Reticular Hyperpigmentation on the Lower Legs

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Reticular Hyperpigmentation on the Lower Legs

The Diagnosis: Erythema Ab Igne

Given the patient's reticulated hyperpigmented lesions in the setting of recent space heater use with heater closer to the more affected leg, erythema ab igne was diagnosed. Patient education was provided and moving the heater away from the lower extremities was advised.

Erythema ab igne first was described by German dermatologist Abraham Buschke as hitze melanose, meaning melanosis induced by heat. The classic skin findings were first observed on the lower legs of patients who worked in front of open fires or coal stoves.1 Over the years, new causes of erythema ab igne secondary to prolonged thermal radiation exposure have been reported.1 In the elderly, hospitalized, and chronic pain patients, erythema ab igne has been observed in areas treated with heating pads and blankets.2 Other triggers such as frequent hot bathing, furniture, steam radiators, space heaters, and laptops also have been reported.3-6 Laptop-induced erythema ab igne is a diagnosis that has been reported in the last decade and its incidence likely will increase in the future.6

The clinical manifestations of erythema ab igne correlate with the frequency and duration of heat exposure. Acutely, a mild and transient erythema develops in the affected area. With chronic heat exposure, these areas subsequently develop a permanent reticulated hyperpigmented pattern and may eventually become atrophic.2,6 All body surfaces are at risk, but erythema ab igne classically involves the legs, lower back, and/or abdomen. Lesions typically are asymptomatic; however, burning and pruritus can be present.2,6 Bullous erythema ab igne, though rare, has been reported,7 suggesting a potential transition from erythema ab igne to burns.6

Biopsy is not recommended for diagnosis; however, the histopathologic changes of erythema ab igne include hyperkeratosis, interface dermatitis, epidermal atrophy with apoptotic keratinocytes, and melanin incontinence. Although this condition typically is benign, histologic findings could resemble actinic keratosis, suggesting that chronic changes induced by infrared thermal radiation may lead to squamous cell carcinoma or rarely Merkel cell carcinoma. The latency for developing carcinoma appears to extend 30 years, with a 30% tendency for recurrence or metastasis. Given the possibility of an increase in erythema ab igne in the pediatric population in the upcoming years, as displayed by our patient, and increasing laptop and electronic use in children and adolescents, it is important to be aware of this skin condition and the potential complications of it going undiagnosed.2,6

 

 

No specific therapy for erythema ab igne exists. Treatment is centered on eliminating exposure to the heat source. With appropriate removal, the reticulated hyperpigmented lesions will resolve, sometimes taking several months.

Differential diagnosis includes livedo reticularis, livedoid vasculopathy, and cutis marmorata. The reticulated purpuric lesions of livedo reticularis involving the extremities often mimic erythema ab igne's cutaneous morphology; however, livedo reticularis frequently is associated with conditions such as drug reactions, infections, thrombosis, and vasculitides,2 as opposed to erythema ab igne, which frequently is associated with conditions causing pain or decreased body temperature, thus necessitating use of heating devices, as seen in our patient. Livedoid vasculopathy is characterized by purpuric macules involving the lower legs and feet that progress to recurrent leg ulcers. Our patient's asymptomatic lesions and absence of ulcers excluded this diagnosis.8 Lastly, cutis marmorata, a congenital condition, is characterized by blue-violet vascular networks that often display ulceration and atrophy of the involved skin as well as hypertrophy or atrophy of the involved limb9; these clinical findings were not present in our patient and this diagnosis would not explain the relationship between the cutaneous lesions and heat exposure. 

