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Biomedical subjects

B Chanu

Publications and source records attributed to B Chanu.

At least 55 records · Page 3Linked to original sources
PubMed1983

[Primary hyperlipoproteinemias. Clinical, biological and physiopathological aspects].

Primary hyperlipoproteinemias are of great interest for the physician and searcher, because of their atherogenic properties; on the other hand, a new type of hyperlipoproteinemia, namely hyperalphaliproproteinemia, seems to be a protective factor against clinical complications of atherosclerosis. The clinical, biological and pathophysiologic aspects of these diseases are studied both from the author's experience and literature data.

Diagnosis, Differential↗
PubMed1983

[Hepatic cholesterolosis. Histological, histochemical and ultrastructural study of 2 cases].

Cholesterol ester storage disease, a mild form of Wolman's disease, is caused by a cholesterol ester lysosomial acid hydrolase deficiency leading to an accumulation of lipids in numerous cells of the organism. The authors have studied the liver parenchyma of two patients. The lipid deposits are found in the hepatocytes, macrophages and Küpffer cells, and in the walls of the biliary canaliculi. Histological study shows them to be rich in triglycerides and cholesterol esters. Ultrastructural study confirms their intralysosomal nature. Finally, examination of a tendinous xanthoma in one of the patients revealed deposits of the same nature in the macrophages.

Cholesterol Esters↗
PubMed1983

[Changes in lipids and lipoproteins caused by the beta-blocking agents used as antihypertensives].

It is certain that atherosclerosis is multi-factorial. Amongst the numerous risk factors two are particularly important: hypertension and primary or secondary abnormalities of plasma lipids and lipoproteins (high levels of total cholesterol, LDL and VLDL cholesterol, triglycerides or VLDL triglycerides, apoprotein B, low levels of HDL cholesterol, apoprotein A1 and probably HDL2). On the basis of a general review of the literature, the authors evaluate the changes in lipids, lipoproteins and apoproteins induced by different beta-blockers. Overall, the most constant and most obvious (particularly in hyperlipidaemic patients) disturbances combine an increase in total triglycerides or VLDL triglycerides and a fall in HDL cholesterol. There is little change in total cholesterol or LDL cholesterol. Side effects seen with most beta-blockers, cardioselective or not, differ in degree from one drug to another. They are particularly marked with some (propranolol) while they are virtually absent with others (pindolol). The mechanism of action is discussed (essentially inhibition of extra-hepatic lipoprotein lipase activity). These findings would seem to lead to the following practical conclusions: 1) Before starting antihypertensive treatment it is important to confirm lipid and lipoprotein levels, particularly bearing in mind the epidemiological links between moderate essential hypertension and lipoprotein abnormalities, especially those with a component of hypertriglyceridaemia. 2) Lipid profile including estimation by precipitation of HDL cholesterol must be studied during antihypertensive therapy and if there is a marked and confirmed deterioration towards an "increased atherogenicity", it is reasonable to envision a change of the antihypertensive agent. With the some efficacy on blood pressure levels and general tolerance, the choice should favour drugs having the least unfavourable effects on lipoprotein metabolism.

Adrenergic beta-Antagonists↗
PubMed1983

[Primary hyperlipoproteinemias. Clinical, biological and physiopathological aspects].

Primary hyperlipoproteinemias are of great interest as for the physician, as for the searcher, because of their atherogenic properties; on the other hand, a new type of hyperlipoprotenemia, namely hyperalphalipoproteinemia, seems to be a protective factor against clinical complications of atherosclerosis. The clinical, biological and pathophysiologic aspects of these diseases are studied both from author's experience and from the literature data.

Humans↗
PubMed1983

[Lipids, lipoproteins, apoproteins and clinical arteriopathic manifestations].

The authors present a historical review of the epidemiologic and pathophysiologic data which have supported the relations between the clinical complications of atherosclerosis on one hand, plasma lipids (cholesterol and triglycerides), lipoproteins (on electrophoretic basis), lipoproteins lipids (separated by ultracentrifugation or precipitation), and currently the plasma apolipoproteins on the other hand. The clinical applications of these data are considered.

Apoproteins↗
PubMed1983

[Genetic hypolipoproteinemia].

The very rare inherited hypolipoproteinemias are of great help to understand the relations between lipoproteins and atherosclerosis; moreover, they raise questions in this field, which are discussed in this paper.

Abetalipoproteinemia↗
PubMed1983

[Dyslipoproteinemic xanthoma].

The authors recall the clinical and histo-chemical aspects of xanthomas and their relations with serum lipids and lipoproteins disturbances. The experimental works in animals and in human clinic are then reviewed. At the light of these results the xanthoma development physiopathology and its relation to atherogenesis is considered.

Acute Disease↗
PubMed1983

[Angiodysplasias of the colon and small intestine: a not uncommon cause of gastrointestinal hemorrhage. 3 cases].

Three cases of bowel angiodysplasia with digestive bleeding were reported. In all cases, diagnosis was confirmed by arteriographic and/or histological data. Angiodysplasia of the colon was the most often an acquired and degenerative disease, and most commonly affecting patients after the seventh decade of life. This condition was a frequent and misinterpreted cause of bleeding per rectum in patients after fifty years. Selective superior mesenteric angiography, after colonoscopy (except during major bleeding) was the best investigation, showing pathognomonic images and specifing the site, often located in the caecum and/or ascending colon. Treatment was surgical, but endoscopic methods provided encouraging results.

