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  • 1
    ISSN: 1432-0428
    Keywords: Key words Nicotinamide ; insulin-dependent diabetes mellitus ; C-peptide ; insulin therapy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nicotinamide has been recently introduced, in addition to intensive insulin therapy for patients with recent-onset insulin-dependent diabetes mellitus (IDDM) to protect beta cells from end-stage destruction. However, available data are conflicting. A double blind trial in 56 newly-diagnosed IDDM patients receiving nicotinamide for 12 months at a dose of 25 mg/kg body weight or placebo was designed in order to determine whether this treatment could improve the integrated parameters of metabolic control (insulin dose, glycated haemoglobin and C-peptide secretion) in the year after diagnosis. In addition to nicotinamide or placebo, patients received three to four insulin injections daily to optimize blood glucose levels. Patients treated with nicotinamide or placebo received similar doses of insulin during follow-up and 1 year after diagnosis with comparable glycated haemoglobin levels (6.7 ± 1.8 % nicotinamide vs 7.1 ± 0.6 % placebo). Basal and glucagon stimulated C-peptide secretion detectable at diagnosis were similarly preserved in the course of 12 months follow-up both in nicotinamide and placebo treated patients. No adverse effects were observed in patients receiving nicotinamide. When age at diagnosis was taken into account, nicotinamide treated older patients ( 〉 15 years of age) showed significantly higher stimulated C-peptide secretion than placebo treated patients (p 〈 0.02). These results suggest that nicotinamide can preserve and improve stimulated beta-cell function only in patients diagnosed after puberty. We conclude that in these patients nicotinamide can be added to insulin at the time of disease diagnosis to maintain and possibly improve residual beta-cell function. However, further studies on patients diagnosed after puberty are needed to confirm whether nicotinamide can be considered an additional tool to insulin in early-onset IDDM. [Diabetologia (1995) 38: 848–852]
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-5233
    Keywords: Hypertension ; Non-insulin-dependent diabetes ; Microalbuminuria ; Lisinopril ; Nifedipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of the angiotensin-converting enzyme lisinopril were compared with those of the calcium antagonist nifedipine in 162 non-insulin-dependent diabetic hypertensive patients for a 24-week period. In 83 and 79 patients, respectively, lisinopril and slow-release nifedipine produced similar reductions in blood pressure (systolic/diastolic: −16/−13 mmHg supine and −14/−11 mmHg standing after lisinopril; −15/−12 mmHg supine and −14/−11 mmHg standing after nifedipine). Fasting and post-prandial plasma glucose, glycosylated haemoglobin and plasma lipids appeared to be unaffected by either agent. Also, 28% of the patients on lisinopril and 30% of those on nifedipine presented microalbuminuria. Both drugs induced a reduction in the albumin excretion rate (AER). The geometric meanxx: tolerance factor of the reduction in AER among the 23 microalbuminuric patients on lisinopril (−10.0xx:1.3 μg/min) was greater, though not significantly so, than that observed in the 26 on nifedipine (−0.9x:1.2 μg/min). Moreover, lisinopril appeared to be better tolerated than nifedipine in our study population. Microalbuminuria is an important risk factor for cardiovascular mortality in non-insulin-dependent diabetic patients as well as in the general population. To what extent a reduction in the AER could ameliorate the cardiovascular prognosis in non-insulin-dependent diabetic patients is, at present, unknown. Finally, both lisinopril and nifedipine showed a similar antihypertensive effect in these patients which was not associated with significant differences in plasma glucose, insulin or lipid concentrations. The clinical consequences of the insignificant differences in AER remain unclear.
    Type of Medium: Electronic Resource
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