Clinical Endocrine Section, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
Endocrinology. 2020 Oct 1;161(10). doi: 10.1210/endocr/bqaa112.
The ongoing coronavirus disease 2019 (COVID-19) pandemic is caused by the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Individuals with metabolic syndrome are at increased risk for poor disease outcomes and mortality from COVID-19. The pathophysiologic mechanisms for these observations have not been fully elucidated. 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 COVID-19 patients with metabolic syndrome. Moreover, the pro-inflammatory milieu observed in patients with metabolic syndrome may contribute toward COVID-19-mediated host immune dysregulation, including suboptimal immune responses, hyperinflammation, microvascular dysfunction, and thrombosis. This review describes the spectrum of clinical features, the likely pathophysiologic mechanisms, and potential implications for the management of metabolic syndrome in COVID-19 patients.
正在持续的 2019 年冠状病毒病（COVID-19）大流行是由新型冠状病毒，即严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）引起的。患有代谢综合征的个体发生 COVID-19 不良疾病结局和死亡的风险增加。这些观察结果的病理生理机制尚未完全阐明。SARS-CoV-2 与血管紧张素转换酶 2（ACE2）之间的关键相互作用有助于病毒进入宿主细胞。ACE2 在胰岛、血管内皮和脂肪组织中表达，SARS-CoV-2-ACE2 在这些组织中的相互作用以及其他因素决定了代谢综合征 COVID-19 患者的临床表现谱和严重程度。此外，代谢综合征患者中观察到的促炎环境可能导致 COVID-19 介导的宿主免疫失调，包括免疫反应不佳、过度炎症、微血管功能障碍和血栓形成。这篇综述描述了 COVID-19 患者代谢综合征的临床表现谱、可能的病理生理机制以及对其管理的潜在影响。
