Biomedical subjects

X Debussche

Publications and source records attributed to X Debussche.

22 records · Page 2Linked to original sources

PubMedDate not supplied

Overwhelming strongyloidiasis in a diabetic patient following ACTH treatment and keto-acidosis.

A non insulin-dependent Zairian patient developed ketoacidosis and then overwhelming strongyloidiasis following ACTH treatment. Severe cardiovascular and respiratory failure, associated with severe acute hypoprotidemia, preceded death, which occurred within three days. Pathologic examination revealed a massive parasitic infiltration of the gastro-enteric mucosa, mesenteric lymph nodes, and the pulmonary tissue and vessels. We suggest that ACTH treatment and keto-acidosis induced immune deficiency and triggered the acute parasitic episode, in a patient originating from an endemic area. Badly controlled diabetes should be known as a risk factor of hyperinfection by Strongyloides stercoralis in latent carriers.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Course of pancreatic beta cell destruction in prediabetic NOD mice: a histomorphometric evaluation.

The course of pancreatic beta cell destruction during the prediabetic period of autoimmune diabetic syndromes is not precisely known. We have analyzed the course of insulitis (n = 140) and the beta cell and lymphocytic volume densities by morphometric methods (n = 80) in NOD mice aged 6 to 45 weeks. In the absence of diabetes the mean beta cell density was only slightly reduced with age: 0.64 +/- 0.04% glandular tissue (mean SEM; n = 12) in 6 wk-old mice, 0.52 +/- 0.06% in 45 wk-old mice (n = 12; ns). However, a minority of pancreases were free of insulitis or showed isolated periinsulitis at the end of the 45-wk follow-up period. Invasive insulitis (i.e. mononuclear cells invading the islet area) was detected in 60-85% of mice from the 12th week on. In non overtly diabetic mice, beta cell density was reduced only when insulitis was invasive in more than 40% of islets: 0.30 +/- 0.03%, (n = 11) vs 0.59 +/- 0.04% (n = 34) in moderately invasive insulitis (p < 0.05). These mice had significant metabolic abnormalities. In diabetic mice, the beta cell density was markedly decreased: 0.02 +/- 0.01% (n = 7; p < 0.001). On the whole, a lymphocytic infiltrate affecting less than 50% of the islet volume was compatible with a normal beta cell density. Beyond this 50% lymphocytic infiltration threshold, beta cell density was tightly and negatively related to the lymphocytic volume density.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMedDate not supplied

Metformin effects on peripheral sensitivity to insulin in non diabetic obese subjects.

Using the euglycaemic insulin-clamp technique we examined the effects of one-month metformin treatment on peripheral glucose utilization in non diabetic obese subjects. Two groups of obese subjects were studied in comparison with untreated lean women. Group 1 (n = 6) experienced weight loss (BMI: 32.6 +/- 1.7 vs 34.8 +/- 1.6 kg/m2, p < 0.05) but not group 2 (n = 7; BMI before and after treatment: 34.6 +/- 3.2 and 34.8 +/- 3.1 kg/m2). After a continuous insulin infusion of 40, 100, and 350 mU/m2/min we estimated the tissue sensitivity to insulin by the determination of Km, the glucose disposal (M), and the amount of glucose metabolized per U insulin (M/I ratio). After the metformin treatment the mean Km decreased by 31% in group 1 (p < 0.05) but not significantly in group 2; M and M/I were not modified in the two study groups. In conclusion, in non diabetic obese subjects, metformin seems not to affect peripheral insulin-mediated glucose metabolism unless there is weight loss.

Adolescent↗

PubMedDate not supplied

Pentamidine-induced dysglycaemia: experimental models in the rat.

In order to analyse further the pathophysiology of pentamidine effects on blood glucose regulation, the following experimental models were established in rats: impairment of the renal function, bile duct ligation, inhibition of the P450 cytochrome enzyme system. In otherwise intact rats, 7.5 mg/day pentamidine was well tolerated whereas doses of 15 mg/day induced severe, relapsing and eventually lethal hypoglycaemia within a few days. Induction of a renal insufficiency of graded severity by treatment with gentamycin, subtotal nephrectomy and total bilateral nephrectomy resulted in repetitive, severe (sometimes lethal) hypoglycaemia, alternating with hyperglycaemia, glucosuria and ketonuria in pentamidine-treated rats (7.5 mg/d). No long-standing insulin-dependent diabetes was observed. In the dysglycemic animals, plasma insulin levels were inappropriate to the concomitant glycaemia; no stimulation was obtained by i.v. glucose. Glucagon levels were higher than normal, suppressible by i.v. glucose, responsive to IV arginine and to hypoglycaemia. Dysglycemic events were more frequent and marked in the rats with the most severe renal functional derangement. They were more frequent in the rats treated with pentamidine mesylate than in those treated with the isethionate salt. Control uremic rats (free of pentamidine) remained euglycaemic. The islets of Langerhans displayed severe vascular congestion and degranulation and necrosis of the B cells, while the non B cells (and particularly the A cells) were intact. Exocrine pancreatitis was occasionally observed in the most severely uremic rats. In contrast with uremic rats, neither surgical ligation of choledocus, nor treatment by P450 cytochrome inhibitors (particularly ketoconazole) precipitated dysglycaemia in the pentamidine-treated rats. These experimental data: 1) strengthen the concept of inappropriate insulin release from pentamidine-lesioned islet B cells due to pentamidine accumulation; 2) indicate a predominant role for renal insufficiency in determining the accumulation of this drug; 3) emphasize the clinical importance of renal insufficiency as a risk factor for pentamidine-induced dysglycaemia. Association with ketoconazole does not appear to be a risk factor.

Animals↗