Vanadium and sodium retention in cirrhosis.
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Biomedical subjects
Publications and source records attributed to P Couzigou.
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Chronic calcifying pancreatitis (CCP) is rare in countries with low alcohol consumption except in some tropical countries where malnutrition is widespread (southwest India) and in which CCP occurs in young non-alcoholics. In Black Africa sporadic cases of CCP have been reported in English-speaking countries (Uganda, Nigeria). The purpose of this study was to: a) assess the geographical distribution of CCP in French-speaking Africa; b) estimate the relative proportion of alcoholic CCP (ACCP) and juvenile tropical pancreatitis (JCCP). A total of 92 cases were included in this study, conducted in 16 French-speaking African countries (including Madagascar). There were no cases in countries with partly desert to climates and Moslem populations. Of these 92 cases, 86 corresponded to ACCP due to over consumption of various types of alcoholic beverages depending on the region. All were males with a mean age at diagnosis of 40.7 yrs. The remaining 6 cases were JCCP which were observed in areas of malnutrition with low intakes of animal protein and lipids. In this group the male/female ratio was 1/1 and the mean age at discovery was 15 yrs. Manioc toxicity did not appear to play any role. The "mixed" form, i.e. associating current alcohol consumption with childhood malnutrition, which has been described in young moderate drinkers in Burundi, was a possibility in 4 of the 86 cases of ACCP.
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Twelve, healthy fasting, subjects received 200 mg cimetidine orally either with water or 1 g sucralfate in a randomized, single dose, two-way crossover study. Blood samples were taken for 12 h and urine was collected for 24 h. Cimetidine in plasma and urine was analysed by HPLC. There was no significant difference between the two treatments in peak plasma concentration, time to peak plasma concentration, area under the plasma concentration-time curve and urinary excretion. The results indicate that sucralfate did not reduce the bioavailability of cimetidine.
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A case of hepatic encephalopathy revealing congenital hepatic fibrosis in a 47-year-old woman is reported. The characteristic features of this observation were: a) the long clinical latency of a congenital disease usually discovered in childhood or in adolescence; b) the existence of hepatocellular insufficiency which appeared without any other reason than an ordinary infection; c) the absence of digestive bleeding or portacaval shunt, factors always found in the rare, previously described cases of encephalopathy in congenital hepatic fibrosis.
Following acute intoxication with alcohol, 8 patients developed 16 episodes of arrhythmia, including 15 supraventricular tachycardias and one torsade de pointe. Seven of the 8 patients were chronically abusing of alcoholic drinks. None of the patients had clinically obvious cardiac pathology nor echocardiographic evidence of myocardiopathy. In 7 of them, however, baseline electrocardiograms disclosed disorders of intra-atrial conduction. The role of the different factors which might determine the occurrence of arrhythmia (notably alcohol, the autonomic nervous system, associated metabolic abnormalities and absorption of medicines) is discussed.
Moderate alcohol consumption is associated with lower cardiovascular mortality. The effect of moderate alcohol intake during 5 weeks on lipoproteins, especially on the high density lipoprotein (HDL) cholesterol total (of which the levels are inversely predictive of coronary heart disease) and apoproteins A, A1 and B, was studied in 7 normal men. HDL cholesterol total appreciated by the heparin manganese precipitation method and phosphotungstate magnesium method increased (p less than 0.01) during alcohol consumption. The composition of HDL was modified by alcohol consumption: increase of the esterified/total cholesterol ratio (p less than 0.05) and phospholipids (p less than 0.05) without significant modification of triglycerides. Low density lipoprotein and very low density lipoprotein did not vary significantly. Apoprotein A1 increased during alcohol consumption (p less than 0.05) with a transitory increase of apoprotein A. There was no significant modification of apoprotein B.
