Enalapril, captopril, and blood glucose.
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Biomedical subjects
Publications and source records attributed to P Passa.
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Opinions diverge as to the frequency of hypoglycaemia in patients under continuous subcutaneous insulin infusion (CSII). In this prospective study the incidence and severity of hypoglycaemia were evaluated in 10 type I brittle diabetic patients under conventional treatment (period A), then under chronic treatment with CSII for at least 1 year (period B: the first 3 months; period C: the last 3 months). Metabolic control (as assessed from mean blood glucose, glycaemia lability indices and glycosylated haemoglobin A1) significantly improved between periods A and B (p less than 0.01). The occurrence of biochemical hypoglycaemia (less than 3 mmol/l) was reduced by 52% and that of clinical hypoglycaemia by 60%. The results observed in period C were not different from those observed in period B. One hypoglycaemic coma occurred under CSII (as opposed to 4 during period A); it was secondary to reduction in food intake and had no sequelae. Thus, in this study, the improvement in metabolic control was associated with a reduction in the frequency and severity of hypoglycaemia. We consider that patients presenting with frequent and severe attacks of hypoglycaemia under conventional insulin treatment can and should benefit from CSII.
The relation between blood glucose control and erythrocyte adhesion to cultured human vascular endothelial cells was studied in 12 Type 1 (insulin-dependent) diabetic patients. Erythrocyte adhesion was measured before, 8 days and 6 weeks after continuous subcutaneous insulin infusion (CSII). Compared to controls, erythrocyte adhesion expressed as an adhesion ratio was increased in 10 diabetic patients at the first examination (adhesion ratio greater than 1.52). After 8 days, adhesion ratio was normalized in 5 patients. After 6 weeks, adhesion ratio was normal in 7 patients and significantly lower in the group of 12 patients (p less than 0.01). The adhesion ratio was significantly correlated with glycosylated haemoglobin values (p less than 0.001). Insulin did not directly affect erythrocyte adhesion. Adequate insulin treatment modifies erythrocyte adhesion through a metabolic effect which needs longer than 1 week to be effective.
A patient with typical clinical and biochemical features of a glucagonoma also presented obvious signs of hypokalemia, indicating combined secretion of renin by the tumor. The latter was voluminous, was located in the tail of the pancreas and was of a malignant nature as shown by the development of secondary hepatic metastases. Syndromes associated with glucagonoma and mixed or combined insular tumors are reviewed in detail.
Renal Kallikrein, an enzyme of the distal tubule acting through kinin liberation, may participate to the control of renal circulation and blood pressure. To study if an impairment of its secretion may exist in diabetics, a cross-sectional study was carried out on 40 non-hypertensive and 29 hypertensive diabetics, compared to 30-age related controls. Urinary Kallikrein Activity (UKA) was measured by its kininogenase activity with and without trypsin preincubation. Compared to UKA in controls (86 +/- 9 micrograms lysyl-bradykinin [LBK] produced per minute of incubation), UKA was significantly reduced either in non-hypertensive diabetics (59 +/- 8 micrograms LBK. min.-1; p less than 0.05) and in hypertensive diabetics (26 +/- 6 micrograms LBK. min.-1; p less than 0.001). The ratio of total/active urinary kallikrein was similar in diabetics and in controls. The decline of UKA in diabetics was related to the duration of their disease (r = -0.38; p less than 0.05) and to their stage of retinopathy (r = -0.46; p less than 0.001). UKA values were proportional to creatinine clearance in diabetics (r = 0.58; p less than 0.001). The lowest UKA values were found in patients with a high urinary excretion of albumin (above 500 mg/day): 8 +/- 2 micrograms LBK. min-1 (p less than 0.001) and beta-2-microglobulin (above 382 micrograms/day): 12 +/- 4 micrograms LBK. min-1 (p less than 0.001). These findings support that an impaired secretion of renal kallikrein in diabetics can be related to the duration of diabetes and to the severity of microangiopathy.
Eighty insulin treated diabetics from North or West Africa were interviewed and compared to 80 French controls matched for sex, age and duration of insulin-therapy. Modalities and access to medical care in a specialized clinic were studied. African people were predominantly blue collar workers (49%) and French people employees (70%). The percentage of unemployed people was similar. Africans performed blood glucose self testing less frequently (35.5% vs 60.5%). Only 40% (vs 75%) participated in specific educational activities because 40% of the migrants did not read French. Despite insulin treatment being similar, metabolic control was worse among migrants (HbA1: 10.5 +/- 2.4 vs 9.3% +/- 1.9; p less than 0.01). In migrants, there was an increased prevalence of degenerative complications which did not reach statistical significance. Three parameters may explain these differences: less strict follow-up, poorer knowledge, lower socioeconomic status.
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The treatment of arterial hypertension in diabetic patients still raises numerous problems. In this type of patients, the most commonly prescribed drugs (beta-blockers, diuretics, antihypertensive agents acting on the central nervous system) have troublesome and potentially detrimental effects (e.g. effects on lipids). The new categories of antihypertensive drugs recently introduced (angiotensin-converting enzyme inhibitors, calcium antagonists) are likely to be most useful in these patients. In an open trial in non-insulin-dependent diabetics with arterial hypertension followed-up for 1 year, enalapril administered alone has proved effective and devoid of clinical and biochemical side-effects. If these results are confirmed, angiotensin-converting enzyme inhibitors will rank high as first-choice treatment of arterial hypertension in diabetics.