Adult↗
PubMed1982

'Pseudohypertriglyceridemia' caused by hyperglycerolemia due to congenital enzyme deficiency.

A 76-year-old man was found to have a false hypertriglyceridemia due to a 40-fold increased glycerolemia. This metabolic change was due to a deficiency in glycerol kinase (ATP:glycerol phosphotransferase, EC 2.7.1.30) activity in the cells of this patient as shown by incubation of his white blood cells with [14 C]glycerol. Several chromatographic analyses and quantitative assays were performed on plasma and urine of this patient and of his relatives. The small number of this family's members did not allow to specify the mode of transmission of this genetic trait.

Aged↗
PubMed1982

[Xanthelasma palpebrarum and dyslipoproteinaemia: two retrospective studies (author's transl)].

In a retrospective study about 600 hyperlipoproteinaemic patients (390 men and 210 women, mean age 47), xanthelasma palpebrarum was infrequent (25 cases or 4.16 p. 100), since it was only at the third rank of chronic extra-vascular lipid deposits after arcus corneus and tendineous xanthomas. It was twice as frequent in men (5.12 p. 100) as in women (2.38 p. 100) and of regularly increasing occurrence until the sixth decade. Among the atherosclerotic risk factors, only obesity was significantly associated. The existence of atherosclerotic diseases was observed more frequently in patients with xanthelasma palpebrarum (40 p. 100) than in total hyperlipoproteinaemic population (28 p. 100). In a second retrospective study concerning 29 patients (15 men and 14 women, mean age 50), selected from the only presence of one or several xanthelasma palpebrarum, a lipoproteinaemic abnormality was observed in 27 cases (93 p. 100): 23 patients (71 p. 100) were hyperlipoproteinaemic (type IIa, IIb or IV) and in 4 out of 6 normolipidemic patients we observed an abnormal lipoprotein cholesterol distribution (LDL + VLDL cholesterol increase and HDL cholesterol decrease). In this group, we observed in nine patients (31 p. 100) unknown atherosclerotic diseases and tendineous xanthomas in other nine patients (31 p. 100).

Adolescent↗
PubMed1981

[Tendinous hyperlipoproteinaemic xanthomatosis associated with supravalvular aortic xanthomatosis (author's transl)].

A 56-year-old woman with familial heterozygous type II hyperlipoproteinaemia and tendinous xanthomas, presented the unusual findings of acquired supravalvular aortic stenosis associated with a congenital stenosis of the orifice. Analysis of clinical, paraclinical, and particularly pathological data confirmed the existence of several associated lesions: congenital hypoplasia of the aortic ring and proximal aorta, calcified valve stenosis probably increased by the dyslipidaemia, and finally and principally, supravalvular stenosis formed of a veritable circular rim of atheromatous material, making up a second haemodynamic obstacle. It is probable that the pre-existing congenital aortic lesions in this case, apart from the hyperlipoproteinaemia, account for the observation, not previously reported in a heterozygous type II hyperlipoproteinaemia, of massive supravalvular atheromatous deposits. This latter of acquired lesion is described in 9 cases reported in the literature with a homozygous form of familial hypercholesterolaemic xanthomatosis, the atheromatous deposits in the proximal aorta appearing earlier in these patients, and in the absence of pre-existing anatomical anomalies.

Aorta↗
PubMed1980

[Fenofibrate: hypolipaemic activity and safety in long-term treatment. Effects on HDL, LDL, VLDL and apoprotein B in short-term treatment (author's transl)].

In a study started in 1973 and still in progress (1100 patient-years so far) fenofibrate in daily doses of 200-400 mg consistently proved effective, without any loss of activity with time. The drug lowered serum total cholesterol levels by 17-27% in type IIa, IIb and III primary hyperlipoproteinaemia (HLP) and serum triglyceride levels by 35-51% in type IIb and III HLP and by 46-54% in type IV HLP. Clinically and biologically fenofibrate was always well tolerated, even after 5 years' treatment. Side-effects were uncommon (4%) and mild, and they obliged to discontinue treatment in only 1% of the patients. Abnormal manifestations encountered during therapy appeared to be fortuitous. The effects of the drug on cardiovascular morbidity and mortality could not be determined from this trial. In a short-term study involving 21 patients with type IIa and IIb primary HLP, fenofibrate in doses of 200-400 mg/day produced a significant decrease in total cholesterol, LDL-cholesterol and apoprotein B. It is also reduced triglycerides and VLDL-triglycerides in type IIb HLP. The increase in HDL-cholesterol observed under fenofibrate was significant in type IIa HLP but not in type IIb HLP. In both types, there was a significant rise in HDL: LDL + VLDL ratio.

Adolescent↗
PubMed1980

[Effects of medium-term probucol treatment on plasma lipids and lipoproteins. 16 cases of type IIa and IIb hyperlipoproteinaemia (author's transl)].

Probucol was used to treat 16 patients with atherogenic hyperlipoproteinaemia. The duration of treatment varied between 30 days (16 patients) and 510 days (4 patients). The drug was found to be remarkably well tolerated, without any clinical or biological side-effects. There was an 8 to 13 p. cent reduction in plasma total cholesterol, a 4 to 17 p. cent reduction in LDL cholesterol and a very favorable increase (19 to 23 p. cent) in the HDL/LDL + VLDL cholesterol ratio. Little or no change was found in triglyceride and HDL cholesterol levels.

Cholesterol↗