Relationship of magnesemia with myocardial damage and mortality in patients with COVID-19.

Magnesium (Mg) is the second most abundant intracellular cation and plays a significant role in immune system and cardiac protection. Mg deficiency contributes to chronic low-grade inflammation leading to cardiovascular diseases, and low Mg level exacerbates virus-induced inflammation. The aim of the study was to investigate whether serum magnesium level is associated with myocardial damage and prognosis of COVID-19. This was a single-center, observational retrospective study of patients with COVID-19. The study population was divided into two groups according to in-hospital mortality: a survivor group (SG) and a non-survivor group (NSG). Myocardial damage was defined as blood levels of cardiac troponin I (cTnI) above the 99th percentile upper reference limit. Magnesium, variables regarding inflammation, and myocardial damage were compared between the groups. A total of 629 patients with COVID-19 were included. Mortality rate was 11.85% (n = 82). There were 61 (74.4%) and 294 male patients (53.7%) in NSG and SG, respectively (p = 0.001). The median age of NSG was 64.5 years (min-max: 37-93) and the median age of SG was 56.0 years (min-max: 22-92) (p < 0.001). Median serum magnesium levels of NSG and SG were 1.94 mg/dL (min-max: 1.04-2.87) and 2.03 mg/dL (min-max: 1.18-2.88), respectively (p = 0.027). Median cTnI levels of NSG and SG were 25.20 pg/mL (min-max: 2.10-2240.80) and 4.50 pg/mL (min-max: 0.50-984.3), respectively (p < 0.001). The cTnI levels were lower in those patients whose serum Mg levels were higher than 1.94. Although serum magnesium level was not a predictor for in-hospital mortality, there was a significant negative correlation between magnesemia and myocardial damage.

Serum magnesium in patients with severe acute respiratory syndrome coronavirus 2 from Wuhan, China.

The aim of the study was to evaluate the significance of hypomagnesemia in patients with coronavirus disease 2019 (COVID-19) and clarify its possible pathogenesis. A retrospective cohort study was conducted by reviewing 83 patients hospitalized in Guanggu district, Wuhan Third Hospital, China. Clinical histories, laboratory findings and outcome data were collected. Eighteen patients had hypomagnesemia during hospitalization. Fourteen patients were in the critical group and six died. In the critical group, serum magnesium (0.72 ± 0.15 mmol/L) was much lower than that in the moderate and severe groups. At the same time, we also found that several indicators are correlated with the level of magnesium. The level of magnesium was positively associated with the lymphocyte count (r = 0.203, P = 0.004) and platelet count (r = 0.217, P = 0.002) but negatively related to the levels of CRP (r = -0.277, P = 0.000), LDH (r = -0.185, P = 0.011) and α-hydroxybutyrate dehydrogenase (r = -0.198, P = 0.008) in the critical group. Hypomagnesemia might increase symptoms and may be associated with mortality in COVID-19 by affecting enzyme activity and activating the inflammatory response. Thus, magnesium might play a key role in the pathogenesis of COVID-19.

Magnesium and Vitamin D Deficiency as a Potential Cause of Immune Dysfunction, Cytokine Storm and Disseminated Intravascular Coagulation in covid-19 patients.

Magnesium and vitamin D each have the possibility of affecting the immune system and consequently the cytokine storm and coagulation cascade in COVID-19 infections. Vitamin D is important for reducing the risk of upper respiratory tract infections and plays a role in pulmonary epithelial health. While the importance of vitamin D for a healthy immune system has been known for decades, the benefits of magnesium has only recently been elucidated. Indeed, magnesium is important for activating vitamin D and has a protective role against oxidative stress. Magnesium deficiency increases endothelial cell susceptibility to oxidative stress, promotes endothelial dysfunction, reduces fibrinolysis and increases coagulation. Furthermore, magnesium deficient animals and humans have depressed immune responses, which, when supplemented with magnesium, a partial or near full reversal of the immunodeficiency occurs. Moreover, intracellular free magnesium levels in natural killer cells and CD8 killer T cells regulates their cytotoxicity. Considering that magnesium and vitamin D are important for immune function and cellular resilience, a deficiency in either may contribute to cytokine storm in the novel coronavirus 2019 (COVID-19) infection.

Magnesium in Infectious Diseases in Older People.

Reduced magnesium (Mg) intake is a frequent cause of deficiency with age together with reduced absorption, renal wasting, and polypharmacotherapy. Chronic Mg deficiency may result in increased oxidative stress and low-grade inflammation, which may be linked to several age-related diseases, including higher predisposition to infectious diseases. Mg might play a role in the immune response being a cofactor for immunoglobulin synthesis and other processes strictly associated with the function of T and B cells. Mg is necessary for the biosynthesis, transport, and activation of vitamin D, another key factor in the pathogenesis of infectious diseases. The regulation of cytosolic free Mg in immune cells involves Mg transport systems, such as the melastatin-like transient receptor potential 7 channel, the solute carrier family, and the magnesium transporter 1 (MAGT1). The functional importance of Mg transport in immunity was unknown until the description of the primary immunodeficiency XMEN (X-linked immunodeficiency with Mg defect, Epstein-Barr virus infection, and neoplasia) due to a genetic deficiency of MAGT1 characterized by chronic Epstein-Barr virus infection. This and other research reporting associations of Mg deficit with viral and bacterial infections indicate a possible role of Mg deficit in the recent coronavirus disease 2019 (COVID-19) and its complications. In this review, we will discuss the importance of Mg for the immune system and for infectious diseases, including the recent pandemic of COVID-19.