Although the impact of hypertension as a risk factor for brain infarction in diabetes mellitus is evident, the beneficial effect of antihypertensive therapy has not been demonstrated. Therefore, we designed a prospective cohort study to elucidate the effects of antihypertensive therapy on the development of ischemic stroke in diabetic outpatients. Two hundred forty patients, 219 non-insulin-dependent diabetes mellitus (NIDDM) and 21 insulin-dependent diabetes mellitus (IDDM), without history of cerebrovascular accident were followed for 8 years, from January 1981 until December 1988, in our diabetic clinic. Forty-eight of 88 hypertensive patients had received antihypertensive drugs. Among 40 untreated hypertensive and 152 initially normotensive diabetics, 14 hypertensives and 11 normotensives required antihypertensive therapy during followup period. Twenty-three patients were dropped out because of the unidentified reasons. Cerebrovascular accident occurred in 24 patients (10%): 18 brain infarctions, 4 transient ischemic attack (TIA), 1 subarachnoidal hemorrhage, and 1 brain hemorrhage. The percent incidence of ischemic strokes in the hypertension-treated patients was 8.9% which was similar to the 8.1% of the normotensives. In contrast, ischemic strokes developed in 29% of the untreated hypertensives, being significantly more frequent than in the former two groups. Multivariate analysis showed that serum total cholesterol and male gender were independent significant precursors of brain infarction in diabetic patients. In conclusion, antihypertensive treatment decreased the incidence of ischemic stroke in diabetics. Serum total cholesterol turned to independent risk factors for ischemic stroke in diabetic patients.

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PubMedDate not supplied

Effect of nicardipine versus enalapril on plasma endothelin-1 in hypertensive patients with type 2 diabetes mellitus.

We compared the effects of dihydropyridine type Ca channel blocker slow-release nicardipine and angiotensin converting enzyme inhibitor enalapril on plasma endothelin-1 (ET-1) levels in hypertensive type 2 diabetic patients (n=20). Nicardipine or enalapril was administered for 6 months by a crossover design. Nicardipine and enalapril comparably lowered blood pressure. Enalapril significantly reduced urinary albumin excretion in microalbuminuric patients, whereas nicardipine did not. Urinary beta2-microglobulin excretion was significantly increased during nicardipine treatment. However, both drugs significantly reduced plasma ET-1 as compared with pretreatment levels, close to that in healthy control (2.9 +/- 0.3 pg/ml in control, 4.8 +/- 0.3 pg/ml before treatment, 3.2 +/- 0.3 pg/ml during nicardipine vs before treatment p<0.05, 2.9 +/- 0.4 pg/ml during enalapril vs before treatment p<0.01). The decrease in plasma ET-1 was significantly correlated with the increase in natriuresis in normoalbuminuric patients treated with enalapril ( r= -0.82, p<0.01) but not in those treated with nicardipine. Although nicardipine and enalapril had different renal effects, both drugs equally suppressed plasma ET-1 levels in hypertensive patients with type 2 diabetes.

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PubMedDate not supplied

A case of insulin dependent diabetes mellitus following systemic treatment for Vogt-Koyanagi-Harada syndrome.

A 29-year-old man developed acute visual impairment, cough, and headache. Both eyes showed serous retinal detachment in the posterior fundus. Fluorescein angiography showed subretinal pooling of fluorescein in the late phase. A diagnosis of Vogt-Koyanagi-Harada (VKH) syndrome was made based on clinical features. Treatment with systemic corticosteroids resulted in improvement of uveitis and both eyes showed "sunset glow" fundus 11 months later. Insulin-dependent diabetes mellitus (IDDM) developed 13 months later (3 months after systemic corticosteroid therapy). Despite treatment with insulin, glycemic control was poor. Human leukocyte antigen (HLA) typing showed HLADR9 and DQB 1*0303 related to IDDM. We postulated that treatment with corticosteroids precipitated IDDM, a yet unknown common autoimmune mechanism might have caused IDDM and VKH, or both conditions occurred coincidentally.

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