LAUSR

Congenital triangular alopecia (CTA), also known as temporal triangular alopecia, is a nonscarring alopecia presenting at birth or early in life. It is thought to be acquired rather than congenital.1 It typically presents as a unilateral triangular alopecia patch in the frontotemporal area that remains unchanged. The pathogenesis is unknown but localized follicular miniaturization has been described. There is no gender predilection, and its incidence is around 0.11%.1,2 A 54yearold female presented with a 2year history of diffuse loss of hair density (balding) over the frontal scalp in association with telogen effluvium (Sinclair stage 6 hair shedding).3 Her past medical history included adultonset acne treated with spironolactone 200 mg/day for the last 5 years. On examination, in addition to Sinclair two female pattern hair loss (FPHL),4 she was noted to have an incidental patch of triangular alopecia on her right temple of 4 × 3 cm. (Figure 1a) Trichoscopy showed hair single hair follicular units and hair fibre miniaturization on the midfrontal scalp and within the triangular alopecia. No yellow dots or exclamation hairs were noted. On direct questioning, this triangular alopecia had been present since birth. The clinical diagnoses were FPHL and CTA. Alopecia areata (AA) was excluded based on clinical presentation and history. Treatment for FPHL was initiated via sublingual minoxidil 0.6 mg/day. The patient declined hair restoration surgery for CTA. At 3 months, patient reported a reduction in hair shedding and improvement of overall hair density including regrowth in her temporal alopecia patch (Figure 1b). On trichoscopy, terminal hairs were seen within the patch. The dose of sublingual minoxidil was further increased to 0.9 mg/day, as a dosedependent increase in terminal hair count and density has been reported in FPHL.5 At 18 months, additional regrowth of terminal hair in the CTA patch was observed (Figure 1c). The diagnosis of CTA can be made based on trichoscopy which shows normal skin without signs of inflammation or atrophy, normal follicular openings and vellus hairs. Differential diagnosis includes AA, trichotillomania, traction alopecia, tinea capitis and aplasia cutis. These typically show other features including yellow dots, exclamation hairs, inflammation and scaling, broken hairs or atrophic skin.6 Clinicians should recognize these clues on trichoscopy, as it is frequently mistreated as AA with intralesional steroid injections. The most common treatment for CTA is a follicular unit extraction (FUE) hair transplant. Surgical excision of the patch has also been described with long lasting improvement. Less invasive treatments including topical and intralesional steroids have been tried without improvement.2 Three case reports have been published suggesting rapid regrowth of terminal hair with the use of 3%– 5%