Melatonin is a hormone secreted by the pineal gland in accordance with the circadian rhythm when the light level decreases. Reduction of melatonin secretion with age may be associated with physiological aging in neurodegenerative diseases by affecting the suprachiasmatic nucleus or of the neuronal pathways of transmission to the pineal gland. A significant decrease in melatonin synthesis has been reported in various disorders and diseases, including cardiovascular diseases, metabolic disorders (particularly diabetes type 2), cancer and endocrine diseases. In addition to the fact, that melatonin is a sleep inducer, it also exerts cytoprotective properties as an antioxidant and free radical scavenger. The therapeutic role of melatonin has been demonstrated in sleep disorders, eye damage and cardiovascular disease. The association between melatonin and β-blockers has had a positive impact on sleep disorders in clinical trials. Previous studies have reported the anti-inflammatory effect of melatonin by adjusting levels of pro-inflammatory cytokines, including interleukin (IL)-6, IL-1β and tumor necrosis factor-α. Melatonin treatment has been demonstrated to decrease IL-6 and IL-10 expression levels and efficiently attenuate T-cell proliferation. Currently, there is an inconsistency of scientific data regarding the lowest optimal dose and safety of melatonin for long-term use. The aim of the present review was to summarize the evidence on the role of melatonin in various clinical conditions and highlight the future research in this area.

The coronavirus disease 2019 (COVID-19) pandemic imposed arestructuring of global health systems by rethinking spaces used for the care of these patients and the additions of intensive care, infectious diseases and pneumology departments. This paper provides evidence on the presence of severe acute respiratory syndrome coronavirus 2 in hepatocytes and its direct cytopathic activity, as well as the degree of liver damage due to drug toxicity, inflammation and hypoxia in COVID-19. A review of clinical trials has quantified liver damage through both pathology and biochemistry studies. Additionally, we briefly present the results of a study conducted in our clinic on 849 patients admitted for COVID-19 treatment, of which 31 patients had pre-existing chronic liver disease and 388 patients had values above the normal limit for alanine aminotransferase, aspartate aminotransferase, and total bilirubin. It was observed that patients with abnormal liver tests were significantly statistically older, had more comorbidities and had a higher percentage of unfavourable evolution (death or transfer to intensive care). The conclusion of this paper is that the main causes of liver damage are direct viral aggression, coagulation dysfunction and endothelial damage, and patients with impaired liver function develop more severe forms of COVID-19 which requires special care by a multidisciplinary team that includes a hepatologist.