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 Table of Contents  
Year : 2020  |  Volume : 2  |  Issue : 3  |  Page : 64-65

D Vitamin, Coronavirus, and Neurological Injuries

1 Department of Surgery, Clínica Sahagún IPS, Córdoba, Colombia
2 Latinoamerican Council of Neurocritical Care, Cartagena de Indias, Colombia
3 Medical Research, Neuro-Critical Care, Center for Biomedical Research; Neurotrauma Research Group, Faculty of Medicine, University of Cartagena, Cartagena de Indias, Colombia

Date of Submission25-May-2020
Date of Acceptance20-Aug-2020
Date of Web Publication31-Dec-2020

Correspondence Address:
Dr. William Andres Florez Perdomo
Department of Surgery, Clínica Sahagún IPS, Córdoba
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jtccm.jtccm_5_20

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How to cite this article:
Perdomo WA, Ucros HE, Moscote-Salazar LR. D Vitamin, Coronavirus, and Neurological Injuries. J Transl Crit Care Med 2020;2:64-5

How to cite this URL:
Perdomo WA, Ucros HE, Moscote-Salazar LR. D Vitamin, Coronavirus, and Neurological Injuries. J Transl Crit Care Med [serial online] 2020 [cited 2023 Mar 31];2:64-5. Available from: http://www.tccmjournal.com/text.asp?2020/2/3/64/305797

Dear Editor,

Coronavirus (CoV) infection has spread around the world rapidly, becoming a pandemic.[1] This has represented a risk for human beings due to the different systems that this new enemy affects. On March 11, 2020, the WHO declared this disease officially as a pandemic and at the same time the number of cases has grown exponentially and concern has grown for all the implications of this virus.[2],[3] The new CoV-2 (severe acute respiratory syndrome [SARS]) belongs to the family of Coronaviridae of the order Nidovirales and the Orthocoronaviridae subfamily with four genera named: alpha, beta, delta, and gamma coronaviruses.[4] Despite limited data, the neurotropism and invasiveness of COVID-19 are known.[5]

Vitamin D is a micronutrient that is used for maintaining the body's economy. It is necessary to maintain the calcium concentration within physiological ranges. The function it performs is essential because the calcium ion has effects on cellular and metabolic processes. After its intestinal absorption, calcium is stored in the skeleton and it acts as a calcium reservoir which is controlled by parathyroid hormone and Vitamin D. Vitamin D is produced by exposure to sunlight and even radiation ultraviolet. Vitamin A and Vitamin D deficiency leads to various avoidable pathologies such as osteoporosis. Vitamin D comprises a group of molecules called calciferol. The main form occurs in foods as cholecalciferol (Vitamin D3) and ergocalciferol (Vitamin D2). Vitamin D participates in the maturation and differentiation of mononuclear cells, facilitation of cytokines, and inhibition and proliferation of malignant cells and facilitates in the differentiation of malignant cells. This effect is independent of hypercalcemia. Vitamin D also affects muscles and the function of the central nervous system.[6]

Vitamin D plays a role in decreasing the pro-inflammatory response in both the innate and adaptive immune response, decreasing the expression of cytokines such as tumor necrosis factor-alpha and interleukin-1, present in the immune response to pathogenic germs such as SARS-CoV-2, thus reducing the cytokine storm preventing the development of the severe form of the disease.[7]

The immune response to a viral infection is mediated by cytotoxic T lymphocytes (CD8+), which destroys the infected cell; this response would be responsible for the neurological damage caused in patients with COVID-19.[8] According to recent studies in autopsies, cytokine storm syndrome (CSS) is involved with COVID-19, which has to be considered a therapeutic target.[9],[10]

Vitamin D may be related to impact as a protector factor, according to studies.[11] Physiologically, the blood–brain barrier (BBB) is a semipermeable membrane; what it is known from sepsis process has contributed to understand that BBB is highly sensitive to the immune system.[12] A probable starting point in sepsis acute brain dysfunctions is neuroinflammation; many cytokines enter the brain trough receptor-mediated endocytosis, and in a septic process when there is systemic inflammatory process involving multiple organ systems, the BBB may increase its permeability as a response to highly immune system reaction as CSS.[13] There are evidence that support neurologic complications in COVID-19, perhaps of a process when disrupting the BBB it is involved.[14],[15],[16]

