Sodium fusidate and increased remission rate of insulin-dependent diabetes mellitus.
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Biomedical subjects
Publications and source records attributed to D Papalia.
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The antihypertensive effect of nitrendipine, 20 mg once daily was studied in 30 patients with mild or moderate hypertension and type II diabetes mellitus under metabolic control. Blood pressure was measured at the end of a 15-day washout period from previous antihypertensive treatment and on the 15th, 30th, 60th, and 90th day of treatment. Systolic blood pressure and diastolic blood pressure were significantly reduced by nitrendipine. The reduction involved lying and orthostatic blood pressure and was maintained throughout the treatment period. Heart rate, fasting and postprandial glycemia, and lipid profile were not significantly affected by nitrendipine. It is concluded that this drug effectively lowers blood pressure in diabetic hypertensive subjects with no alteration of lipid and glucose metabolism.
Recent studies suggest that opioid peptides may influence the secretion of pituitary gland hormones. Since obese patients often show impaired growth hormone (GH), prolactin (PRL) and cortisol responses to stimuli and raised beta endorphin levels, the opioid regulation of such hormone secretion could be different from that in normal weight subjects. In order to verify this hypothesis we studied the effect of iv naloxone, an opiate receptor antagonist, on GH, PRL and cortisol response to insulin-induced hypoglycemia in 9 obese female subjects. Seven normal weight females were used as control group. A control test using saline showed that the PRL and GH responses to insulin stress were impaired in obese subjects, whereas no difference was seen in the cortisol response. Naloxone did not modify the PRL and GH response but provoked a rise in the cortisol response in both obese and normal weight subjects. These findings suggest that while the opioid peptides do not play an important role in regulating the GH and PRL response to insulin hypoglycemia, they influence the cortisol response. In obese patients the impairment in GH and PRL response to stimuli cannot be related to alterations in opioid peptide regulation.
symptomatic dilated cardiomyopathy were studied in order to evaluate the effect of long term sympathetic beta-blockade with metoprolol. Clinical evaluation, stress test, two-dimensional echocardiography, 24 hour ambulatory electrocardiography and hemodynamic assessment with Swan-Ganz catheter were performed before enrollment in the study. Patients were randomly assigned to the relative placebo (8 pts) or metoprolol group (12 pts) in a single-blind fashion. The placebo group received standard therapy (digitalis, diuretics, vasodilators and anticoagulants as needed), while the metoprolol group, along with standard therapy received low-dose beta-blockade, starting with 6.25 mg twice daily and then doubling every 4 days on the two daily administrations. The therapeutic end-point was 100 mg. Patients received less than 100 mg if their systolic blood pressure was less than 100 mmHg or if their resting heart rate was less than 55 beats/min. Patients were clinically assessed every month and a 24-hour electrocardiography, echocardiography and hemodynamic control was repeated after six months. In the metoprolol group there was one sudden death and two drop-outs.(ABSTRACT TRUNCATED AT 250 WORDS)
It is well known that many cardiovascular drugs affect digoxin kinetics, but nothing is defined on propafenone-digoxin interaction. To clarify this problem, we studied digoxin kinetics in 8 healthy men, who received digoxin oral dose (0.50 mg) in the control state and again during maintenance therapy with propafenone (150 mg q.i.d.). Statistically significant changes were observed during propafenone in a number of digoxin kinetic indexes: a rise in peak serum digoxin concentration (4.30 vs 3.07 ng/ml - p less than 0.005), in area under the serum-digoxin concentration curve (4 h: 520.4 vs 368.9; 10 h: 789.6 vs 621.3 ng X min/ml - p less than 0.005; 24 h: 1187.6 vs 954.7 ng X min/ml - p less than 0.05) and urinary excretion of digoxin (277.7 vs 203.5 mcg - p less than 0.005). Renal digoxin clearance was not affected by propafenone. We conclude that propafenone interact kinetically with digoxin in healthy subjects, perhaps increasing digoxin bioavailability.
The aim of this study is to test left ventricular diastolic function in coronary artery disease patients with preserved systolic performance. Two groups of patients (25 coronary artery disease patients with angiographic proved coronary artery stenosis, but with normal hemodynamic and angiographic indices of systolic phase, first group; and 14 normal subjects for control, second group) were tested comparing their systolic and diastolic ventricular function indices, obtained by using a Millar microtip catheter and a computerized program. Systolic ventricular function was similar in the two groups (EF: 0.61 +/- 0.05 vs 0.62 +/- 0.03, p: n.s.; Vmax:120 +/- 28 vs 112 +/- 24 sec-1, p: n.s.), while diastolic indices were significantly different (lowest diastolic pressure: 3.7 +/- 2.4 vs -1.72 +/- 1.45 mmHg, p less than 0.01; end-diastolic pressure: 11.2 +/- 4.2 vs 6.5 +/- 2.8 mmHg, p less than 0.05; T constant: 45 +/- 8 vs 35 +/- 6 mmHg, p less than 0.001; end-diastolic compliance: 2.79 +/- 0.3 X 10(-2) vs 5.68 +/- 0.4 X 10(-2) mmHg-1, p less than 0.001; Kp: 0.041 +/- 0.006 vs 0.003 +/- 0.004 p less than 0.001). In conclusion, impairment of left ventricular diastolic phase may be one of the earliest manifestations of functional alterations of ischemic ventricle.
The effects of somatostatin (SRIF) infusion on blood sugar, immunoreactive insulin (IRI), immunoreactive glucagon (IRG) and C-peptide after administration of oral glucose load (100 g) to 23 obese subjects were examined. The latter were divided in two groups according to oral glucose tolerance (OGTT): (1) normal OGT; (2) impaired OGT. During SRIF infusion IRI and C-peptide response to oral glucose was significantly reduced in both groups as compared with the response under saline infusion. Blood sugar values fell markedly in the second group. After SRIF infusion ended a marked increase in C-peptide, IRG and blood sugar was observed. The results suggest that SRIF infusion is only able to inhibit the release of IRI and IRG temporarily. They do not demonstrate if the behaviour of blood sugar is influenced by variations of these hormones or by the direct effect of SRIF infusion on absorption of the glucose load.
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