[Experience with 110 medium-length therapeutic trials of ethyl chlorophenoxyisobutyrate with or without androsterone in various types of idiopathic hyperlipidemia].
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Biomedical subjects
Publications and source records attributed to J Truffert.
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Prenatal diagnosis of homozygous hypercholesterolemia was achieved at the 24th week of gestation by analysis of lipid values in a fetal blood sample obtained by a needle guided by ultrasound. These abnormal values were compared to values in blood obtained from normal fetuses at the same stage of gestation. After abortion, the diagnosis was confirmed by measuring LDL receptor activity on fibroblast cultures from a skin biopsy. The main advantages of this procedure over measuring LDL receptor activity on cultured amniotic cells are its simplicity and speed.
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The cardiovascular consequences of mixed hyperlipideamia have been determined using a very large series of 950 cases. The early development and the prevalence of complications renders the disease severe, even in its minor forms of the grave forms of essential hypercholesterolaemia. Certain special features are worthy of mention:--the total loss of any parallelism between the biological severity and the development of vascular complications;--the probable role of slow pre-beta-lipoprotein in the determination of complications above all forms resistant to therapeutic reduction where its persistence is remarkable, which justifies the addition to known electrophoretic types III and II b a type, in the opinion of the authors just as common, with pre-beta-lipoprotein without any increase in L.D.L.
Lp(a) is a lipoprotein present in all individuals in concentrations that are genetically determined. Its structure is characterized by the presence of an apoprotein with a high carbohydrate content called apoprotein a. Since 1972, numerous concordant data have endowed Lp(a) with a high risk of atherogenesis. This risk applies to the coronary and cervico-encephalic arteries. For the latter, Lp(a) even is a lipid parameter regarded as a major risk factor. The origin and metabolism of Lp(a) are little known, by they seem to differ from those of low-density lipoproteins. Its specific apoprotein of Lp(a). At the moment, there is no simple dietetic or medicinal treatment that can lower substantially the serum level of Lp(a).
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