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Biomedical subjects

G Turpin

Publications and source records attributed to G Turpin.

At least 199 records · Page 11Linked to original sources
PubMed1977

[Clinical, biological and genetic study of 500 cases of mixed hyperlipemia].

Based on 500 case histories, the writers discuss the main clinical signs, cardiovascular complications, lipide, glucide, and puride anomalies, and the genetic transmission observed in mixed hyperlipidemia. They stress a certain number of criteria which enable them to make mixed hyperlipidemia a specific clinical, highly frequent, and extremely formidable form of essential hyperlipidemia, falling between hyprecholesterolemia of type IIIa and endogenous hypertriglyceridemia of type IV. The variability of the electrophoretic phenotype from one patient to another, and in the same patient from one day to another, leads them to recommend a classification based on the values of plasma lipide fractions. A predominately late appearing genetic transmission of the autosome type supports this view.

Adolescent↗
PubMed1976

Apolipoprotein of the low density lipoprotein of human plasma: structural study in familial hyperbetalipoproteinemia.

Isolation of the low density lipoprotein (LDL) from human plasma was accomplished within a narrow density interval (1.030-1.045 g/ml). After covalent modification by maleic anhydride of the protein moiety and delipidation it was possible to fractionate, by ion-exchange chromatography, up to 35% of the protein into three peptides with distinctive amino acid compositions. These fractions appeared to be identical in normal individuals and in patients with familial hyperbetalipoproteinemia (FH). Our findings provide further evidence that in FH the abnormal catabolism of the protein moiety of LDL is not related to a modification of its structure.

Amino Acids↗
PubMed1975

[Mixed hyperlipidemia resistant to ordinary dietetic and medical treatment. 30 cases].

From 30 cases of mixed hyperlipidemia which were resistant to apparently correctly managed treatment, combining an adapted diet and Clofibrate, the authors confirmed that there is no specific clinical or laboratory picture in these cases: except for the constant presence of two beta-lipoproteins, with a high percentage of slow pre-beta, on electrophoresis on agarose, persisting throughout the length of inactive treatment. Analysis of the factors of resistance, whether exogenous and/or endogenous show that: bad adhesion to the "anticholesterol" diet (persistance of the supply of alcohol and/or sugar, insufficiency of unsaturated fats) and the incomplete reduction of a residual plethoric overload however minimal, constitute the two factors of resistance which are most easily picked out and overcome, but such factors are fat to be constantly causal. And in other cases, the contribution of drug interference or of considerable glycoregulation disorder remains to be excluded or discussed. In the absence of such factors or of their decisive role, a more specific cause of metabolic resistance had to be looked for. A disorder in Clofibrate mechanism, detected by gaseous chromatography in the form of an abnormal peak at C15 (clofibric acid) is found 12 hours or more after the last ingestion of the drug in certain cases. Binding of this molecule with VLDL, and perhaps with slow pre-betalipoprotens and nolonger with albumin, could explain the fault in metabolic clearance and in good metabolic utilization of this drug.

Adult↗