According to several studies, the Vitamin D, supplementation could reduce the risk of mortality, progression to severe disease and neurological damage in patients with COVID 19.[17],[18] However, to confirm this association, several clinical trials and meta-analysis are required.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kofi Ayittey F, Dzuvor C, Kormla Ayittey M, Bennita Chiwero N, Habib A. Updates on Wuhan 2019 novel coronavirus epidemic. J Med Virol 2020;92:403-7.  Back to cited text no. 1
WHO. Available from: https://www.who.int/health topics/ coronavirus.WHO. [Last accessed on 2020 Apr 12].  Back to cited text no. 2
Lipsitch M, Swerdlow DL, Finelli L. Defining the epidemiology of Covid-19-Studies needed. N Engl J Med 2020;382:1194-6.  Back to cited text no. 3
Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol 2004;203:631-7.  Back to cited text no. 4
Conde Cardona G, Quintana Pájaro LD, Quintero Marzola ID, Ramos Villegas Y, Moscote Salazar LR. Neurotropism of SARS-CoV 2: Mechanisms and manifestations. J Neurol Sci 2020;412:116824.  Back to cited text no. 5
Brustad M, Meyer HE. Vitamin D–how much is enough, and is more better for your Health? Tidsskr Nor Laegeforen 2014;134:726-8.  Back to cited text no. 6
Grant WB, Lahore H, McDonnell SL, Baggerly CA, French CB, Aliano JL, et al. Evidence that Vitamin D supplementation could reduce risk of influenza and COVID-19 infections and deaths. Nutrients 2020;12:1-19.  Back to cited text no. 7
Roe K. Explanation for COVID-19 infection neurological damage and reactivations. Transbound Emerg Dis 2020;67:1414-5.  Back to cited text no. 8
Hanley B, Lucas SB, Youd E, Swift B, Osborn M. Autopsy in suspected COVID-19 cases. J Clin Pathol 2020;73:239-42.  Back to cited text no. 9
Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ, et al. COVID-19: Consider cytokine storm syndromes and immunosuppression. Lancet 2020;395:1033-4.  Back to cited text no. 10
Loeb M, Dang AD, Thiem VD, Thanabalan V, Wang B, Nguyen NB, et al. Effect of Vitamin D supplementation to reduce respiratory infections in children and adolescents in Vietnam: A randomized controlled trial. Influenza Other Respir Viruses 2019;13:176-83.  Back to cited text no. 11
Nwafor DC, Brichacek AL, Mohammad AS, Griffith J, Lucke Wold BP, Benkovic SA, et al. Targeting the blood brain barrier to prevent sepsis associated cognitive impairment. J Cent Nerv Syst Dis 2019;11:1-14.  Back to cited text no. 12
Kuperberg SJ, Wadgaonkar R. Sepsis-associated encephalopathy: The blood-brain barrier and the sphingolipid rheostat. Front Immunol 2017;8:597.  Back to cited text no. 13
Bridwell R, Long B, Gottlieb M. Neurologic complications of COVID 19. Am J Emerg Med 2020;38:1549.e3–1549.e7.  Back to cited text no. 14
Radmanesh A, Derman A, Lui YW, Raz E, Loh JP, et al. COVID 19 –associated diffuse leukoencephalopathy and microhemorrhages. Radiology 2020;297:E223–E227.  Back to cited text no. 15
Poyiadji N, Shahin G, Noujaim D, Stone M, Patel S, Griffith B. COVID 19–associated Acute Hemorrhagic Necrotizing Encephalopathy: CT and MRI. Radiology 2020;296:E119–E120.  Back to cited text no. 16
Greiller CL, Martineau AR. Modulation of the immune response to respiratory viruses by vitamin D. Nutrients 2015;7:4240-70.  Back to cited text no. 17
Zhou J, Du J, Huang L, Wang Y, Shi Y, Lin H. Preventive effects of Vitamin D on seasonal influenza a in infants: A multicenter, randomized, open, controlled clinical trial. Pediatr Infect Dis J 2018;37:749-54.  Back to cited text no. 18

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