Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong.
Diabetes Metab J. 2024 Jul;48(4):763-770. doi: 10.4093/dmj.2023.0175. Epub 2024 Mar 11.
We evaluated changes in glycemic status, over 1 year, of coronavirus disease 2019 (COVID-19) survivors with dysglycemia in acute COVID-19.
COVID-19 survivors who had dysglycemia (defined by glycosylated hemoglobin [HbA1c] 5.7% to 6.4% or random glucose ≥10.0 mmol/L) in acute COVID-19 were recruited from a major COVID-19 treatment center from September to October 2020. Matched non-COVID controls were recruited from community. The 75-g oral glucose tolerance test (OGTT) were performed at baseline (6 weeks after acute COVID-19) and 1 year after acute COVID-19, with HbA1c, insulin and C-peptide measurements. Progression in glycemic status was defined by progression from normoglycemia to prediabetes/diabetes, or prediabetes to diabetes.
Fifty-two COVID-19 survivors were recruited. Compared with non-COVID controls, they had higher C-peptide (P< 0.001) and trend towards higher homeostasis model assessment of insulin resistance (P=0.065). Forty-three COVID-19 survivors attended 1-year reassessment. HbA1c increased from 5.5%±0.3% to 5.7%±0.2% (P<0.001), with increases in glucose on OGTT at fasting (P=0.089), 30-minute (P=0.126), 1-hour (P=0.014), and 2-hour (P=0.165). At baseline, 19 subjects had normoglycemia, 23 had prediabetes, and one had diabetes. Over 1 year, 10 subjects (23.8%; of 42 non-diabetes subjects at baseline) had progression in glycemic status. C-peptide levels remained unchanged (P=0.835). Matsuda index decreased (P=0.007) and there was a trend of body mass index increase from 24.4±2.7 kg/m2 to 25.6±5.2 (P=0.083). Subjects with progression in glycemic status had more severe COVID-19 illness than non-progressors (P=0.030). Reassessment was not performed in the control group.
Subjects who had dysglycemia in acute COVID-19 were characterized by insulin resistance. Over 1 year, a quarter had progression in glycemic status, especially those with more severe COVID-19. Importantly, there was no significant deterioration in insulin secretory capacity.
我们评估了新冠肺炎（COVID-19）急性发病期间伴发糖代谢异常的幸存者在 1 年内血糖状态的变化。
我们从 2020 年 9 月至 10 月间的一家大型 COVID-19 治疗中心招募了急性 COVID-19 期间伴发糖代谢异常（糖化血红蛋白 5.7%~6.4%或随机血糖≥10.0mmol/L）的 COVID-19 幸存者。同期从社区招募了配对的非 COVID 对照组。在急性 COVID-19 后 6 周（基线）和 1 年后进行了 75g 口服葡萄糖耐量试验（OGTT），并检测了糖化血红蛋白、胰岛素和 C 肽。血糖状态的进展定义为从正常血糖进展为糖尿病前期/糖尿病，或从糖尿病前期进展为糖尿病。
共招募了 52 名 COVID-19 幸存者。与非 COVID 对照组相比，COVID-19 幸存者的 C 肽水平更高（P＜0.001），且稳态模型评估的胰岛素抵抗（HOMA-IR）趋势更高（P=0.065）。有 43 名 COVID-19 幸存者接受了 1 年的重新评估。糖化血红蛋白从 5.5%±0.3%增加至 5.7%±0.2%（P＜0.001），空腹（P=0.089）、30 分钟（P=0.126）、1 小时（P=0.014）和 2 小时（P=0.165）时 OGTT 的血糖水平升高。基线时，19 名受试者血糖正常，23 名受试者为糖尿病前期，1 名受试者为糖尿病。1 年后，42 名非糖尿病患者中有 10 名（23.8%）血糖状态进展。C 肽水平无变化（P=0.835）。Matsuda 指数降低（P=0.007），体重指数呈上升趋势，从 24.4±2.7kg/m2增加至 25.6±5.2kg/m2（P=0.083）。血糖状态进展者的 COVID-19 病情比无进展者更严重（P=0.030）。对照组未进行重新评估。
急性 COVID-19 伴发糖代谢异常的患者表现为胰岛素抵抗。1 年后，四分之一的患者血糖状态进展，尤其是 COVID-19 病情更严重者。重要的是，胰岛素分泌能力没有明显恶化。
