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Biomedical subjects

J Rouffy

Publications and source records attributed to J Rouffy.

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

Comparative effects of prazosin and atenolol on plasma lipids in hypertensive patients.

Adverse modifications of blood lipid fractions are thought to be an additional risk factor in hypertensive patients treated with some antihypertensive drugs. The purpose of this study was to compare the changes in concentrations of lipid fractions in patients treated with either the cardioselective beta blocker atenolol or the selective alpha 1 blocker prazosin. When used in approximately equipotent doses for antihypertensive effect, prazosin and atenolol demonstrated different effects on lipid metabolism. Prazosin lowered total levels of cholesterol, low-density lipoprotein cholesterol and B-apolipoproteins, but increased the levels of high-density lipoprotein cholesterol, high-density lipoprotein2 cholesterol and A1-apolipoproteins. Changes opposite to those induced by prazosin were observed during atenolol therapy.

Adult↗
PubMed1984

[Dyslipoproteinemic xanthomas].

The authors recall the clinical and histochemical aspects of xanthomas and their relations with disturbances in serum lipids and lipoproteins. Experiments in animals and clinical studies in humans are then reviewed. In the light of these results, physiopathological mechanisms involved in development of xanthomas and their connections with atherogenesis are discussed.

Animals↗
PubMed1984

[Riedel's thyroiditis and retroperitoneal fibrosis. Apropos of a case of multiple fibrosing disease].

The authors report a case of a 53 year old woman with Riedel's thyroiditis and retroperitoneal fibrosis. The thyroiditis has been diagnosed a year before the retroperitoneal fibrosis. This one was idiopathic and has been responsible of the death of the patient during an operation performed for ureterolysis. Fifteen other similar cases have been reported in the literature: four of them associated also mediastinal and biliary ducts fibrosis. The existence in one patient of multiple fibrosclerosis locations and the similitude of histological patterns (inflammatory diffuse fibrosis) lead to the concept of a multiple sclerosing disorder involving Riedel's thyroiditis, Ormond's disease, mediastinal fibrosis, sclerosing cholangitis, and the pseudotumors of the orbit. The etiopathogenic processes remain unclear.

Female↗
PubMed1983

[Genetic hypolipoproteinemias].

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

Humans↗
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↗