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新冠感染引发的新发自身免疫性糖尿病:基于病例的综述。

Newly-onset Autoimmune Diabetes Mellitus Triggered by COVID 19 Infection: A Case-based Review.

机构信息

Faculty of Medicine, Division of Endocrinology, Cukurova University, Adana, Turkey.

出版信息

Endocr Metab Immune Disord Drug Targets. 2023;23(7):887-893. doi: 10.2174/2666145415666221004111511.

Abstract

The devastating global pandemic Coronavirus disease 2019 (COVID 19) isolated in China in January 2020 is responsible for an outbreak of pneumonia and other multisystemic complications. The clinical picture of the infection has extreme variability: it goes from asymptomatic patients or mild forms with fever, cough, fatigue and loss of smell and taste to severe cases ending up in the intensive care unit (ICU). This is due to a possible cytokine storm that may lead to multiorgan failure, septic shock, or thrombosis. Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV -2), which is the virus that causes COVID 19, binds to angiotensin-converting enzyme 2 (ACE2) receptors, which are expressed in key metabolic organs and tissues, including pancreatic beta cells, adipose tissue, the small intestine and the kidneys. Therefore it is possible to state that newly-onset diabetes is triggered by COVID 19 infection. Although many hypotheses have clarified the potential diabetogenic effect of COVID 19, a few observations were reported during this pandemic. Two male patients admitted to us with devastating hyperglycemia symptoms were diagnosed with type 1/autoimmune diabetes mellitus within 3 months following COVID 19 infection. Autoantibodies and decreased C peptide levels were detected in these patients. We speculated that several mechanisms might trigger autoimmune insulitis and pancreatic beta-cell destruction by COVID 19 infection. We aim to raise awareness of the possible link between SARS-CoV-2 and newly onset type 1 diabetes mellitus. Further studies are needed to determine a more definitive link between the two clinical entities.

摘要

2020 年 1 月在中国被隔离的导致 2019 年冠状病毒病(COVID-19)的毁灭性全球大流行是导致肺炎和其他多系统并发症爆发的原因。感染的临床表现具有极端的可变性:它可以从无症状患者或伴有发热、咳嗽、疲劳和嗅觉味觉丧失的轻度病例发展为严重病例,最终进入重症监护病房(ICU)。这是由于可能发生细胞因子风暴,从而导致多器官衰竭、败血症性休克或血栓形成。导致 COVID-19 的严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)与血管紧张素转换酶 2(ACE2)受体结合,ACE2 受体在包括胰腺β细胞、脂肪组织、小肠和肾脏在内的关键代谢器官和组织中表达。因此,可以说新发糖尿病是由 COVID-19 感染引发的。尽管许多假说阐明了 COVID-19 的潜在致糖尿病作用,但在此次大流行期间仅报道了少数观察结果。我们收治的两名男性患者因严重高血糖症状入院,在 COVID-19 感染后 3 个月内被诊断为 1 型/自身免疫性糖尿病。这些患者检测到自身抗体和 C 肽水平降低。我们推测,COVID-19 感染可能通过几种机制引发自身免疫性胰岛炎和胰腺β细胞破坏。我们旨在提高对 SARS-CoV-2 与新发 1 型糖尿病之间可能联系的认识。需要进一步的研究来确定这两种临床实体之间更明确的联系。

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