Efficacy and Safety of Tumour Necrosis Factor-α Antagonists for Folliculitis Decalvans: A Retrospective Case-series Pilot Study.

Folliculitis decalvans is a chronic inflammatory skin disease leading to scarring alopecia. Management of this disabling disease is difficult and no treatment is currently approved. Current knowledge regarding the pathogenesis of folliculitis decalvans suggests the benefit of using anti-tumour necrosis factor-α. This pilot study aimed to evaluate the clinical efficacy of anti-tumour necrosis factor-α for management of folliculitis decalvans. A single-centre retrospective pilot study included patients with refractory folliculitis decalvans treated by tumour necrosis factor-α inhibitors. An Investigator's Global Assessment (IGA) score was designed and validated to assess the efficacy of the therapy. Response to treatment was considered good to excellent when an IGA ≤ 2 was obtained at month 12. Eleven patients were included, with a mean time from diagnosis of folliculitis decalvans to the introduction of infliximab (n = 9) or adalimumab (n = 2) of 8.55 ± 1.26 years. Nine patients had failed on at least 2 lines of systemic therapies before starting anti-tumour necrosis factor-α. The median IGA score at baseline was 3. At the end of follow-up, 5 patients were considered responders. Overall, the safety profile of anti-tumour necrosis factor-α was good. The results suggest that the clinical benefit of anti-tumour necrosis factor-α is obtained after at least 6 months of treatment. However, further prospective studies are needed to confirm these results.

Folliculitis decalvans and dystrophic epidermolysis bullosa: a significant association.

This work reports 30 cases of folliculitis decalvans (FD) in patients with dystrophic epidermolysis bullosa (DEB) among a cohort of 125 DEB patients seen between 2010 and 2021 in 2 French expert centers for the management of inherited epidermolysis bullosa. Such an association between two rare diseases cannot be fortuitous and implies a physiopathological link that we discuss in this paper. This association is a new significant fact to add to the reflexion on FD causes, suggesting that skin abnormality of DEB could act as a factor of a specific skin barrier alteration which could favor FD. Scarring alopecia with tufted folliculitis and pustules on inflamed skin at the vertex of a woman with dominant dystrophic epidermolysis bullosa.

Folliculitis decalvans is characterized by a persistent, abnormal subepidermal microbiota.

Folliculitis decalvans (FD) is a chronic inflammatory disease of unknown aetiology. Although Staphylococcus aureus, frequently found on lesional skin, is thought to play a causal role, the importance of its involvement remains controversial. To examine the role of S aureus, we compared superficial and subepidermal microbiota in 20 FD patients who had S aureus on lesional skin and in 20 healthy controls using culture techniques and genomic identification, before and after an anti-staphylococcal treatment; we also screened for S aureus virulence factors. When present on lesional skin, S aureus colonized non-lesional and subepidermal skin in 80% of cases. These data imply a break in the epidermal barrier integrity and that an abnormal non-lesional skin microbiota persists in FD. S aureus had no superantigenic toxin in 31% of cases and no toxin specificity. Clinical improvement obtained in most cases upon treatment was associated with the disappearance of S aureus in all studied areas, with an incomplete restoration of normal microbiota and a significant increase in negative bacterial samples. This persistent unbalanced, subepidermal microbiota may act as a reservoir of abnormal flora and explain the chronicity of FD, suggesting new avenues of research to restore normal microbiota.

Epidermal psoriasiform hyperplasia, an unrecognized sign of folliculitis decalvans: A histological study of 26 patients.

BACKGROUND: Follicular hyperkeratosis along with hyperplasia of the follicular and interfollicular epithelia are major histopathological characteristics of hidradenitis suppurativa (HS). The presence of an occasional thickening of lesional skin in some folliculitis decalvans (FD) patients and histological similarities between FD and HS led us to look for epidermal hyperplasia and follicular hyperkeratosis in FD patients. PATIENTS AND METHOD: We performed a retrospective histological analysis of 26 patients with FD. OBJECTIVE: We sought to find out whether the presence of hyperplasia of the interfollicular epidermis and of the follicular epithelia could be verified in FD, with reference to the work of von Laffert et al. concerning HS. RESULTS: The main quantitative and qualitative data were: follicular hyperkeratosis (77%), hyperplasia of the interfollicular epidermis (92%) with a psoriasiform aspect (88%), atrophy of the follicular epithelia (85%), plasma cells in infiltrate (92%) in large quantities (42%), follicular microcysts (60%), atrophy of the sebaceous glands (85%) and polytrichia (54%). CONCLUSION: Epidermal hyperplasia, sometimes psoriasiform and follicular microcysts, are significant histological signs of FD, which have been ignored until now although they seem very common.