sur la prévention de complications à long terme sont insuffisantes. Les effets bénéfiques du traitement paraissent être liés en premier lieu au degré de réduction du taux de glycémie. L’étude UKPDS [4] a comparé trois classes de médicaments hypoglycémiants (sulfonylurées, metformine et insuline), mais cette étude n’a pas pu démontrer la supériorité d’une thérapie par rapport aux autres, hormis la metformine pour les complications cardiovasculaires. Le choix des antidiabétiques repose donc sur leur efficacité sur le contrôle glycémique et leurs autres effets susceptibles de réduire les complications à long terme, ainsi que sur leur profil de sécurité, leur tolérance et leurs coûts.

Diabetes mellitus ist die häufigste Stoffwechselerkrankung. In der Schweiz leiden etwa 250 000 Patienten daran. Etwa 90% der Fälle betreffen den Diabetes Typ II. Die Resultate der bisher grössten klinischen Studie auf dem Gebiet des Diabetes mellitus Typ II (United Kingdom Prospective Diabetes Study [UKPDSStudie]) zeigten, dass durch bessere und strengere Kontrollen des Blutzuckers und des Blutdrucks mikround makroangiopathische Komplikationen (d.h. Retinopathie und Nephropathie bzw. Myokardinfarkt und Apoplexie) signifikant vermindert werden können [1]. Im Rahmen von anderen grossen Studien (CARE, LIPID, 4S) wurde überdies gezeigt, dass durch Senkung der Blutlipidwerte sowohl die Mortalität als auch die Morbidität signifikant gesenkt werden kann [2–4]. Angesichts der Resultate dieser Studien wurde die Forderung nach besseren Kontrollen des Blutzuckers, des Blutdrucks und der Blutlipide in der ärztlichen Praxis erhoben. Auf diese Weise sollte eine Reduktion der Komplikationen, eine bessere Lebensqualität sowie günstige Auswirkungen auf die Krankheitskosten erreicht werden. Um die aktuelle Situation und den Wissensstand der Diabetiker in der Schweiz zu erfassen, wurde 1999 im Rahmen einer Initiative der Schweizerischen Diabetes-Gesellschaft (SDG) eine Umfrage durchgeführt. Die daraus gewonnenen Erkenntnisse sollen dazu dienen, gezielte Massnahmen zur Verbesserung der Lebensqualität von Diabetikern einzuleiten. Diese Umfrage stellt eine Ergänzung zur bereits 1995 durchgeführten Diabetiker-Befragung dar [5]. Die Ergebnisse der neuen Umfrage werden in diesem Artikel vorgestellt und mit den Ergebnissen der früher durchgeführten Umfrage verglichen.

The case is reported of a 36-year-old woman presenting with progressive hypercalcemia which led to the diagnosis of adrenocortical insufficiency of recent origin. Adrenal failure developed soon after septic shocks in this heparin anticoagulated patient post leg amputation for Buerger's disease. The clinical, biological and radiological (CT scan) data are consistent with bilateral adrenal hemorrhage as the cause of primary adrenal insufficiency. The pathogenesis of hypercalcemia in this condition is discussed.

The effect of glibenclamide treatment on insulin-mediated glucose disposal was studied in eight C-peptide-negative type I diabetic patients. The patients were studied twice by the euglycemic insulin clamp technique. One of the two experiments was preceded by glibenclamide treatment at the dose of 5 mg, three times daily for 15 days; half of the patients had the first test before and the second test after sulfonylurea treatment, and vice versa. Insulin was infused for four periods of 2 h each sequentially at 0.5, 1.0, 2.0, and 5.0 mU kg-1 min-1; for each insulin infusion period, the steady state plasma free insulin levels were comparable with or without glibenclamide. The mean +/- SEM plasma glucose concentration was 88 +/- 2 mg/dl in both experiments. The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). However, glucose disposal rates did not differ in the diabetic patients with or without glibenclamide treatment during the second, third, and fourth insulin infusion periods, which generated plasma free insulin levels in the supraphysiological range. These results provide evidence for an extrapancreatic effect of glibenclamide at low insulin concentrations during euglycemic clamping in patients with insulin-dependent diabetes mellitus. However, this effect was not reflected clinically in either an increased rate of hypoglycemic reactions or decreased insulin needs during the short term period of treatment.

Sensitivity to insulin in vivo was studied in six Type 1 diabetic patients without residual insulin secretion and without clinical insulin resistance, and in eight non-diabetic subjects, using the euglycaemic insulin clamp technique. Insulin was infused for four periods of 2 h sequentially at 0.5, 1.0, 2.0 and 5.0 mU · kg-1 · min-1; for each insulin infusion period the steady-state plasma free insulin levels were comparable in the diabetic and non-diabetic subjects. The mean ±SEM plasma glucose concentration was 4.9±0.03 mmol/l in the diabetic subjects (coefficient of variation of plasma glucose values: 5.7±0.7%) and 4.6±0.01 mmol/l in the control subjects (coefficient of variation: 5.1±0.6%). Insulin-mediated glucose disposal was lower in the diabetic than in the non-diabetic subjects at the two lower insulin infusion rates (mean±SEM = 2.03±0.27 versus 4.8±0.64 mg · kg-1 · min-1 at the first insulin infusion rate, p<0.01, and 5.59±0.59 versus 8.36±0.61 mg · kg-1 · min-1 at the second insulin infusion rate, p<0.01). However, insulin-induced glucose uptake did not differ significantly between the two groups at the third and fourth rates of insulin infusion. These results show that impaired insulin sensitivity in Type 1 diabetes is dependent on insulin concentration.

In vivo sensitivity to insulin was assessed by the euglycaemic insulin clamp technique in 5 type I diabetic subjects without residual insulin secretion and in 5 non-diabetic control subjects. Insulin was infused at increasing rates of 0.5, 1.0, 2.0 and 5.0 mU/kg/min in 4 periods of 2 hours. The diabetic subjects were resistant to insulin during the 1st and 2nd insulin infusion periods corresponding to the rates of 0.5 and 1.0 mU/kg/min, when compared to the non-diabetic subjects. However, glucose disposal rates were similar in the diabetic and control subjects at the 2 higher insulin infusion rates (2.0 and 5.0 mU/kg/min). Thus insulin resistance in type I diabetes is dependent on insulin concentration.