References
  1. Nilic M, Adams BB. Erythema ab igne induced by a laptop computer. J Am Acad Dermatol. 2004;50:973-974.
  2. Riahi RR, Cohen PR, Robinson FW, et al. Erythema ab igne mimicking livedo reticularis. Int J Dermatol. 2010;49:1314-1317.
  3. Lin SJ, Hsu CJ, Chiu HC. Erythema ab igne caused by frequent hot bathing. Acta Derm Venereol. 2002;82:478-479.
  4. Meffert JJ, Davis BM. Furniture-induced erythema ab igne. J Am Acad Dermatol. 1996;34:516-517.
  5. Kligman LH, Kligman AM. Reflections on heat. Br J Dermatol. 1984;110:369-375.
  6. Arnold AW, Itin PH. Laptop computer−induced erythema ab igne in a child and review of the literature [published online October 4, 2010]. Pediatrics. 2010;126:e1227-e1230.
  7. Kokturk A, Kaya TI, Baz K, et al. Bullous erythema ab igne. Dermatol Online J. 2003;9:18.
  8. Khenifer S, Thomas L, Balme B, et al. Livedoid vasculopathy: thrombotic or inflammatory disease? Clin Exp Dermatol. 2009;35:693-698.  
  9. Pernet C, Guillot B, Bigorre M, et al. Focal and atrophic cutis marmorata telangiectatica congenital. J Am Acad Dermatol. 2013;69:e268-e269.
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The authors report no conflict of interest.

Correspondence: Leslie Castelo-Soccio, MD, PhD, Department of Pediatrics, Section of Dermatology, The Children’s Hospital of Philadelphia, 3550 Market St, 2nd Floor, Philadelphia, PA 19104 (castelosocciol@email.chop.edu).

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From The Children’s Hospital of Philadelphia, Pennsylvania. Dr. Castelo-Soccio is from the Department of Pediatrics, Section of Dermatology.

The authors report no conflict of interest.

Correspondence: Leslie Castelo-Soccio, MD, PhD, Department of Pediatrics, Section of Dermatology, The Children’s Hospital of Philadelphia, 3550 Market St, 2nd Floor, Philadelphia, PA 19104 (castelosocciol@email.chop.edu).

Author and Disclosure Information

From The Children’s Hospital of Philadelphia, Pennsylvania. Dr. Castelo-Soccio is from the Department of Pediatrics, Section of Dermatology.

The authors report no conflict of interest.

Correspondence: Leslie Castelo-Soccio, MD, PhD, Department of Pediatrics, Section of Dermatology, The Children’s Hospital of Philadelphia, 3550 Market St, 2nd Floor, Philadelphia, PA 19104 (castelosocciol@email.chop.edu).

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The Diagnosis: Erythema Ab Igne

Given the patient's reticulated hyperpigmented lesions in the setting of recent space heater use with heater closer to the more affected leg, erythema ab igne was diagnosed. Patient education was provided and moving the heater away from the lower extremities was advised.

Erythema ab igne first was described by German dermatologist Abraham Buschke as hitze melanose, meaning melanosis induced by heat. The classic skin findings were first observed on the lower legs of patients who worked in front of open fires or coal stoves.1 Over the years, new causes of erythema ab igne secondary to prolonged thermal radiation exposure have been reported.1 In the elderly, hospitalized, and chronic pain patients, erythema ab igne has been observed in areas treated with heating pads and blankets.2 Other triggers such as frequent hot bathing, furniture, steam radiators, space heaters, and laptops also have been reported.3-6 Laptop-induced erythema ab igne is a diagnosis that has been reported in the last decade and its incidence likely will increase in the future.6

The clinical manifestations of erythema ab igne correlate with the frequency and duration of heat exposure. Acutely, a mild and transient erythema develops in the affected area. With chronic heat exposure, these areas subsequently develop a permanent reticulated hyperpigmented pattern and may eventually become atrophic.2,6 All body surfaces are at risk, but erythema ab igne classically involves the legs, lower back, and/or abdomen. Lesions typically are asymptomatic; however, burning and pruritus can be present.2,6 Bullous erythema ab igne, though rare, has been reported,7 suggesting a potential transition from erythema ab igne to burns.6

Biopsy is not recommended for diagnosis; however, the histopathologic changes of erythema ab igne include hyperkeratosis, interface dermatitis, epidermal atrophy with apoptotic keratinocytes, and melanin incontinence. Although this condition typically is benign, histologic findings could resemble actinic keratosis, suggesting that chronic changes induced by infrared thermal radiation may lead to squamous cell carcinoma or rarely Merkel cell carcinoma. The latency for developing carcinoma appears to extend 30 years, with a 30% tendency for recurrence or metastasis. Given the possibility of an increase in erythema ab igne in the pediatric population in the upcoming years, as displayed by our patient, and increasing laptop and electronic use in children and adolescents, it is important to be aware of this skin condition and the potential complications of it going undiagnosed.2,6

 

 

No specific therapy for erythema ab igne exists. Treatment is centered on eliminating exposure to the heat source. With appropriate removal, the reticulated hyperpigmented lesions will resolve, sometimes taking several months.

