Chronic diseases are frequent in homeless people. The aims of this study were to estimate the prevalence of diabetes in people living in shelters and to describe the characteristics of homeless people previously diagnosed with diabetes. Diabetes screening was systematically performed in nine shelters in Paris, from October to December 2006. We found a high prevalence of diabetes comparable with those of the general population, but a high frequency of major complications, in spite of a relatively young age, short duration since diabetes diagnosis and moderate glycaemic control. This study underlines the burden of diabetes among precarious people and supports the development of more effective strategies to improve diabetes management in this population, especially regarding podiatric care.
We have studied the pharmacokinetics and the effects of BIM 23,014 (BIM), a new, long-acting octapeptide somatostatin analogue, on basal and stimulated GH secretion in normal men. BIM 250 micrograms sc significantly reduced a GHRH-induced increase in plasma GH. The continuous sc administration of BIM for 24 h dramatically blunted spontaneous GH secretion; 2000 and 3000 micrograms daily reduced GH secretion to a greater extent than 1000 micrograms daily. During these experiments a significant negative correlation (r - 0.66) was found between plasma GH and BIM levels. Acute sc administration of 1000 micrograms BIM significantly reduced the rise in plasma GH observed in the second part of the oral glucose tolerance test. Plasma BIM levels peaked around 30 min, and the elimination half life was 90 min. Plasma BIM levels were below 1 ng/ml 6 h after the injection of 1000 micrograms BIM, and at that time GH started to rise again. We conclude that BIM 23,014 250 to 1000 micrograms sc is able to reduce the plasma GH response to GHRH or to the fall in glucose following an oral glucose tolerance test; a constant infusion of BIM, in doses 1000 micrograms daily, dramatically suppresses spontaneous GH secretion; 2000 micrograms/day by chronic subcutaneous infusion was the most effective dose of BIM in the suppression of GH secretion, and was associated only with minor adverse effects.
Changes in blood glucose homeostasis induced by the new somatostatin analogue BIM 23014 (BIM) were studied. Eight normal men (study 1) received either vehicle or 1000, 2000 and 3000 micrograms BIM as a 24 h s.c. infusion. Blood glucose, plasma insulin, C-peptide, glucagon and growth hormone (GH) were measured before treatment and then hourly for 24 h. In five normal men (study 2) an oral glucose tolerance test (OGTT) was performed during vehicle infusion and then on days 1 and 7 of a continuous s.c. infusion of 2000 micrograms BIM daily for 7 days. The same biological parameters as in study 1 were measured before OGTT and then twice-hourly for 5 h. Dose-dependent and transient glucose intolerance was observed in the first half of study 1. Except for glucagon, BIM significantly (P < 0.01) reduced plasma insulin, C-peptide and GH levels. In study 2 BIM infusion induced glucose intolerance and a drop in plasma insulin and C-peptide on day 1 which disappeared on day 7 of infusion. Higher on day 7 than on day 1, plasma GH secretion was significantly (P < 0.01) reduced throughout BIM infusion. In contrast plasma glucagon levels were not modified at any time. Side-effects were abdominal cramps and diarrhoea which were observed in most subjects when increasing BIM daily dose. In conclusion, BIM infusion induced transient changes in glucose homeostasis and insulin secretion in normal men. By contrast, plasma GH levels remained reduced throughout the treatment. BIM appears to be a useful tool to selectively inhibit GH secretion.
In order to evaluate the peripheral antiglucocorticoid activity of RU 486 in man we examined its ability to antagonize the effects of acutely administered glucocorticoids on blood leukocyte counts. The study was performed on eight normal male subjects. They were given 400 mg RU 486 (or placebo) orally at 0730 h and 1 mg dexamethasone (or placebo) orally at 0830 h, using a double-blind, cross-over, latin-square design with a one week interval between each of the four different treatments. Circulating eosinophils, lymphocytes, and neutrophils were counted at 0730 h and 1330 h, and their variations (1330 h counts/0730 h counts x 100) were compared under each treatment. For each cell type, dexamethasone induced variations (eosinophil and lymphocyte drop, neutrophil rise) which were significantly (P less than 0.05) different from those under the three other treatments; these latter treatments (placebo, RU 486, and RU 486 + dexamethasone) were equivalent to each other, inducing no variations of leucocyte counts. These data show that RU 486 inhibits dexamethasone induced leukocyte changes; this simple test provides a useful means to further analyse the peripheral antiglucocorticoid activity of RU 486 in man.
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