicate treatment regimens, contributing to the chronic course of these infections.⁶ 

Diagnosis is based on clinical and microscopic findings. Nodules on hair shafts can be prepared with potassium hydroxide and placed on glass slides for examination.⁴ Dyes such as toluidine blue or chlorazol black E stain can be used to assist in identifying fungal structures.² Sabouraud agar with cycloheximide may be the best choice for culture medium.² Black piedra slowly grows into small dome-shaped colonies. White piedra will grow more quickly into cream-colored colonies with wrinkles and sometimes mucinous characteristics.³

The best treatment of black or white piedra is to cut the hair, thereby eliminating the fungi,⁷ which is not an easy option for many patients, such as ours, because of the aesthetic implications. Alternative treatments include azole shampoos such as ketoconazole.^2,4 Treatment with oral terbinafine 250 mg daily for 6 weeks has been successfully used for black piedra.⁷ Patients must be careful to thoroughly clean or discard hairbrushes, as they can serve as reservoirs of fungi to reinfect patients or spread to others.^5,7

The Diagnosis: Piedra

Microscopic examination of the hair shafts revealed brown to black, firmly adherent concretions (Figure 1). Scanning electron microscopy of the nodules was performed, which allowed for greater definition of the constituent hyphae and arthrospores (Figure 2). 

Photograph courtesy of Eric Hossler, MD (Danville, Pennsylvania).

Photograph courtesy of Fred E. Hossler, PhD (Johnson City, Tennesse).

Fungal cultures grew Trichosporon inkin along with other dematiaceous molds. The patient initially was treated with a combination of ketoconazole shampoo and weekly application of topical terbinafine. She trimmed 15.2 cm of the hair of her own volition. At 2-month follow-up the nodules were still present, though smaller and less numerous. Repeat cultures were obtained, which again grew T inkin. She then began taking oral terbinafine 250 mg daily for 6 weeks.

This case of piedra is unique in that our patient presented with black nodules clinically, but cultures grew only the causative agent of white piedra, T inkin. A search of PubMed articles indexed for MEDLINE using the terms black piedra, white piedra, or piedra, and mixed infection or coinfection yielded one other similar case.¹ Kanitakis et al¹ speculated that perhaps there was coinfection of black and white piedra and that Piedraia hortae, the causative agent of black piedra, was unable to flourish in culture facing competition from other fungi. This scenario also could apply to our patient. However, the original culture taken from our patient also grew other dematiaceous molds including Cladosporium and Exophiala species. It also is possible that these other fungi could have contributed pigment to the nodules, giving it the appearance of black piedra when only T inkin was present as the true pathogen.

White piedra is a rare fungal infection of the hair shaft caused by organisms of the genus Trichosporon, with Trichosporon ovoides most likely to infect the scalp.² Black piedra is a similar fungal infection caused by P hortae. Piedra means stone in Spanish, reflecting the appearance of these organisms on the hair shaft. It is common in tropical regions of the world such as Southeast Asia and South America, flourishing in the high temperatures and humidity.² Both infectious agents are found in the soil or in standing water.³ White piedra most commonly is found in facial, axilla, or pubic hair, while black piedra most often is found in the hair of the scalp.^2,4 Local cultural practices may contribute to transfer of Trichosporon or P hortae to the scalp, including the use of Brazilian plant oils in the hair or tying a veil or hijab to wet hair. Interestingly, some groups intentionally introduce the fungus to their hair for cosmetic reasons in endemic areas.^2,3,5

Patients with white or black piedra generally are asymptomatic.⁴ Some may notice a rough texture to the hair or hear a characteristic metallic rattling sound as the nodules make contact with brush bristles.^2,3 On inspection of the scalp, white piedra will appear to be white to light brown nodules, while black piedra presents as brown to black in color. The nodules are often firm on palpation.^2,3 The nodules of white piedra generally are easy to remove in contrast to black piedra, which involves nodules that securely attach to the hair shaft but can be removed with pressure.^3,5 Piedra has natural keratolytic activities and with prolonged infection can penetrate the hair cuticle, causing weakness and eventual breakage of the hair. This invasion into the hair cortex also can complicate treatment regimens, contributing to the chronic course of these infections.⁶ 

Diagnosis is based on clinical and microscopic findings. Nodules on hair shafts can be prepared with potassium hydroxide and placed on glass slides for examination.⁴ Dyes such as toluidine blue or chlorazol black E stain can be used to assist in identifying fungal structures.² Sabouraud agar with cycloheximide may be the best choice for culture medium.² Black piedra slowly grows into small dome-shaped colonies. White piedra will grow more quickly into cream-colored colonies with wrinkles and sometimes mucinous characteristics.³

The best treatment of black or white piedra is to cut the hair, thereby eliminating the fungi,⁷ which is not an easy option for many patients, such as ours, because of the aesthetic implications. Alternative treatments include azole shampoos such as ketoconazole.^2,4 Treatment with oral terbinafine 250 mg daily for 6 weeks has been successfully used for black piedra.⁷ Patients must be careful to thoroughly clean or discard hairbrushes, as they can serve as reservoirs of fungi to reinfect patients or spread to others.^5,7