Differential diagnosis includes livedo reticularis, livedoid vasculopathy, and cutis marmorata. The reticulated purpuric lesions of livedo reticularis involving the extremities often mimic erythema ab igne's cutaneous morphology; however, livedo reticularis frequently is associated with conditions such as drug reactions, infections, thrombosis, and vasculitides,2 as opposed to erythema ab igne, which frequently is associated with conditions causing pain or decreased body temperature, thus necessitating use of heating devices, as seen in our patient. Livedoid vasculopathy is characterized by purpuric macules involving the lower legs and feet that progress to recurrent leg ulcers. Our patient's asymptomatic lesions and absence of ulcers excluded this diagnosis.8 Lastly, cutis marmorata, a congenital condition, is characterized by blue-violet vascular networks that often display ulceration and atrophy of the involved skin as well as hypertrophy or atrophy of the involved limb9; these clinical findings were not present in our patient and this diagnosis would not explain the relationship between the cutaneous lesions and heat exposure. 

The Diagnosis: Erythema Ab Igne

Given the patient's reticulated hyperpigmented lesions in the setting of recent space heater use with heater closer to the more affected leg, erythema ab igne was diagnosed. Patient education was provided and moving the heater away from the lower extremities was advised.

Erythema ab igne first was described by German dermatologist Abraham Buschke as hitze melanose, meaning melanosis induced by heat. The classic skin findings were first observed on the lower legs of patients who worked in front of open fires or coal stoves.1 Over the years, new causes of erythema ab igne secondary to prolonged thermal radiation exposure have been reported.1 In the elderly, hospitalized, and chronic pain patients, erythema ab igne has been observed in areas treated with heating pads and blankets.2 Other triggers such as frequent hot bathing, furniture, steam radiators, space heaters, and laptops also have been reported.3-6 Laptop-induced erythema ab igne is a diagnosis that has been reported in the last decade and its incidence likely will increase in the future.6

The clinical manifestations of erythema ab igne correlate with the frequency and duration of heat exposure. Acutely, a mild and transient erythema develops in the affected area. With chronic heat exposure, these areas subsequently develop a permanent reticulated hyperpigmented pattern and may eventually become atrophic.2,6 All body surfaces are at risk, but erythema ab igne classically involves the legs, lower back, and/or abdomen. Lesions typically are asymptomatic; however, burning and pruritus can be present.2,6 Bullous erythema ab igne, though rare, has been reported,7 suggesting a potential transition from erythema ab igne to burns.6

Biopsy is not recommended for diagnosis; however, the histopathologic changes of erythema ab igne include hyperkeratosis, interface dermatitis, epidermal atrophy with apoptotic keratinocytes, and melanin incontinence. Although this condition typically is benign, histologic findings could resemble actinic keratosis, suggesting that chronic changes induced by infrared thermal radiation may lead to squamous cell carcinoma or rarely Merkel cell carcinoma. The latency for developing carcinoma appears to extend 30 years, with a 30% tendency for recurrence or metastasis. Given the possibility of an increase in erythema ab igne in the pediatric population in the upcoming years, as displayed by our patient, and increasing laptop and electronic use in children and adolescents, it is important to be aware of this skin condition and the potential complications of it going undiagnosed.2,6

 

 

No specific therapy for erythema ab igne exists. Treatment is centered on eliminating exposure to the heat source. With appropriate removal, the reticulated hyperpigmented lesions will resolve, sometimes taking several months.

Differential diagnosis includes livedo reticularis, livedoid vasculopathy, and cutis marmorata. The reticulated purpuric lesions of livedo reticularis involving the extremities often mimic erythema ab igne's cutaneous morphology; however, livedo reticularis frequently is associated with conditions such as drug reactions, infections, thrombosis, and vasculitides,2 as opposed to erythema ab igne, which frequently is associated with conditions causing pain or decreased body temperature, thus necessitating use of heating devices, as seen in our patient. Livedoid vasculopathy is characterized by purpuric macules involving the lower legs and feet that progress to recurrent leg ulcers. Our patient's asymptomatic lesions and absence of ulcers excluded this diagnosis.8 Lastly, cutis marmorata, a congenital condition, is characterized by blue-violet vascular networks that often display ulceration and atrophy of the involved skin as well as hypertrophy or atrophy of the involved limb9; these clinical findings were not present in our patient and this diagnosis would not explain the relationship between the cutaneous lesions and heat exposure. 

