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持续皮下胰岛素输注对糖尿病神经病变影响的自身对照研究

A self-controlled study of the effect of continuous subcutaneous insulin infusion on diabetic neuropathy.

作者信息

Haug P J, Kelly T M, Cannon R B, Edwards C Q

机构信息

Department of Medicine, LDS Hospital, Salt Lake City, UT 84143.

出版信息

J Neurol Sci. 1987 Dec;82(1-3):123-32. doi: 10.1016/0022-510x(87)90012-8.

Abstract

Ten patients with poorly controlled type I diabetes mellitus and a documented complication of their disease were observed during 6 months of conventional diabetic management followed by 6 months of insulin infusion pump treatment and home blood glucose monitoring. Median nerve conduction velocity (NCV) was inversely correlated with the glycosylated hemoglobin (HbA1c) level at entry into the study (r = 0.71; P less than 0.05). The mean HbA1c value at the end of the conventional treatment period was 14.3% and fell to 10.1% by completion of the pump treatment period (P less than 0.0001). The median NCV was significantly greater at the completion of the infusion treatment period than it was at the end of the conventional management portion of the study. However, the rate of increase in NCV during the infusion period was not greater than the rate established during the prior treatment period. In addition, change in HbA1c levels during the pump treatment period did not correlate with change in conduction velocity for any of the nerves studies. These results from a self-controlled study of continuous subcutaneous insulin infusion indicate that improved blood glucose control without normalization of metabolic parameters is not sufficient to reverse the functional deterioration of large, fast-conducting nerve fibers that occurs in type I diabetes.

摘要

对10例I型糖尿病控制不佳且有明确疾病并发症的患者进行观察,先进行6个月的传统糖尿病管理,随后进行6个月的胰岛素泵输注治疗及家庭血糖监测。研究开始时,正中神经传导速度(NCV)与糖化血红蛋白(HbA1c)水平呈负相关(r = 0.71;P<0.05)。传统治疗期结束时HbA1c的平均水平为14.3%,至胰岛素泵治疗期结束时降至10.1%(P<0.0001)。输注治疗期结束时正中NCV显著高于研究中传统管理部分结束时。然而,输注期NCV的增加速率并不高于先前治疗期所确定的速率。此外,胰岛素泵治疗期HbA1c水平的变化与所研究的任何神经的传导速度变化均无相关性。这项连续皮下胰岛素输注的自身对照研究结果表明,血糖控制改善但代谢参数未恢复正常不足以逆转I型糖尿病中发生的大的、快速传导神经纤维的功能恶化。

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