糖尿病胃轻瘫的诊断及发病机制

Diagnosis and pathogenic mechanism of diabetic gastroparesis

目的:探讨糖尿病胃轻瘫的早期诊断方法并探讨其可能的发病机制.方法:糖尿病住院患者38例,采用生化及放射免疫方法检测血糖、糖化血红蛋白、胃动素、胃泌素、胰高血糖素水平.以患者卧立位肱动脉收缩压变化检查植物神经功能;并采用标准餐加服小钡条试验,记录排空时间,以胃排空时间>6h诊断为胃轻瘫.结果:糖尿病胃排空异常者与胃排空正常者相比其空腹血糖(12.53±4.13mmol/L vs 7.12±1.37mmol/L,P<0.01)、餐后血糖(19.79±5.69mmol/L vs 14.11±4.21mmol/L,P<0.05)及糖化血红蛋白(9.73%±2.39% vs 7.26%±1.96%,P<0.05)明显升高,同时具有高水平的血清胃动素、胃泌素及胰高血糖素.糖尿病胃排空异常者植物神经功能异常发生率为62%(13/21),而糖尿病胃排空正常者为24%(4/17),糖尿病胃排空异常者胃内小钡条排空时间较正常者明显延长(7.93±1.23h vs 4.35±1.01h,P<0.001).结论:采用临床症状评分、血糖及胃肠道激素等监测及影象学检查可诊断糖尿病胃轻瘫,糖尿病胃轻瘫与神经病变、高血糖、血清胃肠激素异常、微血管病变及代谢紊乱有关.

AIM： To evaluate the clinical diagnosis and explore the pathogenic mechanisms of diabetic gastroparesis. METHODS： A total of 38 in-hospital patients with diabetes were included in this study. Biochemical method and radioimmunoassay （RIA） were used to detect the levels of plasma glucoses, glycosylated hemoglobin （GHG）, gastrin, rnotilin and glucagons. The autonomic nerve function and barium strip emptying time were used to make diagnosis of diabetic gastroparesis. RESULTS： The levels of fast blood glucose （FBG）, postprandial blood glucose （PBG） and GHG were significantly higher in diabetic patients with abnormal gastric emptying than those with normal gastric emptying （FBG： 12.53 ± 4.13 mrnol/L vs 7.12 ± 1.37 mmol/L, P 〈 0.01; PBG： 19.79 ± 5.69 mmol/L vs 14.11 ± 4.21 mmol/ L, P 〈 0.05; GHG： 9.73% ± 2.39% vs 7.26% ± 1.96%, P 〈 0.05）, Meanwhile, high levels of serum too-tilin, gastrin, and glucagons were detected in diabetic patients with abnormal gastric emptying. The occurrence rate of autonomic nerve function abnormality was 62% （13/21） in diabetic patients with abnormal gastric emptying, obviously higher than that in those with normal gastric emptying （24%, 4/17）. The barium strip emptying time was significantly prolonged in patients with diabetic gastroparesis （7.93 ＋ 1.23 h vs 4.35 ＋ 1.01 h, P 〈 0.001）. CONCLUSION： Diabetic gastroparesis can be diagnosed by grading clinical symptom, examining plasma glucoses, gastrin, motilin and glucagons, evaluating autonomic nerve function and barium emptying time. Hyperglycaemia, gut hormone abnormality, neuropathy, microangiopathy, and metabolic disorder participate in the development of diabetic gastroparesis.