[Parodontopathy revealing insulin-dependant diabetes].
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Biomedical subjects
Publications and source records attributed to F Comte.
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Serum and urinary levels of Cinoxacin and pipemidic acid were determined at 7-day intervals in the same 10 healthy volunteers after a single oral dose of respectively 500 and 400 mg of the drugs. Comparison of results shows that Cinoxacin was absorbed faster (absorption half-life, ta 1/2cin = 0.25 h) than pipemidic acid (ta 1/2pip = 0.37 h) and distributed in a smaller apparent volume (AVDcin = 23.5 1/1.73 m2; AVDpip = 60.1 1/1.73 m2). Biological half-lives were identical (tb 1/2cin = 2.10 h; tb 1/2pip = 2.15 h). On the other hand, serum levels for Cinoxacin at 1, 2 and 4 hours (8.1 +/- 1.5 micrograms/ml, 10.6 +/- 1.5 micrograms/ml, 5.6 +/- 1.3 micrograms/ml respectively) were higher than those for pipemidic acid (3.3 +/- 0.3 micrograms/ml, 3.4 +/- 0.5 micrograms/ml, 2.1 +/- 0.5 micrograms/ml respectively). Urinary excretion of the two derivatives during the 12 hours following their administration was similar (Ucin0-12h = 86%; Upip0-12h = 83%). Mean urinary concentrations were particularly high, still attaining respectively 90 +/- 29 micrograms/ml and 131 +/- 38 micrograms/ml in samples collected between the 9th and the 12th hours; these levels were well above the M.I.C. for the Gram-negative organisms included within the spectrum of activity of these two quinolones. In addition, predictive calculations of serum levels reached after multiple dosing indicate that at an administration rate of 500 mg every 6 or preferably every 4 hours, Cinoxacin concentrations should be sufficiently high to be of interest in the treatment of systemic infections by sensitive organisms.
Hyperammonemia is observed in high protein diet fed cirrhotic and is thought to be related to an increased intestinal ammoniagenesis. We studied this problem in control rats and rats with a portal stricture and portal systemic shunts given a high protein or a standard diet. In those animals the systemic, portal and renal venous ammonemia and glutaminemia were measured. In rats with portal stricture on a high protein diet, the increase in systemic ammonemia did not significantly differ from that found in animals on a standard diet. In contrast, the control group exhibited a higher level (P less than 0.001) of systemic ammonemia after a high protein (102 +/- 7 SEM mumol/l) than after standard diet (36 +/- 1). This hyperammonemia appeared to be of renal origin since there was a significantly higher ammonia difference between renal venous and arterial blood with the high protein than with standard feeding, both in rats with a portal stricture (+ 229 +/- 32 vs. + 24 +/- 8 mumol/l; P less than 0.001). and in control rats (+ 196 +/- 23 vs. + 2 +/- 11; P less than 0.001). This increased renal ammonia release into the circulation induced by the high protein diet was associated with a high renal uptake of circulating glutamine. Moreover, a decreased ammonia passage from the digestive tract into the portal vein and disappearance of intestinal uptake of circulating glutamine was also observed with the high protein feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
Insulin secretion is assessed by simultaneous radioimmunological assay of insulin (R.I.I.) and C-peptide (R.I.C.P.) levels under basal conditions, and after stimulation by oral or intravenous glucose administration. Subjects with abnormal glucose tolerance demonstrate an increase in the ratios R.I.C.P. divided by glucose and R.I.C.P. divided by R.I.I. after fasting, increase in R.I.I. and R.I.C.P. occurring later and lasting longer after glucose loading. These anomalies are observed in both obese subjects and those with normal body weights. Simultaneous determination of R.I.I. and R.I.C.P. levels appears of value in a limited number of cases where glucose loading tests do not supply precise information on the quality of glucose tolerance. Obese subjects, in whom abnormal hyperglycemia levels provoked by oral glucose are observed, but in whom the peripheral glucose assimilation coefficient is normal, can be considered to be non-diabetic as shown by the levels of R.I.I. and R.I.C.P. and more particularly by the molar ratio R.I.C.P. divided by R.I.I.