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The mechanisms of tachycardia in hyperthyroidism were investigated by means of Holter recordings of heart rate in 45 patients, 33 of whom had sinus rhythm and were left untreated. In the remaining 12 patients, recordings were taken after 3 days of treatment with either propranolol (120 mg/day; 6 patients) or pindolol (15 mg/day; 6 patients). Propranolol is a beta-blocker devoid of intrinsic sympathetic activity whereas pindolol possesses such activity. Changes in heart rate under the influence of each of these drugs were compared with those observed in 96 controls similarly treated. The difference in baseline heart rare between day and night was significantly higher (p less than 0.01) in patients with hyperthyroidism (17 +/- 1 QRS/min) than in controls (13 +/- 1 QRS/min). Day and night heart rates were increased by pindolol, the increase in night heart rate being significantly greater (p less than 0.05) in patients with hyperthyroidism (23.4 +/- 4.9%) than in controls (11.6 +/- 2.6%). These results suggest that sinus tachycardia in hyperthyroidism is related to an increase in the number of myocardial beta-adrenoceptors. They also indicate that thyrotoxicosis should not be treated with beta-blockers possessing intrinsic sympathetic activity.
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The aim of this prospective, randomized, double-blind, placebo controlled study was to investigate the effect of nifedipine on carbohydrate metabolism in diabetic patients after a 3-day and a 3-month course of treatment. Sixteen non obese, well controlled non-insulin dependent diabetics, (HbA1 less than 10%), with moderate untreated hypertension were divided in two groups: nifedipine (group N, 8 patients) and placebo (group P, 8 patients). An oral glucose tolerance test (OGTT, 75 g glucose) and an arginine infusion were performed before, after a 3-day, and a 3-month course, either of nifedipine 30 mg/D or placebo. Blood samples obtained during OGTT were assayed for glucose and insulin, and during arginine infusion for insulin, glucagon and growth hormone. The differences between basal and peak values during tests were compared between both groups before and after treatment using Wilcoxon's rank sum test. Neither acute nor chronic administration of nifedipine or placebo modified the glucose tolerance. However, basal insulin levels were reduced by 3 month-administration of nifedipine (from 19 +/- 2 micromicrons/ml to 10 +/- 1 micromicrons/ml, p = 0,01). Otherwise the basal and peak hormonal values during tests were not significantly affected by nifedipine either at the start of after 3 months of treatment. These results suggest that nifedipine, when given in standard dosage for 3 months, has minor effects on carbohydrate metabolism in non-insulin dependent diabetic patients.
Insulin release is coupled with a calcium entry into the pancreatic B cells. The use of calcium-antagonists may eventually alter glucose homeostasis. To evaluate this possibility, nicardipine action was tested both in vitro and in vivo: 1. on insulin release and vascular resistances from isolated perfused rat pancreases; 2. on 7 hypertensive patients with an established glucose intolerance, during two oral glucose tolerance tests (OGTT) performed successively under placebo and nicardipine (90 mg daily) at a two-week interval. In vitro, the basal insulin release from isolated perfused rat pancreases (86 +/- 15 ng.min-1; n = 27; M +/- SE) was inhibited according to the nicardipine dose by the 5 th min. of infusion: 7.2 +/- 1.5 p.100 of the initial output at 10(-4) M (n = 6; p less than %.001); 33.4 +/- 2.7 p.100 at 10(-6) M (n = 6; p less than 0.001); 87.5 +/- 14.8 p.100 at 10(-8) M (n = 6; ns). The pancreatic vascular resistances declined significantly for the 3 doses, but no dose-response could be registered. In vivo, the mean arterial blood pressure was significantly reduced by nicardipine from 114 +/- 3 mmHg to 95 +/- 3 mmHg (p less than 0.001) without any significant alteration of either glucose tolerance (glycaemias at the 120 th min of OGTT: 9.2 +/- 1.1 mmol.l-1 vs 8.9 +/- 1.2 mmol.-1) or insulin peak: 70 +/- 20 micrograms U.ml-1 vs 67 +/- 22 microU.ml-1.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovascular diseases represent the major cause of premature death in diabetics. These patients usually die in an intensive care unit or a cardiological clinic, not in a diabetic clinic. In the acute phase of a myocardial infarct the determination of glycosylated haemoglobin is the best indicator for the diagnosis of diabetes. During the first month after the myocardial infarct the mortality among diabetics is double that of the general population. The causes of this phenomenon are multiple, some of which may be prevented. In the case of diabetics coronary insufficiency is characterised by an unquestionable clinical and prognostic specificity whereas, from the therapeutic point of view, the purely cardiological problems are identical with those found in non-diabetics.
Acebutolol may induce the development of antinuclear antibodies and, exceptionally, of a lupus-like syndrome. The purpose of this study was to evaluate the prevalence of antinuclear antibodies in hypertensive diabetics under long-term treatment with acebutolol. Seventy-eight normal subjects, 75 diabetics under antidiabetic therapy only, and 75 hypertensive diabetics who received acebutolol in mean doses of 478 +/- 242 mg/day for at least one year were investigated. The 3 groups were comparable with regard to age and sex. Antinuclear antibodies were detected in 18.6% of diabetics under acebutolol, as against 3.8% and 1.3% respectively of subjects in the other groups (p less than 0.01). There was no correlation between the levels of antinuclear antibodies and the dosage or duration of acebutolol treatment. None of the sera tested contained antinative DNA antibodies, and none of the hypertensive diabetics exhibited signs of lupus-like syndrome.