Metabolic Syndrome as Prognostic Factor for Outcome of Sever SARS-COV-2 Cases.

SARS-COV-2 (Coronavirus Disease-2019), a disease caused by the coronavirus. SARS-CoV-2 (Sever Acute Respiratory Syndrome-Coronavirus-2) has emerged as a rapidly spreading communicable disease affecting more than 100 countries across the globe at present.

The disease is primarily spread through large respiratory droplets, though the possibility of other routes of transmission cannot be ruled out, as the virus has been found in stool and urine of affected individuals.

The disease severity has varied from mild self-limiting flu-like illness to fulminant pneumonia, respiratory failure and death. Several risk groups have been identified as being at higher risk of developing a more severe form of the disease and, subsequently, have higher mortality. In particular, cardiovascular diseases, hypertension, chronic respiratory diseases, metabolic syndrome (MS), and diabetes mellitus (DM) appear to play an important role in developing a more severe form of the disease with several complications.

Metabolic syndrome is a constellation of cardiovascular risk factors that include abdominal obesity, elevated blood pressure, dysglycemia, atherogenic dyslipidemia, pro-thrombotic state, and pro-inflammatory state).

Clinically, metabolic syndrome is defined as the presence of 3 or more of the following factors: increased waist circumference (population and country-specific cutoff), hypertriglyceridemia (>150 mg/dL or on treatment for hypertriglyceridemia), elevated blood pressure (systolic . 130 and/or diastolic . 85 mm Hg or with a history of hypertension on treatment), reduced high-density lipoprotein cholesterol (<40 mg/dL in males; <50 mg/dL in females), and dysglycemia (.100 mg/dL or on treatment for hyperglycemia)

. Components of metabolic syndrome such as hypertension, type 2 diabetes mellitus (T2DM), and obesity are highly prevalent and significantly increase the risk of hospitalization and mortality in SARS-COV-2 patients.

The pathophysiologic mechanisms for these observations have not been fully explained. A critical interaction between SARS-CoV-2 and the angiotensin-converting enzyme 2 (ACE2) facilitates viral entry into the host cell. ACE2 is expressed in pancreatic islets, vascular endothelium, and adipose tissue, and the SARS-CoV-2 -ACE2 interaction in these tissues, along with other factors governs the spectrum and the severity of clinical manifestations among SARS-COV-2 patients with metabolic syndrome.

Moreover, the pro-inflammatory milieu observed in patients with metabolic syndrome may contribute toward SARS-COV-2-mediated host immune dysregulation, including suboptimal immune responses, hyper inflammation, micro-vascular dysfunction, and thrombosis.