Abstract
Calcium is involved in all vital processes of the body: synaptic transmission, memory development, immunity, blood clotting, heart contractions, etc. In this regard, it is important to understand the involvement of calcium in the development of SARS-CoV-2 virus infection and COVID-19 disease. We have studied the existing scientific literature, looking for the involvement of both calcium and calcium-regulating hormones (parathyroid hormone, calcitonin, vitamin D) in COVID contagiousness and severity of disease. Separately, both hypocalcemia and vitamin D deficiency have been identified in a number of large clinical trials as a predictor of mortality in patients hospitalized with COVID-19. Angiotensin-converting enzyme-2 plays a key role in contagiousness with the SARS-CoV-2 virus, and its formation is a calcium-calmodulin-dependent process. In our opinion, in order to prevent the penetration and spreading of the virus in the body, this link should be targeted with the usage of drugs that activate the calcium calmodulin system. Calcium blockers used parallel with hypocalcemia, to some extent, reduce the spreading of the virus in the body in the acute phase of the disease, but it is possible that in the future they lead to deeper and long-term complications - cognitive dysfunction. However, we did not find any study in the literature that aimed to identify calcium-dependent mechanisms in a complex, dynamic study of the same patients. Therefore, this question is still open in science, because without understanding how the amount of calcium-regulating hormones changes during the disease, without understanding how much phosphorus changes in parallel with calcium, it is impossible to get a complete picture of the disease on the role of calcium-dependent mechanisms in development. Only a summary of such combined data will allow us to reach a scientifically based conclusion, to explain the mechanisms by which hypocalcemia occurs, and by what possible mechanisms it can be prevented.
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