Why the study?
COVID-19 and obesity are co-occurring pandemics that both mediate inflammation, creating a harmful interaction that impairs multiorgan function and increases thrombotic risk.
This review highlights the synergistic inflammatory and pathophysiological mechanisms between COVID-19 and obesity, emphasizing the increased risk of severe complications in this patient population.
Warrants vigilance for obese COVID-19 patients; leaves open targeted anti-inflammatory trials.
COVID-19 and obesity are two pandemic diseases that the world is currently facing. Both activate the immune system and mediate inflammation. A sequence of disease phases in patients with severe COVID-19 results in a cytokine storm, which amplifies the subclinical inflammation that already exists in patients with obesity. Pro-inflammatory cytokines and chemotactic factors increase insulin resistance in obesity. Therefore, a greater systemic inflammatory response is establishe, along with an increased risk of thrombotic phenomena and hyperglycemic conditions. These changes further impair pulmonary, cardiac, hepatic, and renal functions, in addition to hindering glycemic control in people with diabetes and pre-diabetes. This review explains the pathophysiological mechanisms of these two pandemic diseases, provides a deeper understanding of this harmful interaction and lists possible therapeutic strategies for this risk group.
No takes yet. Share an insight, caveat, or question.
Brandão et al. (2020) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: