Risk of vitiligo in patients with SARS-CoV-2 vaccination or infection: a nationwide cohort study.

As recent sporadic case reports of newly developed vitiligo after SARS-CoV-2 infection or vaccination have been -published, a convincing large-scale study addressing this association is warranted. To investigate the association between SARS-CoV-2 infection or vaccination and vitiligo using the Korean National Health Insurance Service database. SARS-CoV-2-positive patients and those vaccinated against SARS-CoV-2 were recruited. In studies 1 and 2, control groups were selected based on 1:1 propensity score matching with vaccinated and SARS-CoV-2-positive patients, respectively. The occurrence of vitiligo was the main outcome. Each individual was monitored for six months. The hazard ratio (HR) for vitiligo was calculated using the Cox proportional hazards model. In study 1, the incidence of vitiligo in the vaccination group was 2.22-fold higher than that in the non-vaccination group (adjusted HR [aHR]: 2.22; 95% confidence interval [CI]: 1.54-3.19). Rheumatoid arthritis was a risk factor for vitiligo (aHR: 1.99; 95% CI: 1.12-3.54). Conversely, two factors associated with decreased incidence of vitiligo were male sex (aHR: 0.58; 95% CI: 0.40-0.82) and rural residency (aHR: 0.68; 95% CI: 0.49-0.96). In study 2, the incidence of newly-diagnosed vitiligo was not significantly different between SARS-CoV-2-positive patients and uninfected controls (aHR: 0.95; 95% CI: 0.51-1.78). SARS-CoV-2 vaccination may increase the risk of developing vitiligo in South Korea, although additional studies in other countries or with extended periods are needed. Clinicians should be aware of the impact of SARS-CoV-2 infection and vaccination on autoimmune skin diseases, including vitiligo.

Risk of Alopecia Areata After COVID-19.

This cohort study examines the incidence, prevalence, and risk of alopecia areata after COVID-19.

Facial tinea incognito: a clinical, dermoscopic and mycological study of 38 cases.

BACKGROUND: Tinea incognito (TI) is a dermatophytic infection of the skin that is modified by steroid use. As a result, it shows atypical clinical presentations that can lead to misdiagnosis. TI occurring on the face is most frequently misdiagnosed as cutaneous fungal infection, however, very limited information is available on facial TI. OBJECTIVES: This study aimed to characterize the clinical, dermoscopic and mycological features of facial TI. MATERIALS & METHODS: We retrospectively evaluated 38 patients with mycologically proven facial TI at a single institution in Korea between July, 2014 and July, 2021. RESULTS: The patients had a mean age of 59.6 ± 20.4 years and showed a slight female predominance (male-to-female ratio of 1:1.38). The most common clinical presentation was an eczema-like pattern (47.4%), followed by rosacea-like (15.8%), psoriasis-like (10.5%), lupus erythematosus-like (10.5%), cellulitis-like (7.9%), and folliculitis-like (7.9%) patterns. The mean duration from disease onset to diagnostic confirmation was 3.4 months. Overall, 78.9% of the patients had accompanying chronic systemic diseases, and 57.9% had concurrent tinea infections at other skin sites, mainly the feet and toenails. On dermoscopy, scales and dilated vascular patterns (arborizing vessels and telangiectasia) were commonly observed on glabrous skin, with follicular patterns, such as black dots, broken hairs, and empty follicles. The characteristic trichoscopic features were comma, corkscrew, Morse code-like, and translucent hairs. CONCLUSION: The clinical characteristics and distinct dermoscopic features described in this article may aid in the differential diagnosis of facial TI while reducing diagnostic delays and unnecessary treatments.

SIRT1 downregulation provokes immune-inflammatory responses in hair follicle outer root sheath cells and may contribute to development of alopecia areata.

BACKGROUND: Silent information regulator 1 (SIRT1), a type III histone deacetylase, is involved in various cutaneous and systemic autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis, and psoriasis. However, little is known about the role of SIRT1 in the development of alopecia areata (AA). OBJECTIVES: This study investigated whether SIRT1 regulates the hair follicle immune system and is involved in AA pathogenesis. METHODS: SIRT1 expression in human scalp tissue was analyzed using immunohistochemical staining, qPCR, and western blotting. The regulatory effect of SIRT1 was evaluated after stimulation with the double-stranded RNA mimic polyinosinic:polycytidylic acid (poly I:C) in hair follicle outer root sheath (ORS) cells and C3H/HeJ mice. RESULTS: SIRT1 expression was significantly reduced in the AA scalp compared to the normal scalp. SIRT1 inhibition upregulated MHC class I polypeptide-related sequence A and UL16 binding protein 3 in hair follicle ORS cells. SIRT1 inhibition also promoted the production of Th1 cytokines (IFN-γ and TNF-α), IFN-inducible chemokines (CXCL9 and CXCL10), and T cell migration in ORS cells. Conversely, SIRT1 activation suppressed the autoreactive inflammatory responses. The counteractive effect of the immune response by SIRT1 was mediated through the deacetylation of NF-κB and phosphorylation of STAT3. CONCLUSION: SIRT1 downregulation induces immune-inflammatory responses in hair follicle ORS cells and may contribute to AA development.