References
  1. Nilic M, Adams BB. Erythema ab igne induced by a laptop computer. J Am Acad Dermatol. 2004;50:973-974.
  2. Riahi RR, Cohen PR, Robinson FW, et al. Erythema ab igne mimicking livedo reticularis. Int J Dermatol. 2010;49:1314-1317.
  3. Lin SJ, Hsu CJ, Chiu HC. Erythema ab igne caused by frequent hot bathing. Acta Derm Venereol. 2002;82:478-479.
  4. Meffert JJ, Davis BM. Furniture-induced erythema ab igne. J Am Acad Dermatol. 1996;34:516-517.
  5. Kligman LH, Kligman AM. Reflections on heat. Br J Dermatol. 1984;110:369-375.
  6. Arnold AW, Itin PH. Laptop computer−induced erythema ab igne in a child and review of the literature [published online October 4, 2010]. Pediatrics. 2010;126:e1227-e1230.
  7. Kokturk A, Kaya TI, Baz K, et al. Bullous erythema ab igne. Dermatol Online J. 2003;9:18.
  8. Khenifer S, Thomas L, Balme B, et al. Livedoid vasculopathy: thrombotic or inflammatory disease? Clin Exp Dermatol. 2009;35:693-698.  
  9. Pernet C, Guillot B, Bigorre M, et al. Focal and atrophic cutis marmorata telangiectatica congenital. J Am Acad Dermatol. 2013;69:e268-e269.
References
  1. Nilic M, Adams BB. Erythema ab igne induced by a laptop computer. J Am Acad Dermatol. 2004;50:973-974.
  2. Riahi RR, Cohen PR, Robinson FW, et al. Erythema ab igne mimicking livedo reticularis. Int J Dermatol. 2010;49:1314-1317.
  3. Lin SJ, Hsu CJ, Chiu HC. Erythema ab igne caused by frequent hot bathing. Acta Derm Venereol. 2002;82:478-479.
  4. Meffert JJ, Davis BM. Furniture-induced erythema ab igne. J Am Acad Dermatol. 1996;34:516-517.
  5. Kligman LH, Kligman AM. Reflections on heat. Br J Dermatol. 1984;110:369-375.
  6. Arnold AW, Itin PH. Laptop computer−induced erythema ab igne in a child and review of the literature [published online October 4, 2010]. Pediatrics. 2010;126:e1227-e1230.
  7. Kokturk A, Kaya TI, Baz K, et al. Bullous erythema ab igne. Dermatol Online J. 2003;9:18.
  8. Khenifer S, Thomas L, Balme B, et al. Livedoid vasculopathy: thrombotic or inflammatory disease? Clin Exp Dermatol. 2009;35:693-698.  
  9. Pernet C, Guillot B, Bigorre M, et al. Focal and atrophic cutis marmorata telangiectatica congenital. J Am Acad Dermatol. 2013;69:e268-e269.
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A 13-year-old otherwise healthy adolescent girl presented to the pediatric dermatology clinic for evaluation of a rash on the legs. The patient noticed the rash 1 month prior to presentation. The rash initially involved the left shin and gradually spread to involve the shins bilaterally. The rash was asymptomatic with no pain, pruritus, or muscular asymmetry of the legs. She denied recent fevers, chills, or travel. The patient reported using a space heater daily that was directed at the legs, approximately 0.5 m away. Physical examination revealed a well-nourished adolescent girl in no acute distress with reticular hyperpigmentation of the lower extremities located on the left anterior shin and knee, with mild involvement of the right shin. The reticulated hyperpigmented areas were arranged in a rectangular distribution. Lower extremity musculoskeletal examination was symmetric.  

