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Biomedical subjects

J Fabre

Publications and source records attributed to J Fabre.

At least 163 records · Page 9Linked to original sources
PubMed1978

[Metabolites of hypoglycemic sulfonylureas in kidney failure. Experience with glibenclamide].

Renal insufficiency is a factor which predisposes to hypoglycemic accidents in subjects treated with hypoglycemic sulfonylureas. Glibenclamide (glyburide) is eliminated from the body mainly by metabolism, with the result that renal insufficiency has little effect on its biotransformation. In order to determine to what extent the retention of the metabolities intervenes in such hypoglycemic accidents, rats with ligatured ureters received intraperitoneal injections of 1 mg/kg glibenclamide or hydroxy-glibenclamide (the main metabolite), or of saline. For each animal there was a control animal which had undergone a simulated operation. For six rats with renal insufficiency, glibenclamide caused hypoglycemia of the same intensity as in the control group but more prolonged. With hydroxy-glibenclamide the glycemia was signficantly lower than in the control group. Hydroxy-glibenclamide has an obvious hypoglycemic activity which represents 1/6 of that of the parent drug, but 50--100 times that of tolbutamide. Its retention contributed to the intensification and prolongation of the hypoglycemic effect of glibenclamide in rats with renal insufficiency.

Acute Kidney Injury↗
PubMed1978

[Behavior of gentamicin in the kidney parenchyma. Studies on rats during and after treatment with therapeutic doses].

The injection in rats of 4 mg/kg gentamicin results in accumulation and continued presence of the antibiotic in the renal parenchyma compared with its rapid elimination from other tissues. With repeated injections at 24-hour intervals over a period of 3 weeks, gentamicin concentrations in the cortex reach 356 +/- 139 microgram/g after 1 week of treatment, i.e. levels 50 times higher than the maximum serum levels. They then stay at a saturation plateau before decreasing very slowly to levels of 50 microgram/g 2 weeks and 15 microgram/g 15 weeks after the last injection. The accumulation takes place mainly in the cells of the proximal convoluted tubule. In the medulla, gentamicin behaves similarly but the levels are lower. Weeks after the last injection, urine levels of gentamicin are still appreciable. In spite of this enormous accumulation, the treatment does not result in disturbance of renal function or striking morphological changes. These observations are based on dosages of gentamicin corresponding to those used clinically. Compared to earlier observations based on the supratherapeutic administration of the antibiotic, the present study provides a better understanding of the mechanisms involved in gentamicin nephrotoxicity.

Animals↗
PubMed1978

[Cutaneous plasmacytosis and polyclonal cryo-immunoglobulinemia].

A 65-year-old male patient is described who presented with (1) large violet cutaneous plaques on the left side of the body, characterized by dense plasmocyte infiltration of the dermis which appeared benign and largely negative to immunofluorescence, (2) massive polyclonal cryoglobulinemia (type III) without paraproteins, and (3) intermittently marked peripheral monocytosis and thrombopenia without significant medullary changes. Compared with the cases reported in the literature, and after a thorough immunological investigation, this syndrome cannot be entirely assimilated to any entity described up to the present time. Hypothetically, a reactional disorder is the most likely.

Aged↗
PubMed1978

[Complex pneumoconiosis in dental laboratory technicians].

Five cases of complex pneumoconiosis are described in dental prosthesis makers. The histo-spectrographic analysis with Castaing's microprobe of the lung fragment obtained by surgical biopsy revealed a complex disease associating silicosis of cobalt pneumoconiosis.

Adult↗
PubMed1978

Nephrotoxicity of gentamicin. Action on subcellular organelles and pharmacokinetics in the kidney.

Our findings on the renal pharmacokinetics of gentamicin explain why: (1) gentamicin concentrations in the kidney reach levels high enough to provoke injuries to the organelles; (2) the morphological manifestations of toxicity involve primarily the convoluted proximal tubule (which constitutes the largest part of the cortex), since antibiotic concentrations in this area are especially high; (3) nephrotoxicity is related to duration of treatment; (4) urine may contain small quantities of gentamicin up to 3 weeks after the end of therapy (14, 22, 30); (5) nephrotoxicity continues after discontinuance of the treatment, and (6) the hepatocytes, whose lysosomes are very sensitive to the action of gentamicin, show no obvious signs of toxicity, since the antibiotic never attains a high enough concentration in this organ.

Animals↗