Impaired glucose tolerance in pancreas grafted diabetic patients is due to insulin secretory defects.

INTRODUCTION: Pancreas transplantation in diabetic patients can sustain insulin independence for years. The aim of the study was to measure the incidence of an impaired or diabetic glucose tolerance in patients after successful transplantation and analyse insulin resistance and insulin secretion. METHODS: 174 Type 1 diabetic recipients of simultaneous pancreas/kidney (SPK) transplants were investigated early (three months) and 95 patients late (five years) after transplantation using an oral glucose tolerance test combined with an iv arginine load. RESULTS: Although mean fasting blood glucose and HbA1c levels were within the normal range, only 65% of the patients displayed a normal glucose tolerance (NGT), whereas 25% had an impaired (IGT) and 10% showed a diabetic glucose tolerance (DGT). Fasting blood glucose and HbA1c values were significantly lower in patients with NGT compared to graft recipients with IGT or DGT, either three months or five years after SPK. Indicators of insulin resistance (fasting insulin, HOMA-IR, Matsuda/de Fronzo Index) were elevated in all graft recipients, but no differences were found between groups. In contrast insulin secretion was significantly reduced in patients with IGT and DGT early and late after transplantation. SUMMARY: Insulin resistance is a common feature after pancreas transplantation. However, either three months or five years after SPK abnormal glucose tolerance was mainly due to a reduced glucose- and arginine-induced secretory response of insulin.

[Hyponatraemic encephalopathy and rhabdomyolysis. Complications after preparation for colonoscopy with mannitol]. / Hyponatriämische Enzephalopathie und Rhabdomyolyse. Komplikationen nach Koloskopievorbereitung mit Mannit.

In the preparation for colonoscopy, it is necessary to drink a great deal of often hypo-osmotic fluid. Therefore, the electrolytes and intra- and extracellular water are disequilibrated. Most of the patients tolerate this without any subjective or objective symptoms. In our case, a young male patient suffered from a severe hyponatriaemia with encephalopathy for more than 48 h through the preparation for an elective ambulant colonoscopy with mannite. Furthermore, he developed a rhabdomyolysis (either through lying on the floor in coma for more than 9 h, through the hyponatriaemia itself or through compensation of the hyponatriaemia) that lasted for ca. 1 week.

Role of basic fibroblast growth factor in the pathogenesis of nodular goiter.

Thyroid epithelial cells are known to produce several growth factors and cytokines which influence thyroid cell growth and function in an autocrine and/or paracrine manner. It is already known that insulin-like growth factor I (IGF I) is overexpressed in toxic adenomas whereas epidermal growth factor (EGF) is found predominantly in thyroid neoplasia. We now investigated the expression of bFGF by immunohistochemistry in thyroid tissue of patients with toxic adenoma (n = 27), cold nodules (n = 27) and for comparison in Graves' disease (n = 5). In addition bcl-2-oncoprotein expression in these tissues were also detected by immunohistochemistry. Most of bFGF immunostaining was found in the connective tissue of all thyroid tissues with a predominance in adenomas and in Graves' diseases. The collagen surrounding the thyroid follicles close to their basal membrane were homogeneously and intensively stained. All the cytoplasm of fibroblast in the connective tissue were strongly positive. Within the cytoplasm of only 2-10% thyroid epithelial cells bFGF immunostaining was found without any difference between toxic adenomas or cold nodules. In the tissue of patients with Graves' disease, less than 2% of thyrocytes were stained. All thyroid epithelial cell showed clearly an immunostaining for bcl-2-oncoprotein in nodular goiter as well as Graves' disease.