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Patch of Hair Loss on the Scalp

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Patch of Hair Loss on the Scalp

The Diagnosis: Temporal Triangular Alopecia

Temporal triangular alopecia (TTA), also known as congenital triangular alopecia, was first described in the early 1900s.1 It presents clinically as a triangular-shaped area of nonscarring alopecia either unilaterally or bilaterally. Limited clinical data suggest that most unilateral cases are on the left frontotemporal region of the scalp. In bilateral cases, there may be asymmetry in size of the area involved.2 Dermatoscopically, TTA is characterized by decreased terminal hair follicle density as well as the presence of vellus hairs with an absence of inflammation.3 The majority of TTA is noted between birth and 6 years of life with the areas staying stable thereafter. Large areas of TTA may suggest cerebello-trigeminal-dermal dysplasia (Gomez-Lopez-Hernandez syndrome), a rare neurocutaneous syndrome characterized by rhombencephalosynapsis, trigeminal anesthesia, and parietooccipital alopecia (Online Mendelian Inheritance in Man 601853).4 Although TTA is largely idiopathic, it has been suggested that the trait may be paradominant, whereby a postzygotic loss of the wild-type allele in a heterozygotic state causes triangular alopecia and reflects hamartomatous mosaicism.5 It also is an important mimicker of alopecia areata. Correct identification prevents unnecessary treatment to the areas of the scalp. Hair restoration surgery has been reported as a tool to treat this disorder.6

References
  1. Tosti A. Congenital triangular alopecia. report of fourteen cases. J Am Acad Dermatol. 1987;16:991-993.
  2. Armstrong DK, Burrows D. Congenital triangular alopecia. Pediatr Dermatol. 1996;13:394-396.
  3. Iorizzo M, Pazzaglia M, Starace M, et al. Videodermoscopy: a useful tool for diagnosing congenital triangular alopecia. Pediatr Dermatol. 2008;25:652-654.
  4. Assoly P, Happle R. A hairy paradox: congenital triangular alopecia with a central hair tuft. Dermatology. 2010;221:107-109.
  5. Happle R. Congenital triangular alopecia may be categorized as a paradominant trait. Eur J Dermatol. 2003;13:346-347.
  6. Wu WY, Otberg N, Kang H, et al. Successful treatment of temporal triangular alopecia by hair restoration surgery using follicular unit transplantation. Dermatol Surg. 2009;35:1307-1310.
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Dr. Castelo-Soccio is from the Department of Pediatrics, Children’s Hospital of Philadelphia, Section of Dermatology, Pennsylvania. Ms. Yang is from Case Western Reserve University, Cleveland, Ohio.

The authors report no conflict of interest.

Correspondence: Leslie Castelo-Soccio, MD, PhD, Children’s Hospital of Philadelphia, 3550 Market St, 2nd Floor Dermatology, Philadelphia, PA 19104 (castelosocciol@email.chop.edu).

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Correspondence: Leslie Castelo-Soccio, MD, PhD, Children’s Hospital of Philadelphia, 3550 Market St, 2nd Floor Dermatology, Philadelphia, PA 19104 (castelosocciol@email.chop.edu).

Author and Disclosure Information

Dr. Castelo-Soccio is from the Department of Pediatrics, Children’s Hospital of Philadelphia, Section of Dermatology, Pennsylvania. Ms. Yang is from Case Western Reserve University, Cleveland, Ohio.

The authors report no conflict of interest.

Correspondence: Leslie Castelo-Soccio, MD, PhD, Children’s Hospital of Philadelphia, 3550 Market St, 2nd Floor Dermatology, Philadelphia, PA 19104 (castelosocciol@email.chop.edu).

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The Diagnosis: Temporal Triangular Alopecia

Temporal triangular alopecia (TTA), also known as congenital triangular alopecia, was first described in the early 1900s.1 It presents clinically as a triangular-shaped area of nonscarring alopecia either unilaterally or bilaterally. Limited clinical data suggest that most unilateral cases are on the left frontotemporal region of the scalp. In bilateral cases, there may be asymmetry in size of the area involved.2 Dermatoscopically, TTA is characterized by decreased terminal hair follicle density as well as the presence of vellus hairs with an absence of inflammation.3 The majority of TTA is noted between birth and 6 years of life with the areas staying stable thereafter. Large areas of TTA may suggest cerebello-trigeminal-dermal dysplasia (Gomez-Lopez-Hernandez syndrome), a rare neurocutaneous syndrome characterized by rhombencephalosynapsis, trigeminal anesthesia, and parietooccipital alopecia (Online Mendelian Inheritance in Man 601853).4 Although TTA is largely idiopathic, it has been suggested that the trait may be paradominant, whereby a postzygotic loss of the wild-type allele in a heterozygotic state causes triangular alopecia and reflects hamartomatous mosaicism.5 It also is an important mimicker of alopecia areata. Correct identification prevents unnecessary treatment to the areas of the scalp. Hair restoration surgery has been reported as a tool to treat this disorder.6

