An observation turned into a clinical hypothesis when researchers noted that there was a high frequency of male pattern hair loss among patients admitted for COVID-19. 71% of men admitted for COVID-19 in two Spanish hospitals were observed to have clinically significant androgenetic alopecia (AGA) as determined by the Hamilton-Norwood Scale of AGA. A limitation of this study is that it only involved 41 patients and was completely observational, without outcome measures or a control group.

A follow up study from the same group was published on Aug 20th titled, “Androgenetic alopecia present in the majority of patients hospitalized with COVID-19: The “Gabrin sign””. The authors evaluated 175 individuals hospitalized with COVID-19 in Madrid, Spain and found that 67% of the overall patients presented with AGA (79% in men and 42% in women). These rates were significantly higher than the rate of AGA in age-matched men (31-53%) and women (38%) in a similar population. The authors hypothesized that hyper-androgenism, which can lead to AGA, may lead to a more severe course of COVID-19 infection.

The first author on this study, Dr. Carlos Wambier from Brown University Department of Dermatology told The Telegraph. “We think androgens or male hormones are definitely the gateway for the virus to enter our cells.” The authors suggest that anti-androgen treatments may be useful for prevention and/or treatment of severe COVID-19 infections. In fact, there are several clinical trials using anti-androgens, such as spironolactone, currently underway as preventative or treatment options for COVID-19. The authors propose the “Gabrin sign,” in memory of Dr. Frank Gabrin, the first American physician to die from COVID-19, as a visual sign of androgenetic alopecia being a risk factor for severe COVID-19 infection.

Observational studies like these are good for idea generation. However, there are confounding factors in this study which need to be taken into account before forming conclusions. For one, this study was small, didn’t have outcome measures of the hospitalized patients, and didn’t have a control group of age-matched patients who did not have AGA. Also, there may have been confounding factors such as obersity, Type 2 diabetes mellitus, or coronary artery disease that were more prevelant in patients that have AGA. Thereby, the association of COVID-19 severity with AGA may be fully explained by these known COVID-19 risk factors, rather than their AGA status. Nonetheless, observational studies such as the ones reviewed above are valuable and may serve as a foundation of more formalized future studies of risk factors for COVID-19.