Prospective Double-blind, Placebo Controlled Study to Assess the Efficacy of Intralesional Corticoid on the Treatment of Frontal Fibrosing Alopecia

Brief Summary

Detailed Description

Frontal fibrosing alopecia (FFA) is a primary lymphocytic cicatricial alopecia, that was first described in postmenopausal women, by Kossard in 1994. Since then, FFA has also been reported in premenopausal women and rarely in men. The exact cause of FFA is unknown. One possible reason can be the disturbed immune response to some component of the scalp hair follicles, however, whether or not the hair loss is caused by hormonal fluctuations is under question. Some authors, consider that FFA is a variant of liquen planopilaris (LPP). Whether FFA is truly an LPP variant or is a distinct entity with shared clinical features remains to be determined. FFA was also diagnosed in family members (mother and daughter) suggesting a possible genetic contribution. Clinically, it is characterized by progressive frontal and temporoparietal recession of the hairline due to inflammatory destruction of hair follicles. Hair loss occurs in a band-like distribution and the depth of recession can be from 0,5-8 cm. Often, a small number of isolated hairs are spared within the band of alopecia. Loss of eyebrows (partial or complete) is a finding in FFA and in some cases, can precede the hairline recession. The affected skin is atrophic, shiny, and often lighter than the chronically sun-exposed forehead skin. The diagnosis of FFA is usually made on the basis of clinical findings, and laboratory tests are rarely required. Dermoscopy, a noninvasive tool can help for the diagnosis of FFA; The dermoscopic features of FFA are: Absence of follicular openings, perifollicular scale, and a feeble perifollicular erythema. Perifollicular erythema at the receding hairline may be a sign of active disease. Since the first description of FFA, many reports have been published, and the number of new cases of FFA appears to be increasing. Currently, there are no evidence-based studies to guide treatment and there is no clearly defined line of treatment for the condition. Therefore treatment options vary among clinicians. The aim of this study is to find if intralesional triamcinolone acetonide (compared to area treated with placebo) may help to halt or slow down the progression of this disease. The patients are divided into two groups (A and B): 1. Group A: right half-head (active border of the disease): treatment with intralesional triamcinolone acetonide left half-head (active border of the disease): placebo (saline solution) 2. Group B: right half-head (active border of the disease):placebo (saline solution) left half-head (active border of the disease): intralesional triamcinolone acetonide The aim of this study is to find if intralesional triamcinolone may help to halt or slow down the progres- sion of this disease. All patients provide written informed consent before participating in the study, which is performed according to the Declaration of Helsinki.

Primary Outcomes

Secondary Outcomes

• Global photographs of the scalp(6 months)