Is melatonin deficiency a unifying pathomechanism of high risk patients with COVID-19?
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Abstract
An article by Zhang et al. [1] published in the March issue of Life
Sciences suggested melatonin as a potential adjuvant treatment for
COVID-19. Besides the antioxidative and immunomodulatory actions of
melatonin, there is another reason supporting melatonin's use as a rational approach to COVID-19 treatment. The population with the
greatest susceptibility to becoming infected and developing a severe
SARS-CoV-2 infection involve the elderly and patients with hypertension, diabetes and various cardiovascular pathologies. The question
arises, what unifying condition accounts for the increased sensitivity to
and risk of poor prognosis of COVID-19 in these groups?
One feature common to these cohorts is their depressed night-time
melatonin rise. The production of melatonin progressively decreases
with increased age, the lowest levels being in the elderly [2]. Impaired
nocturnal melatonin secretion is also observed in non-dipper hypertensive patients [3]. Experimental pinealectomy or continuous light
exposure in rats is associated with reduced levels of melatonin and
hypertension development [4]. Circadian rhythms of melatonin secretion are blunted in type 2 diabetic patients and low melatonin secretion
at night is associated with autonomic neuropathy [5]. Decreased levels
of serum melatonin predict adverse left ventricular remodelling during
the chronic phase after myocardial infarction [6]. Based on these
findings, we suggest that insufficient melatonin production may have
an important role in the increased susceptibility of these patients to
SARS-CoV-2 infection and to its negative prognosis. This pathophysiological association supports using melatonin both in prophylaxis and as
a therapy in COVID-19 especially considering its high safety profile.
Link to resource
https://doi.org/10.1016/j.lfs.2020.117902Collections
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