Hypermagnesemia and hyperphosphatemia are highly prevalent in patients with COVID-19 and increase the risk of death.

OBJECTIVES: Nonrespiratory manifestations of COVID-19 include endocrine disorders, among which are calcium-magnesium-phosphate homeostasis abnormalities, which seem to influence the disease severity and patient outcome. The aim of this study was to evaluate the prevalence and impact of calcium-magnesium-phosphate and vitamin D3 disorders on survival in patients hospitalized for COVID-19 depending on the severity of the disease and kidney function. DESIGN OR METHODS: The study was conducted between April 2020 and May 2021 at Central Clinical Hospital in Warsaw, Poland. A total of 146 patients who had tested concentration of at least one of the studied elements, estimated glomerular filtration ratio, creatinine levels, and blood saturation, and were diagnosed with COVID-19 disease were included in the analysis. RESULTS: We found that hypermagnesemia was common and associated with a 1.5-fold increased risk of death in the whole cohort. Hyperphosphatemia also increased the risk of death, exactly 2.4-fold. Furthermore, we found a statistically significant association between increased mortality in the whole cohort and hypovitaminosis D3 (P <0.05). Serum creatinine concentration and estimated glomerular filtration ratio significantly correlated with serum magnesium and phosphate levels. CONCLUSION: Hypermagnesemia, hyperphosphatemia, and hypovitaminosis D but not hypocalcemia influence the mortality of patients with COVID-19. These parameters should be monitored routinely in this group of patients, especially in those with decreased kidney function.

Could Exogenous Insulin Ameliorate the Metabolic Dysfunction Induced by Glucocorticoids and COVID-19?

The finding that high-dose dexamethasone improves survival in those requiring critical care due to COVID-19 will mean much greater usage of glucocorticoids in the subsequent waves of coronavirus infection. Furthermore, the consistent finding of adverse outcomes from COVID-19 in individuals with obesity, hypertension and diabetes has focussed attention on the metabolic dysfunction that may arise with critical illness. The SARS coronavirus itself may promote relative insulin deficiency, ketogenesis and hyperglycaemia in susceptible individuals. In conjunction with prolonged critical care, these components will promote a catabolic state. Insulin infusion is the mainstay of therapy for treatment of hyperglycaemia in acute illness but what is the effect of insulin on the admixture of glucocorticoids and COVID-19? This article reviews the evidence for the effect of insulin on clinical outcomes and intermediary metabolism in critical illness.

Avoiding the Coming Tsunami of Common, Chronic Disease: What the Lessons of the COVID-19 Pandemic Can Teach Us.

During the past year, clinicians and the public have been focused on the coronavirus disease 2019 (COVID-19) pandemic and its associated societal and economic effects. However, once the acute phase of this crisis has passed, we will face an enormous wave of death and disability as a result of common chronic diseases (CCDs), with cardiometabolic diseases at the crest (Figure). A tsunami results when an earthquake on the ocean floor creates huge waves that can wreak devastation far distant from the original upheaval, especially when warnings are ignored. Similarly, underlying global and national demographic and risk factor profiles have for some time presaged an overwhelming burden of CCDs. However, although the pandemic has created additional impetus that unless heeded will amplify the consequences of this burden, the rapid adaptations and innovations in care and research prompted by the urgent response to it may also offer us the means to stem this flood.

Is Toll-like receptor 4 involved in the severity of COVID-19 pathology in patients with cardiometabolic comorbidities?

The severe form of COVID-19 is marked by an abnormal and exacerbated immunological host response favoring to a poor outcome in a significant number of patients, especially those with obesity, diabetes, hypertension, and atherosclerosis. The chronic inflammatory process found in these cardiometabolic comorbidities is marked by the overexpression of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumoral necrosis factor-alpha (TNF-α), which are products of the Toll-Like receptors 4 (TLR4) pathway. The SARS-CoV-2 initially infects cells in the upper respiratory tract and, in some patients, spread very quickly, needing respiratory support and systemically, causing collateral damage in tissues. We hypothesize that this happens because the SARS-CoV-2 spike protein interacts strongly with TLR4, causing an intensely exacerbated immune response in the host's lungs, culminating with the cytokine storm, accumulating secretions and hindering blood oxygenation, along with the immune system attacks the body, leading to multiple organ failure.

A metabolic handbook for the COVID-19 pandemic.

For infectious-disease outbreaks, clinical solutions typically focus on efficient pathogen destruction. However, the COVID-19 pandemic provides a reminder that infectious diseases are complex, multisystem conditions, and a holistic understanding will be necessary to maximize survival. For COVID-19 and all other infectious diseases, metabolic processes are intimately connected to the mechanisms of disease pathogenesis and the resulting pathology and pathophysiology, as well as the host defence response to the infection. Here, I examine the relationship between metabolism and COVID-19. I discuss why preexisting metabolic abnormalities, such as type 2 diabetes and hypertension, may be important risk factors for severe and critical cases of infection, highlighting parallels between the pathophysiology of these metabolic abnormalities and the disease course of COVID-19. I also discuss how metabolism at the cellular, tissue and organ levels might be harnessed to promote defence against the infection, with a focus on disease-tolerance mechanisms, and speculate on the long-term metabolic consequences for survivors of COVID-19.

Metabolic dysfunction associated fatty liver disease increases risk of severe Covid-19.

BACKGROUND AND AIMS: Liver involvement is common in COVID-19. Elevated aspartate and alanine amino transaminase (AST/ALT) and borderline increase in serum bilirubin and serum alkaline phosphatase (ALP) are the commonest findings. Patients with associated co morbid conditions like obesity, cardiovascular disease, renal disease, malignancy, hypertension and old age are prone to develop severe disease. Limited data is available in patients with COVID-19 and metabolic dysfunction associated fatty liver disease (MAFLD).The aim of this review is to analyse the effect of MAFLD on severity of COVID-19. METHODS: We systematically searched the PubMed database till May 20, 2020 and retrieved all the articles published on COVID-19 and fatty liver/MAFLD/NAFLD. RESULTS: Limited studies done had shown four to six fold high risk of severe COVID-19 in patients with MAFLD. Patients with MAFLD and associated obesity, severe fibrosis and age <60 yrs are more prone to develop severe COVID-19. CONCLUSION: MAFLD is associated with 4-6 fold increase in severity of COVID-19 compared to non MAFLD patients. Physician and hepatologist should follow these patients cautiously and preventive measures to be taken strictly in these high risk patients.