Weidmann P, Boehlen L M, de Courten M, Ferrari P
Medizinische Poliklinik, University of Berne, Switzerland.
J Hum Hypertens. 1992 Dec;6 Suppl 2:S23-36.
Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
糖尿病(DM)相关的代谢改变和高血压会同时加速或引发脑血管疾病和冠心病、肾病、视网膜病变以及广泛的大血管病变,从而使糖尿病患者面临非常高的发病、致残和过早死亡风险。因此,糖尿病患者的长期护理应旨在同时控制代谢和血压(BP)。饮食措施必不可少;建议采用高纤维、低脂肪、低盐饮食,当体重超过理想体重时,辅以热量限制和体育锻炼。抗糖尿病药物治疗存在一个尚未解决的难题。要实现理想的血糖正常水平,需要有效剂量的胰岛素,但高胰岛素血症(由于胰岛素依赖型糖尿病的肠外[过度]治疗)被怀疑会促进动脉粥样硬化形成,是冠心病的危险因素,甚至可能会加重高血压。考虑到抗高血压药物治疗,噻嗪类或袢利尿剂在糖尿病中是有问题的药物,因为它们会加重代谢改变。这些药物对左心室肥厚(LVH)似乎也只有有限的预防或逆转作用;β受体阻滞剂也不被认为是理想的药物,因为它们会降低低血糖的意识,并倾向于促进葡萄糖不耐受。特别是非选择性β受体阻滞剂会促进外周缺血和胰岛素诱导的低血糖,而无内在拟交感活性的β受体阻滞剂会降低血清高密度脂蛋白胆固醇。钙拮抗剂和血管紧张素转换酶(ACE)抑制剂具有同等的降压效果,不会损害碳水化合物和脂质稳态或外周灌注,并且可以有效改善LVH。某些ACE抑制剂甚至可能会轻微改善异常的胰岛素敏感性和血糖水平。虽然α受体阻滞剂具有这些大多数理想的特性,但这些药物在糖尿病患者中更容易引发体位性低血压。非噻嗪类利尿剂吲达帕胺和5-羟色胺2拮抗剂酮色林也兼具降压效果和代谢中性。治疗的最终目标是改善生活预后。在原发性高血压中,基于高剂量利尿剂的传统药物治疗能令人满意地降低脑血管并发症,但不能降低冠心病并发症或猝死。在糖尿病患者中,抗高血压治疗对预后的影响尚未进行前瞻性评估。基于回顾性分析,Warram等人报告,仅接受利尿剂治疗的糖尿病患者的死亡率比未治疗高血压的糖尿病患者高3.8倍(《内科学文献》。1991年;151:1350)。H. H. Parving计算得出,有效控制糖尿病肾病患者的血压可能会使10年死亡率从约65%降至20%(《高血压杂志》。1990年;8[增刊7]:187)。(摘要截取自400字)