In this communication, we present arguments for androgen sensitivity as a likely determinant of COVID‐19 disease severity. The androgen sensitivity model explains why males are more likely to develop severe symptoms while children are ostensibly resistant to infection. Further, the model explains the difference in COVID‐19 mortality rates among different ethnicities. Androgen sensitivity is determined by genetic variants of the androgen receptor. The androgen receptor regulates transcription of the transmembrane protease, serine 2 (TMPRSS2), which is required for SARS‐CoV‐2 infectivity. TMPRSS2 primes the Spike protein of the virus, which has two consequences: diminishing viral recognition by neutralizing antibodies and activating SARS‐CoV‐2 for virus‐cell fusion. Genetic variants that have been associated with androgenetic alopecia, prostate cancer, benign prostatic hyperplasia and polycystic ovary syndrome could be associated with host susceptibility. In addition to theoretical epidemiological and molecular mechanisms, there are reports of high rates of androgenetic alopecia of from hospitalized COVID‐19 patients due to severe symptoms. Androgen sensitivity is a likely determinant of COVID‐19 disease severity. We believe that the evidence presented in this communication warrants the initiation of trials using anti‐androgen agents.
Background: The frequency of different types of alopecia is not clearly reported in recent studies. Objective: To analyze the frequency of the types of alopecia in patients consulting at specialist hair clinics (SHC) and to assess for global variations. Methods: Multicenter retrospective study including data from patients evaluated at referral SHC in Europe, America, Africa and Australia. Results: A total of 2,835 patients (72.7% females and 27.3% males) with 3,133 diagnoses of alopecia were included (73% were non-cicatricial and 27% were cicatricial alopecias). In all, 57 different types of alopecia were characterized. The most frequent type was androgenetic alopecia (AGA) (37.7%), followed by alopecia areata (AA) (18.2%), telogen effluvium (TE) (11.3%), frontal fibrosing alopecia (FFA) (10.8%), lichen planopilaris (LPP) (7.6%), folliculitis decalvans (FD) (2.8%), discoid lupus (1.9%) and fibrosing alopecia in a pattern distribution (FAPD) (1.8%). There was a male predominance in patients with acne keloidalis nuchae, dissecting cellulitis and FD, and female predominance in traction alopecia, central centrifugal cicatricial alopecia, FFA, TE, FAPD and LPP. Conclusion: AGA followed by AA and TE were the most frequent cause of non-cicatricial alopecia, while FFA was the most frequent cause of cicatricial alopecia in all studied geographical areas.