ABSTRACT
Introduction
Alopecia areata (AA) is an autoimmune disease induced by viral infection or vaccination. With the increased incidence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the incidence of AA has also increased. Recently the incidence was found to be 7.8% from a previously reported rate of 2.1%. The physical and psychological damage caused by AA could seriously affect patients’ lives, while AA is a challenging dermatological disease owing to its complex pathogenesis.
Areas covered
This paper presents a comprehensive review of the prevalence, pathogenesis and potential therapeutic targets for AA after infection with SARS-CoV-2 or SARS-CoV-2 vaccine.
Expert opinion
The treatment of AA remains challenging because of the complexity of its pathogenesis. For patients with AA after SARS-CoV-2 infection or vaccination, the use of sex hormones and alternative regenerative therapies may be actively considered in addition to conventional treatments. For preexisting disease, therapeutic agents should be adjusted to the patient’s specific condition.
Article highlights
SARS-CoV-2 infection or vaccination could induce or aggravate alopecia areata.
The updated incidence of alopecia areata during COVID-19 pandemic was fourfold higher than previously reported.
Etiological factors, including genes, autoimmunity, coagulation, and psychological stress account for alopecia areata associated with SARS-CoV-2.
Besides conventional treatments, sex hormone replacement therapies and regenerative therapies are alternative options.
List of abbreviations
SARS-CoV-2 | = | severe acute respiratory syndrome coronavirus 2 |
AA | = | alopecia areata |
HF | = | hair follicle |
IP | = | immune privilege |
COVID-19 | = | coronavirus disease 2019 |
TMPRSS2 | = | transmembrane protease serine 2 |
ACE2 | = | angiotensin-converting enzyme 2 |
Th1 cells | = | T helper-1 cells |
IL | = | interleukin |
IFN | = | interferon |
Th2 cells | = | T helper-2 cells |
DCs | = | dendritic cells |
TNF | = | tumor necrosis factor |
NK cells | = | natural killer cells |
DNA | = | deoxyribonucleic acid |
mRNA | = | messenger RNA |
RNA | = | ribonucleic acid |
TLRs | = | toll-like receptors |
NF-kB | = | nuclear factor-k-gene binding |
JAK | = | Janus tyrosine kinase |
HFSCs | = | hair follicle stem cells |
pDC | = | plasmacytoid dendritic cell |
NLRP3 | = | pyrin domain of the NOD-like receptor containing three inflammasomes |
ASIA | = | autoimmune/inflammatory syndrome induced by adjuvants |
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.