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糖尿病并发症的病理生理学:葡萄糖假说能解释多少?

The pathophysiology of diabetic complications: how much does the glucose hypothesis explain?

作者信息

Nathan D M

机构信息

Diabetes Unit, Massachusetts General Hospital, Boston 02114, USA.

出版信息

Ann Intern Med. 1996 Jan 1;124(1 Pt 2):86-9. doi: 10.7326/0003-4819-124-1_part_2-199601011-00002.

DOI:10.7326/0003-4819-124-1_part_2-199601011-00002
PMID:8554219
Abstract

OBJECTIVE

To examine the putative pathogenetic mechanisms of the long-term, specific complications of diabetes mellitus.

DATA SOURCES

Literature review relevant to long-term diabetic complications and their pathogenesis.

STUDY SELECTION

Studies of animal models of diabetes, epidemiologic investigations of diabetes and its long-term complications, and interventional studies examining intensive treatment of diabetes and its effect on the development and progression of complications.

DATA SYNTHESIS

Diabetic retinopathy, nephropathy, and neuropathy occur in all clinical forms of diabetes mellitus, regardless of the cause of the diabetes. Hyperglycemia appears to be the major variable shared among these different clinical forms; and epidemiologic data, studies in animal models of diabetes, and the results of recent interventional studies such as the Diabetes Control and Complications Trial, all support an important and perhaps dominant role of hyperglycemia in the pathogenesis of complications. However, the diverse complications may not share the same pathogenesis. Different pathogenetic mechanisms may operate in different types of diabetic complications or at different stages of specific complications, or both.

CONCLUSIONS

The level of chronic glycemia is the best established concomitant factor associated with diabetic complications. The mechanism by which hyperglycemia might cause complications remains unknown, and evidence for a uniform pathogenetic mechanism is far from established.

摘要

目的

探讨糖尿病长期特定并发症的假定发病机制。

资料来源

与糖尿病长期并发症及其发病机制相关的文献综述。

研究选择

糖尿病动物模型研究、糖尿病及其长期并发症的流行病学调查,以及探讨糖尿病强化治疗及其对并发症发生和发展影响的干预性研究。

资料综合

糖尿病视网膜病变、肾病和神经病变见于所有临床类型的糖尿病,无论糖尿病的病因如何。高血糖似乎是这些不同临床类型共有的主要变量;流行病学数据、糖尿病动物模型研究以及近期干预性研究(如糖尿病控制与并发症试验)的结果,均支持高血糖在并发症发病机制中起重要且可能占主导地位的作用。然而,各种并发症可能并不具有相同的发病机制。不同的发病机制可能在不同类型的糖尿病并发症中起作用,或在特定并发症的不同阶段起作用,或二者皆有。

结论

慢性血糖水平是与糖尿病并发症相关的最明确的伴随因素。高血糖可能导致并发症的机制尚不清楚,且统一发病机制的证据远未确立。

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