Abstract:
COVID-19 has been shown to affect numerous organ systems, including the adrenal
glands, which play a central role in the body’s stress response. Clinical reports describing early
onset hypocorticism and acute adrenal insufficiency following SARS-CoV-2 infection suggest
that the adrenal glands may be compromised either directly by the virus or indirectly through
systemic disease mechanisms. The purpose of this review is to summarize and evaluate current
evidence regarding structural, functional, and pathophysiological alterations of the adrenal
glands associated with COVID-19.
Autopsy findings consistently demonstrate vascular abnormalities—including thrombosis,
infarction, hemorrhage, and severe endothelitis—represent another recurrent pattern and
highlight substantial microcirculatory disruption. Additional findings such as cellular
hyperplasia, necrosis, lipid degeneration, and focal adrenalitis further support the notion of
notable adrenal involvement. Although expression of ACE2, TMPRSS2,and other viral entry
associated proteins in adrenal tissue provides biological probability for SARS-CoV-2 infection
of adrenal cells, the limited number of virus-positive cells observed suggests that direct
cytopathic injury is unlikely to be the primary mechanism.
Collectively, the available literature underscores the multifactorial nature of adrenal
involvement in COVID-19 and highlights the necessity for further research to better define the
prevalence, underlying mechanisms, and long-term consequences of adrenal dysfunction in
affected patients.
