Capron L
Service de médecine vasculaire, Hôpital Broussais, Paris, France.
Diabete Metab. 1994 Nov;20(3 Pt 2):357-61.
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)
糖尿病大血管病变常被视为动脉粥样硬化的一种加速和加重形式。与糖尿病相关的几种生物紊乱部分解释了动脉粥样硬化可能加重的原因。这些紊乱包括血脂异常(甘油三酯浓度升高、低密度脂蛋白改变)、止血异常(血小板活性增加、纤溶活性降低)或动脉血管舒缩功能异常。然而,许多不确定性和不一致性仍然模糊了糖尿病与动脉粥样硬化之间的联系,这些联系仍属假设且存在争议。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增加。然而,除了动脉粥样硬化恶化之外的其他因素可能解释这些关联。例如,几项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与动脉粥样硬化的关系并不像通常认为的那样密切。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,记录最充分且最合理的是动脉硬化——一种单纯的动脉壁硬化(无脂质沉积),在其晚期可损害组织血管化。动脉硬化被认为是动脉老化的正常结果,而在糖尿病中会加速。慢性高血糖是糖尿病患者动脉风险的一个独立且有影响的标志物。它可通过形成晚期糖基化终产物(AGEs)增强动脉基质各种成分的非酶糖基化,从而刺激动脉硬化。(摘要截取自250词)