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Biomedical subjects

J Truffert

Publications and source records attributed to J Truffert.

At least 37 records · Page 2Linked to original sources
PubMed1981

[Atherogenous mixed hyperlipidaemia with predominant slow pre-betalipoprotein overload: type IVb (author's transl)].

Together with the rare dysbetalipoproteinaemia (type III) and with combined beta- and pre-betalipoproteinaemia (type IIb), slow pre-betalipoproteinaemia (type IVb) belongs to the group of mixed hyperlipidaemias, where both blood cholesterol and triglycerides are raised. From a study of 30 patients, 10 of whom benefited from ultracentrifugal separation of lipoproteins, the authors define type IVb hyperlipidaemia, characterized by an equal increase in triglycerides and cholesterol and by the fact that the cholesterol overload is almost entirely due to slow pre-betalipoproteins. This particular type undoubtedly plays a part in the development of atherosclerosis.

Arteriosclerosis↗
PubMed1981

Double screening test at 8th and 12th hour of overnight fasting for a better classification of idiopathic hyperlipidemias. Large scale study of 505 tests.

Total blood cholesterol, plasma triglycerides, and lipoprotein electrophoresis have been studied 8 and 12 hours after a standard meal. In controls and in familial hypercholesterolemia, plasma triglycerides were normal at 8th and 12th hour of fasting. In mixed hyperlipidemia, as in endogenous hypertriglyceridemia, plasma triglycerides were abnormally high at the 8th hour of fasting. Difference of 8th-12th hour triglycerides levels was greater in these two groups than in controls and in familial hypercholesterolemia. These results suggest than the 8th jour value will rectify a mistaken classification or detect a latent hyperlipidemia.

Adult↗
PubMed1980

[Dynamic study of the changes in the composition of fatty acids in serum lipid fractions under a diet rich in polyunsaturated fatty acids].

Appropriate adjustment of diet and specially reduction of the saturated fatty acids content is the cornerstone of correcting many hyperlipidemias. What we have tried in our study was first to show the evolution of the changes in the serum's fatty acids composition under a rich polyunsaturated fatty acids diet, second to find an index proving that the diet had correctly been taken. Chromatographic analysis were performed after ultracentrifugal separation of the lipoprotein fractions. Seven volunteers, non fat, and normolipemics were selected. Samples were collected every three or five days before and during the diet. The whole test lasted twenty days. What had been shown is that the linoleic acid content increased but the one of the oleic acid decreased in all lipoprotein fractions. Those changes are bestly illustrated by using the (formula: see text) ratio as a kinetic index. The triglycerid fraction modifications are faster than the phospholipid's one. Concerning the other fatty acids, the modifications are less spectacular : the palmitic acid decrease in every lipids fractions and the palmitoleic acid has a significant decrease only in the esterified cholesterol. And the stearic acid has no variation at least significatively.

Adult↗
PubMed1977

[Severe hypercalcemia during hyperthyroidism].

A particularly high hypercalcemia (141 mg/ml) was observed in a man with Graves' disease. An intense muscle asthenia, with lack of dynamism and vomiting which may cause dehydration, are the most suggestive signs of hypercalcemia. Bone biopsy and above all parathormone estimations permit one to eliminate associated hyperparathyroidism. The efficacy of mithramycin used alone, without any other hypocalcemic drug, was remarkable. The direct responsibility of thyrotoxicosis as a cause of the calcium disorder seems undoubted but the precise mechanism of the hypercalcemia remains unexplained.

Adult↗
PubMed1977

Gout and hyperlipidaemia. Effect of overweight on the levels of circulating lipids.

A study of the serum lipids in 90 patients with gout and 90 controls matched for age and weight index demonstrated that in gout there was a significant elevation of the mean serum levels of cholesterol (282 +/- 55 mg/100 ml), triglycerides (183 +/- 161 mg/100 ml) and phospholipids (270 +/- 61 mg/100 ml) compared with the controls whose mean values were respectively 243 +/- 41 mg, 95 +/- 53 mg and 245 +/- 36 mg. Hyperlipidaemia of mixed type was the most common lipid defect in the patients with gout; there was no difference in the frequency of pure hypercholesterolaemia (without hypertriglyceridaemia) between gout and the controls. The frequency of anomalies of blood lipid levels in gout does not result from (or not solely from) obesity since patients with gout and controls were matched for their weight and height. There was a correlation between the serum lipid levels and obesity in the controls but this was not demonstrable in the patients with gout.

Adult↗
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↗
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↗
PubMed1975

[Detection and distriburion of slow pre-betalipoprotein in agar gel electrophoresis of total serum in 204 cases of mixed hyperlipidemia].

The demonstration in certain sera by electrophoresis an Agar gel, according to Noble's technique, of a further band of intermediate pre-betalipoprotein, between the betalipoproteins and the usual rapid pre-betalipoproteins, led to the designation of this fraction under the name of slow pre-betalipoprotein or pre-beta-lipoprotein. To the rare studies so far published on this subject, we bring here our contribution in the form of a routine analysis of the variations, and not only the presence, but also the relative concentration of the slow pre-beta-lipoproteins with regard to the rapid prebetalipoproteins. On the fasting serum, after 12 hours fasting, comparative studies of normal control subjects (104 cases) of essential hypercholesterolemia, with or without tendinous xanthomas, corresponding to type IIa (110 cases), mixed hyperlipidemia of type II + IV or III, on paper electrophoresis, corresponds usually to type IIb (204 cases) and, finally, massive endogenous hypertriglyceridemia, corresponding to type IV (95 cases). These indicate clearly the elective concentration of the band of slow pre-betalipoproteins persisting after 12 hours fasting in cases of mixed hyperlipidemia (73% of cases), whilst it is rare in the other groups (no more than 5% of cases). A more complete study of 204 cases of mixed hyperlipidemia showed that the high frequency of slow pre-betalipoproteins is situated in a fairly narrow range of relatively moderate hypertriglyceridemia, between the lower limit of 1.50 and the upper limit of 6 to 7 g/l: the maximum frequency and intensity is situated within the area of 2.50 to 4 g/l. The cases who have already had cardiovascular accidents are more often found to have this band than the cases without complications in a fairly similar age group. However, longitudinal studies, both midterm in relation to therapeutic correction, and short term throughout the day or between the 8th and 12th hour of fasting, have clearly revealed the potential labile nature of this fraction, and show the pathological nature of its sometimes massive persistence beyond the 8th hour and even beyond the 12th hour of fasting. This is a sign of pathological blocking of its transformation rather than of a constitutional lipoprotein abnormality.

Adult↗