[糖尿病患者大血管受累机制]。

Diabete & metabolisme Pub Date : 1994-11-01
L Capron
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引用次数: 0

摘要

糖尿病大血管病变通常被视为动脉粥样硬化的一种加速和加重形式。几种与糖尿病相关的生物学紊乱部分解释了动脉粥样硬化可能加重的原因。如血脂紊乱(甘油三酯浓度升高,低密度脂蛋白改变)、止血障碍(血小板活性增加,纤溶活性降低)或动脉血管运动障碍。然而,许多不确定性和不一致性仍然混淆了糖尿病和动脉粥样硬化之间的联系,这仍然是假设和有争议的。临床经验和所有临床流行病学研究表明,糖尿病患者缺血性动脉疾病(冠心病、下肢缺血、脑缺血事件)的发病率和严重程度都有所增加。然而,除了恶化的动脉粥样硬化外,中间产物可能解释了这些关联。例如,一些基于常规尸检的解剖学流行病学研究一致发现,糖尿病患者的动脉粥样硬化病变(斑块)比非糖尿病患者更大、更广泛。因此,糖尿病大血管病变的基本机制可能并不像通常认为的那样与动脉粥样硬化密切相关。在可以解释糖尿病患者动脉风险增加的非动脉粥样硬化病变中,最具文献记录和最可信的是动脉硬化——动脉壁的纯粹硬化(没有脂质沉积),其晚期形式可以损害组织血管化。动脉硬化被认为是动脉老化的正常结果,而糖尿病会加速动脉老化。慢性高血糖是糖尿病患者动脉危险的独立而重要的标志。它可以通过晚期糖基化终产物(AGEs)的形成,增强动脉基质各种成分的非酶糖基化,从而刺激动脉硬化。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Mechanisms of macrovascular involvement in diabetic subjects].

Diabetic macroangiopathy is often viewed as an accelerated and aggravated form of atherosclerosis. Several biological disturbances that are associated with diabetes partially account for a possible aggravation of atherosclerosis. Such are disorders of blood lipids (increased triglyceride concentration, modifications of low density lipoproteins) of haemostatis (increased platelet activity, decreased fibrinolytic activity) or of arterial vasomotility. Yet, many uncertainties and inconsistencies still obfuscate the links between diabetes and atherosclerosis, which remain hypothetical, and debatable. Clinical experience and all clinical epidemiological studies show that the incidence and severity of ischaemic arterial diseases (coronary heart disease, lower limb ischaemia, cerebral ischaemic events) are increased in diabetic individuals. However, intermediates other than worsened atherosclerosis may account for these associations. For instance, several anatomical epidemiological studies, based on routine autopsies, have note consistently found that atherosclerotic lesions (plaques) are larger and more extensive in diabetic than in non-diabetic individuals. The basic mechanisms of diabetic macroangiopathy could therefore be not as closely related to atherosclerosis as is usually thought. Among the non-atherosclerotic lesions that could explain the increased arterial risk in diabetic patients, the best documented and most plausible is arteriosclerosis--a pure sclerosis of the arterial wall (without lipid deposition) which, in its advanced forms, can compromise tissue vascularization. Arteriosclerosis is considered as a normal consequence of arterial ageing which would be accelerated in diabetes. Chronic hyperglycaemia is and independent and influent marker of arterial risk in diabetic patients. It could stimulate arterial sclerosis by enhancing non-enzymatic glycation of various components of the arterial matrix, through formation of advanced glycation end-products (AGEs).(ABSTRACT TRUNCATED AT 250 WORDS)

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