Erosive pustular dermatosis of the scalp in the <scp>COVID</scp>‐19 era

Erosive pustular dermatosis of the scalp (EPDS) is a rare inflammatory disorder which occurs mainly in elderly patients, often associated with previous trauma to the scalp.1 It usually resolves with cicatricial alopecia. Herein, we describe a case of EPDS after herpes zoster infection following COVID-19 vaccination. An 88-year-old healthy man presented with a history of erosive, pustular, and crusted lesions on his scalp. The skin lesions started 6 months before, shortly after the first episode of herpes zoster infection in the same region, and slowly progressed in the parietal scalp region. The herpes zoster infection started 3 weeks after the second dose of the BNT162b1 mRNA COVID-19 vaccine (Pfizer–BioNTech). The patient had previously been treated with oral antibiotics and sun protective cream without improvement. Dermatologic examination showed multiple pustules, erosions, scales, and crusts on the occipito-temporal scalp associated with areas of scarring alopecia (Figure 1). There were no other skin or mucosal lesions. Trichoscopic examination revealed follicular keratotic plugging, milky red areas, white patches, hair shaft disorder, and absence of follicular opening (Figure 2A,B). Routine laboratory examinations were within normal limits. Bacterial and fungal cultures were negative. A skin specimen biopsy showed epidermal crust, focal ulceration, broad areas of erosion associated with perivascular and perifollicular inflammatory infiltrate consisting mainly of neutrophils (Figure 2C,D). Clinical and histopathological findings were evaluated as compatible with the diagnosis of EPDS. Clobetasol propionate cream treatment was started twice daily. Within 4 weeks, the lesions resolved with patches of cicatricial alopecia. The treatment was planned to be continued 2 days a week for 3 months and the patient had no recurrence. Erosive pustular dermatosis of the scalp is an uncommon, inflammatory dermatosis which shows nonmicrobial pustules, crusting and erosions.1 The disease is characterized by a chronic and progressive course without spontaneous remission. It may involve large scalp regions and lead to scarring alopecia.1 It was first described in 1979 by Burton and Pye.2 It often affects the scalp of the elderly, mostly in women but may occasionally occur in younger individuals or even children and may affect other skin sites including the face and the extremities.3 EPDS can be clinically confused with bacterial or fungal infections, pemphigus vulgaris, and squamous cell carcinoma. A few reports have described the trichoscopic features of the EPDS. A trophic skin, lack of follicular ostia, and dilated dermal vessels are usually observed in the chronic phase. While perifollicular pustules, perifollicular serous exudate, black crusts, and hyperkeratosis are the main trichoscopic features in the active phase.4 Histopathology is not specific to the disease.1 It varies depending on the stage: early stages, revealed laminated orthokeratosis, psoriasiform hyperplasia, a slight mixed inflammatory infiltrate in the dermis, and normal hair follicular density. Late-stages showed orthokeratosis, atrophic epidermis, dermal fibrosis, and a decrease or lack of hair follicles and sebaceous glands.4 Therefore, the diagnosis of EPDS requires close clinicopathologic correlation. Criteria for the EPDS diagnosis were as follows: a clinical association of pustules, erosions, scales, and crusts on the scalp, negative microbiologic studies, and histopathologic exclusion of other inflammatory skin disorders. The pathogenesis of EPDS is not well known. It is frequently associated with local physical injuries, accidental mechanical trauma, on atrophic and sun-damaged skin. It was suggested that the tissue damage caused by these factors, triggers immune dysregulation or immunologic response with the production of an inflammatory reaction. The fact that EPDS improves with anti-inflammatory agents supports this hypothesis. In our case, the herpes zoster may lead to a local immunologic dysregulation and abnormal neutrophil chemotaxis or chemoattractants and cytokine production against epidermal or follicular antigens. Thus, we consider that the tissue damage caused by herpes zoster might have induced subsequent EPDS. Topical and systemic corticosteroids, topical tacrolimus, photodynamic therapies, systemic acitretin were reported as successful treatments of EPDS.5 To the best of our knowledge, our case is the fifth reported case of EPDS after herpes zoster.6, 7 Interestingly, our patient developed herpes zoster infection 3 weeks following the second dose of the Pfizer–BioNTech COVID-19 vaccine. The association between this COVID-19 mRNA-based vaccine and the first reactivation of the latent zoster infection is a rare cutaneous finding reported in the literature.8 In conclusion, the early identification and management of EPDS is important in order to prevent expansion of scarring alopecia. N.BS., A.A., and L.D. performed the research and contributed essential reagents or tools. N.BS., A.A., L.D., B.S., and M.D. analyzed the data. N.BS. and L.D. wrote the paper. All authors have read and approved the final manuscript. None. Data sharing is not applicable to this article as no new data were created or analyzed in this study.