Search PubMed⌕ Search

Biomedical subjects

G Chabrier

Publications and source records attributed to G Chabrier.

At least 55 records · Page 3Linked to original sources
PubMed1984

[Renal glutamine metabolism in man during treatment with sodium valproate].

The administration of 1500 mg sodium valproate to 20 patients provoked in the kidney an increased glutamine uptake correlated with an increased ammonia release, as shown by the changes of the renal arterial-venous concentration differences of glutamine and ammonia. VPA's action on the renal cell may perhaps constitute a valid model for elucidating the effects of this drug on neurons.

Adult↗
PubMed1984

[Hyperammonemia and decrease of growth and nocturnal locomotion in rats with portal stricture and uremia].

In order to make clearer the pathogenesis of hepatic coma, the clinical tolerance of progressive levels of chronic hyperammonemia were studied in the rat. Increases of blood ammonia in the range of 200 to 600 micrograms/dl were produced within 4 weeks by stricture of the portal vein associated with progressive rises in blood urea resulting from reduction of the renal mass and/or addition of urea to the food. The portal stricture produces a collateral circulation allowing a hepatic bypass of portal blood and the ammonia level of this blood is proportional to the amount of circulating and alimentary urea hydrolyzed in the digestive tract. Only the highest hyperammonemias were associated with decreased nocturnal locomotion of the rats and decrease in the growth rate. The latter was correlated with the ammonia levels. No animal presented signs of coma. These results suggest a good cerebral tolerance by the rat of important chronic hyperammonemias which however seem to have an anorexic effect.

Ammonia↗
PubMed1983

[Apoproteins A1 and B as markers of the severity of cirrhosis].

Since apolipoproteins A1 and B (Apo A1 and Apo B), which are the quantitatively predominant fractions of plasma lipoproteins, are synthetized and/or metabolized in the liver, their variations could represent a significant prognostic factor in patients with cirrhosis. In order to test this theory, the concentrations of Apo A1 and Apo B were measured in 43 patients with confirmed cirrhosis and were found to be reduced. These changes correlated with a number of biochemical tests measuring hepatic function and indicating severe cirrhosis, as well as with a clinico-biological severity index based on these biochemical tests and on the importance of clinical complications during the course of the disease. It is concluded that Apo 1 and Apo B determinations constitute a valuable index of liver synthetizing function.

Apolipoprotein A-I↗
PubMed1983

[Quantitative evaluation of hormonal extraction performed by continuous plasma exchange in euthyroid patients. Application to the treatment of severe hyperthyroidism].

Plasma exchanges (PE) have been successfully used in the treatment of thyroid storm. The dramatic results obtained (as in the case reported here) have prompted the authors to evaluate the effects of PE on plasma thyroid hormone (T4, T3 and unbound T4) levels and thyroxine-binding globulin (TBG) levels in 5 euthyroid patients. PE of one blood volume consistently produced a significant decrease in T4, T3 and TBG levels without changes in unbound T4 or TSH. Hormone extraction was proportional to the volume of blood removed and correlated with the amount of TBG extracted. Compared with the estimated total plasma content, the percentage of unbound T4 extracted was superior to that of total T4, which suggests release of free hormones from the intracellular compartment. Repeated PE in the same patient resulted in a transient decrease in T4 without changes in TSH. These results indicate that PE constitutes a fast, simple and effective means of removing thyroid hormones in all emergencies related to thyrotoxicosis. The fact that TSH levels remain stable after PE shows that the thyroid balance in euthyroid subjects is unaffected by this method.

Evaluation Studies as Topic↗
PubMed1983

Sodium valproate-induced hyperammonemia in the rat: role of the kidney.

The intravenous injection of sodium valproate (VPA) 200 mg/kg provoked in fasting rats a 100% increase in the arterial NH+4 concentration by the 10th min. The increase persisted at this level for at least 100 min. Simultaneous measurements of NH+4 and glutamine concentrations in the carotid artery, renal vein and suprahepatic vein showed that there were increases in the release of NH+4 and the uptake of glutamine by the kidney while the [NH+4] of suprahepatic venous blood remained stable. In binephrectomized rats injected with VPA, NH+4 levels did not change. These results suggest that the VPA-induced arterial hyperammonemia depended on the accelerated catabolism or possibly the reduced synthesis of glutamine by the kidneys. The liver of fasting rats does not seem to play a preponderant role in the VPA-induced hyperammonemia.

Ammonia↗
PubMed1983

Sodium valproate associated with phenobarbital: effects on ammonia metabolism in humans.

Treatment with sodium valproate (VPA) in association with phenobarbital (PB) is accompanied by a greater systemic hyperammonemia than treatment by VPA alone. The anatomical origins of this difference were studied by injecting a dose of 1,500 mg VPA i.v. into six unmedicated patients and six epileptics chronically treated with PB and measuring the ammonium (NH4+) concentration difference between arterial blood and renal, hepatic, internal jugular, and femoral venous blood. In unmedicated patients, arterial [NH4+] rose moderately, secondary to an increased amount of NH4+ released into the general circulation by the kidney; the hepatic metabolism of NH4+ remained normal. In epileptics treated with PB, arterial [NH4+] rose massively, partly as a result of the increased NH4+ release by the kidney and partly because of disturbance of the hepatic metabolism of NH4+. These results provide a clearer understanding of the potentiation of the secondary effects of VPA by PB.

Adult↗
PubMed1983

The renal origin of sodium valproate-induced hyperammonemia in fasting humans.

