NATURAL-HISTORY OF PERIPHERAL NEUROPATHY IN PATIENTS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS
NATURAL-HISTORY OF PERIPHERAL NEUROPATHY IN PATIENTS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS
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DOI：
10.1056/nejm199507133330203
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发表时间：
1995-07-13
影响因子：
158.5
通讯作者：
UUSITUPA, M
中科院分区：
文献类型：
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作者：
PARTANEN, J;NISKANEN, L;UUSITUPA, M
背景关于非胰岛素依赖型糖尿病（NIDDM）患者神经病变的发生率和自然史的信息很少。我们研究了新诊断的NIDDM患者和对照组在基线和5年和10年后。根据临床标准（疼痛和感觉异常）和电诊断研究（神经传导速度和反应幅度值）诊断多发性神经病。我们调查了代谢变量（口服葡萄糖耐量试验结果、血脂和胰岛素浓度以及糖化血红蛋白值）与多发性神经病发展之间的关系。在10年中，36例NIDDM患者和8例对照受试者死亡; 86例患者和121例对照受试者完成了研究。当研究结束时，18%的患者只接受饮食治疗，59%的患者只接受口服降糖药治疗，12%的患者只接受胰岛素治疗，11%的患者同时接受胰岛素和口服降糖药治疗。基线时，NIDDM患者中明确或可能的多发性神经病的患病率为8.3%，而对照组为2.1%。10年后，这些值分别为41.9%和5.8%。腿部和足部神经传导异常的NIDDM患者数量从基线的8.3%增加到5年后的16.7%和10年后的41.9%。感觉和运动振幅的下降，表明轴突破坏，比神经传导速度的减慢，这表明脱髓鞘更明显。在NIDDM患者中，有多发性神经病的患者血糖控制比无多发性神经病的患者差。口服葡萄糖前后的低血清胰岛素浓度与多发性神经病的发生有关，与血糖的程度无关。NIDDM患者多发性神经病的患病率随着时间的推移而增加，并且在低胰岛素血症患者中增加可能更大。
Background. There is little information on the incidence and natural history of neuropathy in patients with non-insulin-dependent diabetes mellitus (NIDDM).Methods. We studied patients with newly diagnosed NIDDM and control subjects both at base line and 5 and 10 years later. Polyneuropathy was diagnosed on the basis of clinical criteria (pain and paresthesias) and electrodiagnostic studies (nerve conduction velocity and response-amplitude values). We investigated the relation between metabolic variables (results of oral glucose-tolerance tests, serum lipid and insulin concentrations, and glycosylated hemoglobin values) and the development of polyneuropathy.Results. In 10 years, 36 patients with NIDDM and 8 control subjects died; 86 patients and 121 control subjects completed the study. When the study ended, 18 percent of the patients were being treated only with diet, 59 percent with oral hypoglycemic drugs alone, 12 percent with insulin alone, and 11 percent with both insulin and oral hypoglycemic agents. At base line the prevalence of definite or probable polyneuropathy among the patients with NIDDM was 8.3 percent, as compared with 2.1 percent among the control subjects. These values 10 years later were 41.9 percent and 5.8 percent, respectively. The number of patients with NIDDM who had nerve-conduction abnormalities in the legs and feet increased from 8.3 percent at base line to 16.7 percent after 5 years and to 41.9 percent after 10 years. The decrease in sensory and motor amplitudes, indicating axonal destruction, was more pronounced than the slowing of the nerve conduction velocities, which indicates demyelination. Among the patients with NIDDM, those with polyneuropathy had poorer glycemic control than those without. Low serum insulin concentrations before and after the oral administration of glucose were associated with the development of polyneuropathy, regardless of the degree of glycemia.Conclusions. The prevalence of polyneuropathy among patients with NIDDM increases with time, and the increase may be greater in patients with hypoinsulinemia.