Siddiqui Raheel S, Zirkiyeva Milana, Saliaj Merjona
Internal Medicine, Icahn School of Medicine at Mount Sinai (New York City Health and Hospitals/Queens), Jamaica, USA.
Cureus. 2020 Oct 3;12(10):e10779. doi: 10.7759/cureus.10779.
Diabetic ketoacidosis is typically associated with type I diabetes mellitus, but it can be associated with type II diabetes mellitus under the conditions of extreme stress or as a presenting manifestation of ketosis-prone type II diabetes mellitus. A 38-year-old prediabetic male presented to the emergency room with hyperglycemia six weeks after recovery from coronavirus disease 2019 (COVID-19) pneumonia. Laboratory results showed severe hyperglycemia, metabolic acidosis, positive ketones in urine and blood, and elevated fasting C- peptide level. COVID-19 polymerase chain reaction (PCR) was negative, and immunoglobulin G (IgG) antibodies were positive. The workup was completely unremarkable for acute infection. Hemoglobin A1C increased from 6.1% to 10.8% within six weeks. The mechanism by which COVID-19 infection may trigger the onset of full-blown diabetes mellitus remains unknown. Viral infection may cause the direct destruction of pancreatic beta cells or trigger the changes in the body that induce the state of insulin resistance. Antibodies against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection may cross-react or interfere with the functioning of endogenous insulin. The association between type II diabetes and COVID-19 infections needs additional investigations to ascertain the exact mechanism by which COVID-19 infection triggers the onset of full-blown diabetes mellitus.
糖尿病酮症酸中毒通常与1型糖尿病相关,但在极端应激条件下或作为酮症倾向2型糖尿病的首发表现时,也可与2型糖尿病相关。一名38岁的糖尿病前期男性在从2019冠状病毒病(COVID-19)肺炎康复六周后因高血糖症被送往急诊室。实验室结果显示严重高血糖、代谢性酸中毒、尿酮和血酮阳性以及空腹C肽水平升高。COVID-19聚合酶链反应(PCR)为阴性,免疫球蛋白G(IgG)抗体为阳性。针对急性感染的检查结果完全无异常。糖化血红蛋白在六周内从6.1%升至10.8%。COVID-19感染引发全面糖尿病发作的机制仍不清楚。病毒感染可能导致胰腺β细胞的直接破坏,或引发体内诱导胰岛素抵抗状态的变化。针对严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染的抗体可能发生交叉反应或干扰内源性胰岛素的功能。2型糖尿病与COVID-19感染之间的关联需要进一步研究,以确定COVID-19感染引发全面糖尿病发作的确切机制。