Acute administration of 1,500 mg of sodium valproate or chronic administration of 30 mg/kg/24 hours induced a more than twofold increase of renal ammoniagenesis in fasting subjects. Hyperammonemia was moderate, as normal hepatic ammonia detoxification persisted. Renal uptake of glutamine increased simultaneously.

Adult↗
PubMed1983

[Role of hyperammonemia in stuporous states induced by sodium valproate].

Stuporous states induced by sodium valproate (VPA) are accompanied by an isolated marked hyperammonemia. In reality, hyperammonemia occurs after administration of VPA even in the absence of neurological complications. The hyperammonemia is of purely renal origin and results from modifications in glutamine metabolism, this compound being the main precursor of amino acid neurotransmitters. Combined administration of VPA and phenobarbitone increases the level of hyperammonemia due to lack of detoxification by the liver of the excess of ammonia produced by the kidneys. The anatomical site of origin of the ammoniogenesis, and its intensity, were studied in two patients with a history of stuporous states during combined VPA-phenobarbitone treatment. A single injection of VPA at a later date when they were being treated by combined phenobarbitone-carbamazepine therapy, induced disturbances in ammonia metabolism which did not differ qualitatively from those observed when intolerance to VPA is lacking. It is therefore not possible to rely on simple biological tests to detect patients at risk. Correlation is also lacking between the degree of hyperammonemia and disorders of vigilance. Ammonia does not therefore appear to be the only factor responsible for neurological complications and the role of other factors must be investigated. These include: disturbances of metabolism of inhibitory and excitatory aminoacid neurotransmitters, the condition of the cerebral parenchyma, and the excitatory effect of sodium valproate which could act to varying degrees in synergy with the hyperammonemia to provoke a stuporous state.

Adult↗
PubMed1982

Effect of diabetic control on the level of circulating thyroid hormones.

Basal plasma levels of thyroxine (T4), triiodothyronine (T3) and reverse T3 were determined by radioimmunoassay in 44 control subjects, 44 Type 1 (insulin-dependent) and 39 Type 2 (non insulin-dependent) diabetic patients aged from 15 to 75 years. All were clinically euthyroid. The quality of diabetic control was assessed by the percentage of glycosylated haemoglobin. In both the diabetic groups there was a significant decrease in T3 and a rise in reverse T3 whereas T4 was normal. We found no significant differences between plasma thyroid hormone levels in Type 1 and Type 2 diabetic patients. In the poorly controlled diabetics (glycosylated haemoglobin greater than or equal to 12%), T3 was 90 +/- 5 ng/dl, which differed significantly from the level found in the better controlled patients (106 +/- 5 ng/dl, p less than 0.01). In the diabetic patients without associated illness, a negative linear correlation was found between T3 and glycosylated haemoglobin and a positive correlation between reverse T3/T3 and glycosylated haemoglobin. No correlation between T3 or reverse T3 and fasting blood glucose could be established. In conclusion, many diabetics showed a low T3 syndrome suggesting that there may be an impairment in the extrathyroidal conversion of T4 to T3. This may well be enhanced by a poor diabetic control (glycosylated haemoglobin greater than or equal to 12%).

Adolescent↗
PubMed1982

[Study of muscular metabolism of ammonia in the posterior limbs of the intact rat].

In order to evaluate the ammonia, glutamine, and alanine muscular uptake and/or release, we have studied the effects of ammonium acetate perfusions, in intact anaesthetized rat hindquarters, by simultaneous measure of blood flow and arterio-venous differences of ammonia, glutamine and alanine concentrations. Increasing doses of ammonium acetate perfusions (1.23-2.46-3.69 nmol/mm/100 g b.w.) result in an increase of ammonia rat hindquarters uptake which is correlated with the amount of ammonium infused and the arterial ammonia levels but without significant release or uptake of glutamine or alanine. However these perfusions induce an arterial hyperglutaminemia and hypoalaninemia likely due to extramuscular metabolic changes in these two amino-acids.

Acetates↗
PubMed1980

[Thyrotoxicosis with low T3 and high reverse T3 levels. 9 cases (author's transl)].

In common forms of hyperthyroidism serum levels of triiodothyronin (T3) are higher than those of thyroxin (T4) and isolated elevations of serum T3 have even been noted. We report 9 cases of proven hyperthyroidism with normal or low levels of T3 and elevated T4 and reverse T3 (rT3). Most out of the patients were more than seventy years old and had associated diseases. Our data show that the low T3 with elevated rT3 syndrome--which has been noted in many metabolic and pathologic conditions--can coexist in hyperthyroidism. They emphasize the lack of diagnostic discrimination of T3 assays in thyroid dysfunction especially in the older patient or one with associated disease.

Adult↗
PubMedDate not supplied

[Hyperthyroidism and immune hemolytic anemia following amiodarone therapy].

We report the cases of two patients who, after prolonged amiodarone therapy developed hyperthyroidism and immune haemolytic anaemia. Antibodies were of the IgG type and non-specific at elution. A search for other causes of haemolytic anaemia with positive Coombs' test gave negative results. Antiamiodarone antibodies have recently been discovered; they reflect an immunological disturbance due to this drug and might be responsible for some of the undersirable effects of amiodarone. In our patients, hyperthyroidism and haemolytic anaemia were induced by a dual mechanism: accumulation of amiodarone and induction of an effect of this drug on the immune system.

Aged↗