Dear Editor,
In recent months, there have been reported several dermatologic manifestations in
COVID‐19 patients such as erythematous rash, widespread urticarial, chickenpox‐like
vesicles, acroischemia, chilblain‐like eruptions and petechial rash mimicking dengue.
1
,
2
In this study, we present a case of alopecia areata (AA) in a patient who tested positive
for COVID‐19. Our purpose is to further characterize dermatologic manifestations of
this disease.
At the end of September, a 38‐year‐old healthy male patient presented to the dermatologic
department because of sudden appearance of bald spots affecting the beard.
The patient had been diagnosed with SARS‐CoV‐2 infection in August, a month before
the appearance of the bald spots.
He referred no other underlying diseases and denied taking any drugs during the last
year, except for the paracetamol used as a symptomatic treatment for SARS‐CoV‐2 infection.
No family history for AA and other autoimmune diseases was present.
Physical examination revealed sharply demarcated bald patches on the beard. The patches
were round, variously distributed on the beard area. The underlying skin was unscarred
and looks superficially normal (Figure 1).
FIGURE 1
Pictures showing round bold patches variously distributed on the beard area
Our diagnosis was confirmed by trichoscopy showing yellow dots, black dots, broken
hairs and short vellus hairs (Figure 2).
FIGURE 2
Pictures showing trichoscopic findings of Alopecia Areata of the beard: black dots,
yellow dots, broken hairs, vellus hairs
Further examination including liver, kidney and thyroid functionality were within
normal limits. Serologic tests were negative for HIV, HBV, HCV and parvovirus B19.
Nasopharyngeal swab was negative for SARS‐CoV‐2 as well. After 2 weeks of treatment
with a trichological lotion with nicotinic acid, resorcinol and hyaluronic acid ,
the patient presented with an important improvement of the old lesions and the appearance
of new ones (Figure 3).
FIGURE 3
Pictures showing an improvement of the old lesions and the appearance of new ones,
after two weeks of treatment with a trichological lotion with nicotinic acid, resorcinol
and hyaluronic acid
Only few cases of AA in SARS‐CoV‐2‐infected patients have been reported in the literature.
3
The interplay among genetic factors (ie, HLA‐DR, CTLA4 and ULBP3) and environmental
factors (ie, emotional/physical stress, hormones and infections) has been shown to
play a key role in the AA etiology and progression.
4
,
5
Although the exact pathophysiology remains unknown, it seems to be related to an autoimmune
reaction against the hair follicles. Supporting the autoimmune genesis of AA, several
studies refer its association with other autoimmune diseases, such as type I diabetes
and vitiligo.
4
We assume that SARS‐CoV‐2 could be an additional risk factor in the pathogenesis of
AA. Referring to this, viral infection seems to be involved in autoimmune pathogenesis
by two mechanisms: According to bystander theory, the presence of pathogens increases
the release of costimulatory signals allowing the dendritic cells to present antigens
more effectively, both pathogen and self‐antigens. If this occurs in genetically predisposed
individuals, the activation of self‐reactive T lymphocytes could develop and progress
(Figure 4).
FIGURE 4
Possible role of SARS‐CoV‐2 in the pathogenesis of Alopecia Areata
As stated in the molecular mimicry theory, the virus could have antigens which cross‐react
with self‐antigens, so that the immune response turns against host tissues.
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Moreover, considering the significant impact of COVID‐19 pandemic on mental health,
psychological stress appears to be another possible risk factor of AA.
5
,
7
SARS‐CoV‐2 could act as a trigger in different autoimmune pathways, by creating an
inflammatory environment which allows the nonspecific activation of the immune system
or by a cross‐reaction between its antigens and host antigens.
In both cases, antigens expressed at the level of the follicles are recognized and
attacked by the immune system. Apart from the psychological effect, we believe that
SARS‐CoV‐2 has an important role in the onset of AA. As we do not know the long‐term
effects of SARS‐CoV‐2 infection, we will make periodical follow‐ups on our patient.
These observations represent a further confirmation of AA as a multifactorial disease,
but further studies are needed to confirm the relation between AA and COVID‐19.
CONFLICT OF INTEREST
The authors declare no potential conflict of interest.
AUTHOR CONTRIBUTIONS
Severino Persechino conceived the research idea. Alessandro Capalbo, Charalampos Georgios
Balampanos and Federica Orrù wrote the paper. Domenico Giordano, Nazareno Gagliostro
and Flavia Persechino collected the data.