P103 Clinical clues for frontal fibrosing alopecia: a case series describing prominent, depressed forehead veins

• Published in: British journal of dermatology (1951) Vol. 191; no. Supplement_1; pp. i64 - i65
• Main Authors: Bala, Laksha, Tsang, Christie, Agarwal, Vani, Elshimy, Noha
• Format: Journal Article
• Language: English
• Published: 28-06-2024
• ISSN: 0007-0963; 1365-2133
• DOI: 10.1093/bjd/ljae090.130

Abstract Frontal fibrosing alopecia (FFA) is a lymphocytic, scarring alopecia characterized by progressive frontotemporal hairline recession, most frequently in postmenopausal women. It is considered a subtype of lichen planopilaris, given the shared histopathological findings of perifollicular lymphocytic infiltration and fibrosis. FFA is a recently reported entity and one of the most common causes of cicatricial alopecia worldwide. Its pathogenesis is not well understood, with immune dysregulation, and hormonal, genetic and environmental factors all postulated to play a role. Clinical features include the characteristic bandlike frontotemporal scarring hair loss, perifollicular hyperkeratosis and erythema (active inflammation), the ‘lonely hair’ sign (terminal hairs within a band of alopecia), loss of eyelashes and eyebrows, and facial lesions (most commonly papules). Visible vascular abnormalities with prominent and/or depressed forehead veins are a much less recognized entity, with only three publications to date reporting this finding (Heymann WR. Vascular abnormalities in FFA, artificial intelligence and Winston Churchill. Dermatol World Insights Inquiries 2023; 5: Aug 23). We present a case series of 15 patients with FFA presenting to our tertiary centre hair clinic, who displayed prominent and/or depressed forehead veins. To the unsuspecting clinician, visibility of frontal veins may mistakenly be attributed to steroid atrophy (in patients receiving corticosteroid treatment). Instead, it has been hypothesized that FFA itself may be responsible. The pathogenesis of FFA involves concentric perifollicular fibrosis, thought to culminate in fibrous tract formation and progressive vertical contraction with dermal constriction. This may be more marked around vasculature, resulting in the characteristic appearance of frontal veins in FFA. Steroids may exacerbate this process, but are not thought to be pathogenic (Vañó-Galván S, Rodrigues-Barata AR, Urech M, Jiménez-Gómez N et al. Depression of the frontal veins: a new clinical sign of frontal fibrosing alopecia. J Am Acad Dermatol 2015; 72: 1087–8). Therapeutic approaches for FFA largely focus on suppression of inflammation driving perifollicular fibrosis. Common therapies include topical corticosteroids or calcineurin inhibitors, corticosteroid injections, and systemic therapies such as oral tetracyclines or hydroxychloroquine. Prominent vasculature in FFA can be challenging to treat, with one study supporting the use of Nd:YAG laser as a potentially safe and effective treatment. The reason for the presence of prominent, depressed forehead veins in FFA and, indeed, the preferential targeting of follicles along the frontal hairline in this disease remains unknown and merits further research. Nevertheless, this clinical sign may serve as a helpful diagnostic tool for the perceptive dermatologist.