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The incidence of alopecia areata significantly increased after COVID-19, a nationwide study involving more than half a million South Koreans found.

In a propensity score-matched analysis, incidence of the autoimmune form of hair loss was 82% higher for individuals with versus those without a prior COVID infection (43.19 vs 23.61 per 10,000 person-years; adjusted HR 1.82, 95% CI 1.60-2.07), reported Jin Park, MD, PhD, of Jeonbuk National University Medical School in Jeonju, South Korea, and colleagues.

Higher incidence was seen in all groups older than 20 years, with a greater risk observed both in women and men, they detailed in a research letter.

The study also revealed an increased incidence of telogen effluvium -- rapid hair loss triggered by stress or other changes to the body -- among the cohort with COVID compared with the control group (adjusted HR 6.40, 95% CI 4.92-8.33).

"These findings support the possible role of COVID-19 in AA [alopecia areata] occurrence and exacerbation, although other environmental factors, such as psychological stress, may have also contributed to AA development during the pandemic," Park and co-authors added. " of AA following COVID-19 include antigenic molecular mimicry between SARS-CoV-2 and hair follicle autoantigens, cytokine shifting, and bystander activation."

Alopecia areata "occurs in susceptible individuals by environmental triggers, such as viruses, vaccinations, and psychological stress," the researchers said, adding that while documented new onset, exacerbation, and recurrence of alopecia areata after COVID have been increasing, evidence linking alopecia areata to COVID has been limited.

Danilo Del Campo, MD, a dermatologist with the Chicago Skin Clinic, described the study findings as "more confirmatory" than "surprising."

"Anything that can stimulate the immune system can trigger other problems, and alopecia areata, in particular, stems from a strong immune reaction," he told MedPage Today.

He likened the immune system to a web of "secret spies," constantly "on the hunt" for infiltrators. Sometimes it simply has the wrong target -- in this case hair stem cells instead of virus cells -- which is known as antigenic molecular mimicry.

Another explanation is that COVID infection leads to a "huge influx of cytokines," which has other downstream effects. Alternatively, it may be that hair stem cells are too close to infected cells or to "helper cells" trying to clean the infected cells, and are inadvertently targeted, known as bystander activation.

Shoshana Marmon, MD, PhD, of New York Medical College in New York City, told MedPage Today in an email that while the "plausible mechanisms" described by Park and his team are "theoretically sound, their specific roles in the context of COVID-19 and alopecia areata require further empirical validation through research and clinical studies."

For their propensity score-matched study, the authors used data from the Korea Disease Control and Prevention Agency-COVID-19-National Health Insurance Service cohort from October 2020 through September 2021. The cohort included 259,369 patients with COVID and 259,369 patients without COVID. Patients were matched along demographic characteristics and comorbidities.

Looking at clinical subtypes, incidence of patchy alopecia areata or alopecia totalis and alopecia universalis (AT/AU) were higher in patients with COVID, at 35.94 and 7.24 per 10,000 person-years, respectively, as compared with 19.43 and 4.18 per 10,000 person-years among controls. Meanwhile, the prevalence of alopecia areata and AT/AU was 70.53 and 12.39 per 10,000 person-years in the COVID group versus 52.37 and 8.97 per 10,000 person-years in controls.

"During the study period, the age- and sex-adjusted incidence and prevalence of AA [alopecia areata] and AT/AU in COVID-19-infected patients were considerably higher than in the prepandemic period in Korea, in which incidence and prevalence of AA and AT/AU remained constant from 2006 to 2015," they wrote.

Park and team acknowledged "potential detection or misclassification bias" in their study, despite using validated sensitivity analyses with several matching variables. They said that "further studies are necessary to validate the association between different populations and elucidate the causal relationship between the two conditions."

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