The Diagnosis: Temporal Triangular Alopecia

Temporal triangular alopecia (TTA), also known as congenital triangular alopecia, was first described in the early 1900s.1 It presents clinically as a triangular-shaped area of nonscarring alopecia either unilaterally or bilaterally. Limited clinical data suggest that most unilateral cases are on the left frontotemporal region of the scalp. In bilateral cases, there may be asymmetry in size of the area involved.2 Dermatoscopically, TTA is characterized by decreased terminal hair follicle density as well as the presence of vellus hairs with an absence of inflammation.3 The majority of TTA is noted between birth and 6 years of life with the areas staying stable thereafter. Large areas of TTA may suggest cerebello-trigeminal-dermal dysplasia (Gomez-Lopez-Hernandez syndrome), a rare neurocutaneous syndrome characterized by rhombencephalosynapsis, trigeminal anesthesia, and parietooccipital alopecia (Online Mendelian Inheritance in Man 601853).4 Although TTA is largely idiopathic, it has been suggested that the trait may be paradominant, whereby a postzygotic loss of the wild-type allele in a heterozygotic state causes triangular alopecia and reflects hamartomatous mosaicism.5 It also is an important mimicker of alopecia areata. Correct identification prevents unnecessary treatment to the areas of the scalp. Hair restoration surgery has been reported as a tool to treat this disorder.6

References
  1. Tosti A. Congenital triangular alopecia. report of fourteen cases. J Am Acad Dermatol. 1987;16:991-993.
  2. Armstrong DK, Burrows D. Congenital triangular alopecia. Pediatr Dermatol. 1996;13:394-396.
  3. Iorizzo M, Pazzaglia M, Starace M, et al. Videodermoscopy: a useful tool for diagnosing congenital triangular alopecia. Pediatr Dermatol. 2008;25:652-654.
  4. Assoly P, Happle R. A hairy paradox: congenital triangular alopecia with a central hair tuft. Dermatology. 2010;221:107-109.
  5. Happle R. Congenital triangular alopecia may be categorized as a paradominant trait. Eur J Dermatol. 2003;13:346-347.
  6. Wu WY, Otberg N, Kang H, et al. Successful treatment of temporal triangular alopecia by hair restoration surgery using follicular unit transplantation. Dermatol Surg. 2009;35:1307-1310.
References
  1. Tosti A. Congenital triangular alopecia. report of fourteen cases. J Am Acad Dermatol. 1987;16:991-993.
  2. Armstrong DK, Burrows D. Congenital triangular alopecia. Pediatr Dermatol. 1996;13:394-396.
  3. Iorizzo M, Pazzaglia M, Starace M, et al. Videodermoscopy: a useful tool for diagnosing congenital triangular alopecia. Pediatr Dermatol. 2008;25:652-654.
  4. Assoly P, Happle R. A hairy paradox: congenital triangular alopecia with a central hair tuft. Dermatology. 2010;221:107-109.
  5. Happle R. Congenital triangular alopecia may be categorized as a paradominant trait. Eur J Dermatol. 2003;13:346-347.
  6. Wu WY, Otberg N, Kang H, et al. Successful treatment of temporal triangular alopecia by hair restoration surgery using follicular unit transplantation. Dermatol Surg. 2009;35:1307-1310.
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An 11-year-old girl presented for evaluation of a patch of hair loss on the right parietal scalp that had been present and stable for 2.5 years. Physical examination revealed a unilateral area of hair loss that was triangular in shape on the right parietal/temporal region, measuring 2.1×2.2 cm. Dermatoscope examination showed vellus hairs throughout. A hair-pull test was negative and the patient confirmed that the area had never been completely smooth. There were no associated symptoms and no family history of autoimmune disease or hair loss. Prior to presentation, the patient underwent a trial of intralesional steroids and topical steroids to the area without effect.

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Recurrent Stevens-Johnson Syndrome Secondary to Mycoplasma pneumoniae Infection

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