The pattern of gammaglutamyl transpeptidase levels was studied in the sera of 25 subjects with hyperthyroidism and 11 subjects with hypothyroidism, before and after treatment, and in 14 age- and sex-matched control subjects. Gammaglutamyl transpeptidase levels were significantly increased in hyperthyroidism (65 +/- 59 U/l) (p less than 0.01) and significantly decreased under treatment (40 +/- 27 U/l) (p less than 0.001). Before treatment, gammaglutamyl transpeptidase levels correlated with alkaline phosphatase levels and 5'-nucleotidase levels, the correlation persisting after treatment with 5'-nucleotidase. Alkaline phosphatase levels significantly increased under treatment (p less than 0.01). The percentages of gammaglutamyl transpeptidase variation correlated with thyroxine (r = 0.44, p less than 0.03), triiodothyronine (r = 0.47, p less than 0.02) and latent fixation capacity (r = 0.44, p less than 0.03) variations. Subjects with hypothyroidism had significantly decreased gammaglutamyl transpeptidase levels before treatment (18 +/- 9 U/l, p less than 0.01). Alkaline phosphatase levels were significantly decreased before treatment, and significantly increased after treatment. For all subjects with hyperthyroidism of hypothyroidism, the percentages of gammaglutamyl transpeptidase variations correlated with thyroxine (r = 0.48, p less than 0.003) and triiodothyronine (r = 0.39, p less than 0.016) variations. These results suggest that variations in gammaglutamyl transpeptidase levels in hyperthyroidism and hypothyroidism are, at least in part, in relation with variations in thyroid hormone levels.
Peripheral lymphocyte subpopulations have been quantified by a direct and indirect, immunofluorescence technique, using monoclonal antibodies, in 22 patients with continued heavy drinking, hepatocellular dysfunction (spider angiomata, ascites, and factor V decrease) (group I), in 16 patients with a history of heavy drinking and abstinence maintained for at least 6 months and hepatocellular dysfunction (group II) and in 28 patients admitted for continued heavy drinking, without hepatocellular dysfunction (group III). Sixteen normal subjects were studied as controls. The total number of lymphocytes and T lymphocytes (OKT3+) were significantly reduced (p less than 0.001) in groups I and II. A significant decrease of B lymphocytes was observed in group II (p less than 0.02). The OKT8+ lymphocytes were significantly reduced in group I (p less than 0.01) and in group II (p less than 0.001); the decrease of the OKT4+ lymphocytes was significant in group II (p less than 0.01) only. The OKT4/OKT8 ratio was higher in group I (p less than 0.05) and group II (p less than 0.01) than in the control group. Normal values of total lymphocytes, B lymphocytes, T lymphocytes subsets and OKT4/OKT8 ratio were observed in group III. In group III, the lymphocyte subpopulations and OKT4/OKT8 ratio were similar in patients with or without abnormalities of liver function tests. In group I and II, no correlation was found between the lymphocyte subpopulations or the OKT4/OKT8 ratio and factor V or nutritional status assessed by anthropometrical and biological tests. T-cell imbalance in alcoholic liver disease does not seem to be related to alcohol consumption, factor V decrease or malnutrition.
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Ethanol metabolism was studied in ten male non-alcoholic subjects following the constant intravenous infusion of ethanol (1.2 g/kg) administered during three hours with and without cimetidine. Pharmacokinetic analysis was performed on the pseudolinear portion of the elimination curve. The mean peak ethanol concentrations were not significantly different with and without cimetidine. There was no acceleration of ethanol metabolism at high concentrations: the ethanol elimination rate was similar above and under 17 mM, with and without cimetidine. Cimetidine administration had no effect on pharmacokinetic parameters of ethanol (area under the curve, Km and Vm). The fact that the ethanol elimination rate is similar whatever be its concentration and the absence of modifications of the pharmacokinetic parameters by cimetidine are not in favor of an important role of the microsomal ethanol oxidizing system (MEOS) in the ethanol metabolism of nonalcoholic subjects. The data do not allow to examine the role of MEOS in ethanol metabolism after chronic alcohol consumption.
Emesis is a common symptom in pheochromocytoma. It occurs in 26% of cases with permanent secretion, and 43% of cases with paroxystic secretion. Emesis may be the initial manifestation as in the present report of a 54-year-old female patient. For more than 15 years she experienced emesis which was ascribed to biliary dyskinesia. Bilateral pheochromocytoma was then diagnosed. With reference to this case, digestive manifestations of pheochromocytoma are reviewed.
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Eleven patients with ascitic cirrhosis and eleven patients without liver disease received 200 mg of cimetidine orally and intravenously. Plasma concentrations of cimetidine were analysed by high pressure liquid chromatography. No differences were observed in cimetidine half-life (2.53 +/- 0.63 and 2.33 +/- 0.40 h) between the two groups. Cimetidine clearance was diminished by about 30 p 100 in cirrhotic patients (0.426 +/- 0.138 vs. 0.649 +/- 0.163 l/h/kg). The apparent volume of distribution was also significantly diminished (1.50 +/- 0.44 vs. 2.14 +/- 0.55 l/kg) in patients with cirrhosis and ascites.
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