伴有或不伴有潜在缺血性心脏病的糖耐量受损患者的代谢紊乱

Q4 Medicine Scripta Medica Pub Date : 2022-01-01 DOI:10.5937/scriptamed53-36711
Milena Brkić, D. Đekić, Jelena Jovanić, Goran Topic, A. Grbić, Tatjana Šutilović
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引用次数: 0

摘要

背景/目的:有证据表明,代谢危险因素胰岛素抵抗(IR)、血脂异常和肥胖在2型糖尿病(DMT2)和冠心病(CHD)的发生发展中起重要作用。除了代谢因素外,炎症标志物如纤维蛋白原和hs-C反应蛋白(hsCRP)的增加在冠心病的发生中也起作用。代谢紊乱被认为也存在于糖耐量受损(IGT)的患者中,并可能促进这些个体冠心病的发展。本研究的目的是探讨IGT患者糖耐量试验中代谢参数和慢性炎症标志物的行为和相关的冠心病。方法:随机分为4组,每组30例:a) IGT合并冠心病,b) IGT不合并冠心病,c)冠心病不合并IGT, d)无冠心病且糖耐量(NGT)正常的对照组。测量各组血糖调节参数(空腹血糖和Hb1Ac)。在75 g糖负荷下进行口服糖耐量试验(OGTT),计算IR参数(采用HOMA-IR、Matsuda指数、Quicki指数、HOMA1%B),测定血脂、腰臀比、纤维蛋白原和hsCRP。通过心电图、超声心动图和/或几何测量的典型心肌梗死体征来确定冠心病的诊断(布鲁斯方案)。结果:与没有IGT的冠心病患者和对照组相比,IGT合并冠心病患者和IGT合并冠心病患者的甘油三酯和胆固醇水平均有统计学意义上的升高,且胰岛素敏感性降低。同时伴有IGT和CHD的组纤维蛋白原和hsCRP浓度明显升高。结论:IR和高脂血症与慢性炎症介质一起,是糖耐量障碍发展的潜在预测因素;因此,在IGT期或高胰岛素血症期间进行介入治疗可以使患者有更好的机会预防或推迟糖尿病及其并发症的发生或发展。
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Metabolic disorders in patients with impaired glucose tolerance, with or without underlying ischaemic heart disease
Background/Aim: The evidence showed that in the development of diabetes mellitus type 2 (DMT2) and coronary heart disease (CHD) significant role is played by metabolic risk factors: insulin resistance (IR), dyslipidaemia and obesity. Beside metabolic factors, increase in inflammatory markers such as fibrinogen and hs-C reactive protein (hsCRP) plays a role in developing CHD. Metabolic disorders are thought to also be present in patients with impaired glucose tolerance (IGT) and could contribute to development of CHD in these individuals. Aim of this study was to investigate the behaviour of metabolic parameters and chronic inflammation markers in patients with IGT on glucose tolerance test and associated CHD. Methods: The trial included 4 groups of 30 subjects: a) IGT with CHD, b) IGT without CHD, c) CHD without IGT and d) control group without CHD and with normal glucose tolerance (NGT). Within each group glucoregulation parameters were measured (fasting glucose and Hb1Ac). Oral glucose tolerance test (OGTT) with 75 g glucose load was performed and IR parameters calculated (using HOMA-IR, Matsuda index, Quicki index, HOMA1%B), lipid profile was done, waist/hip ratio was measured, as well as fibrinogen and hsCRP. CHD diagnosis was determined by typical signs of previous myocardial infarction on ECG, echocardiogram and/or ergometry (Bruce protocol). Results: Subjects with IGT, but no CHD and those with both IGT and CHD had statistically significantly higher triglyceride and cholesterol levels and manifest IR with decreased insulin sensitivity compared to subjects with CHD, but no IGT and control group. Group with both IGT and CHD was found to have significantly higher fibrinogen and hsCRP concentrations. Conclusion: IR and hyperlipidaemia, together with chronic inflammation mediators, are potential predictors of the development of glucose tolerance disorders; hence interventional treatment during IGT period or during hyperinsulinaemia could give patients better opportunity to prevent or postpone onset or development of diabetes and its complications.
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