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R Mordasini

Publications and source records attributed to R Mordasini.

At least 37 records · Page 2Linked to original sources
PubMed1983

[Clinical and pathogenic aspects of secondary hyperlipoproteinemia].

The secondary hyperlipoproteinemias are frequent in "civilized" countries. Through new methods, the interest for secondary hyperlipoproteinemias is increasing, on theoretical and practical points of view. This paper reviews the hyperlipoproteinemias of alcoholism, renal and hepatic diseases, diabetes mellitus, abnormal thyroid function, and those secondary to various medications. For each of them, the clinical, pathophysiologic and therapeutic aspects are described.

Adrenal Cortex Hormones↗
PubMed1983

Effects of indapamide and various diuretics alone or combined with beta-blockers on serum lipoproteins.

A prospective evaluation was started in 1976 to study the influence of diuretics alone or combined with beta-blockers on serum lipoproteins in normal or hypertensive subjects. Compared to placebo conditions, 4 or 6-weeks' monotherapy with various diuretics significantly (p less than 0.05) increased the beta-lipoprotein fraction (furosemide, 80 mg/day or chlorthalidone, 100 mg/day; n = 16) or low-density lipoprotein-cholesterol (LDL-C) (chlorthalidone, 100 mg/day, n = 27 men; tienilic acid, 250 mg/day, n = 16 men, clopamide, 5 mg/day, n = 17 men; or muzolimine, 20 to 40 mg/day, n = 13 men or post-menopausal women). No increase in LDL-C was noted in 43 men (32 normal, 11 with mild hypertension) treated with indapamide, 2.5 mg/day. Serum high-density lipoprotein-cholesterol and apoproteins A1, A2 and B were not consistently changed by any of these agents. In women, chlorthalidone (100 mg/day) significantly increased LDL-C in the (100 mg/day) significantly increased LDL-C in the post-menopausal (n = 18) but not in the pre-menopausal (n = 22) state. Increases in LDL-C caused by chlorthalidone monotherapy were prevented or reversed by the addition of a beta-blocker, usually propranolol or atenolol (n = 18); increases in LDL-C during clopamide monotherapy were reversed after the addition of the beta-blocker pindolol (10 mg/day, n = 17). In all studies, variations in beta-lipoprotein or LDL-C levels could not be explained by changes in blood volume, serum glucose or insulin and did not correlate with alterations in blood pressure, plasma potassium, renin, aldosterone, adrenaline or noradrenaline. These observations indicate that various diuretics may increase serum LDL-C in men or post-menopausal women. Pre-menopausal women may often be protected from this side-effect. Long-term studies are now needed to clarify the pathogenic and prognostic relevance of lipoprotein changes induced by diuretics. In the meantime, it is of clinical interest that indapamide had no significant effect on serum lipoproteins and that certain beta-blockers appear to prevent or reverse increases in LDL-C during diuretic treatment in men and post-menopausal women.

Adrenergic beta-Antagonists↗
PubMed1983

[Clinical and pathogenic aspects of secondary hyperlipoproteinemias].

The secondary hyperlipoproteinemias are frequent in "civilized" countries. Through new methods, the interest for secondary hyperlipoproteinemias is increasing, on theoretical and practical points of view. This paper reviews the hyperlipoproteinemias of alcoholism, renal and hepatic diseases, diabetes mellitus, abnormal thyroid function, and those secondary to various medications. For each of them, the clinical, pathophysiologic and therapeutic aspects are described.

Alcoholism↗
PubMed1983

[Apolipoproteins: valuable indicators of atherogenicity in patients with coronary disease and normal blood lipids].

The lipid, lipoprotein and apolipoprotein B, A-I and A-II fractions in 20 young patients, (mean age 34.4 years) with myocardial infarction were compared with the results of a control group of 20 healthy men (mean age 35.8 years). The apolipoproteins B and A-I distinguished the myocardial infarction from the control patients. The patient group (who had slightly lower total and HDL cholesterol levels) had significantly higher apo B and lower A-I fractions than the controls. There was no significant difference in apo A-II fractions between the two groups. The measurement of the apo B and A-I fractions would appear to improve the lipid diagnosis by distinguishing the patients predisposed to atherosclerosis due to disorders of fat metabolism who may not be detected by less detailed lipid studies.

Adult↗
PubMed1983

Ethanol-induced hyperlipoproteinemia. Crucial role of preceding ethanol intake in the removal of chylomicrons.

Ethanol produces a number of effects in different steps of lipid metabolism which have been suggested to be responsible for the common phenomenon of ethanol-induced hyperlipoproteinemia in man. The occurrence of hyperchylomicronemia has been attributed to an ethanol-specific disturbance of the clearing mechanism of triglyceride-rich lipoproteins. However, the reports on lipolytic activities and the clearance of chylomicrons after ethanol ingestion are contradictory. In this investigation the short-term excess of serum lipoproteins and the lipolytic activities in healthy volunteers were studied after single and prolonged ethanol ingestion followed by an intravenous lipid load. One hour after a single oral dose of ethanol, the intravenous fat tolerance test was unchanged. After an ethanol load over a 5 hr period, the fat tolerance was reduced, although the same ethanol levels at the time of infusion were maintained. In addition, the lipolytic activities of the serum were significantly reduced after 5 hr of ethanol ingestion followed by intravenous fat load. Hence the time relations between ethanol and fat loads determine whether a defect in chylomicron catabolism can be observed or not. A striking difference in the situations when the fat infusions were performed was the development of endogenous hypertriglyceridemia after 5 hr of ethanol ingestion. Since ethanol-dependent differences in the absorption of fat are ruled out by our experimental design, we attribute our findings to a competitive inhibition of chylomicron degradation by VLDL and partial depletion of the lipolytic system by combined endogenous and exogenous hypertriglyceridemia.

Adult↗
PubMed1982

[Alcohol and plasma lipoproteins in acute and long-term studies].

The influence of ethanol on plasma lipids, lipoproteins and on the activity of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL), the major enzymes in the catabolism of triglyceride rich lipoproteins, was studied in 14 healthy young volunteers who were given 50 g ethanol daily for 4 weeks together with a standardized isocaloric diet. Marked hypertriglyceridemia occurred initially, mainly due to increased VLDL, but chylomicronaemia was also present in all probands. While HTGL activity remained unaltered there was a marked decrease in LPL activity. At the end of the study serum triglycerides and VLDL almost returned to initial levels, while Chylomicronaemia had totally disappeared. Furthermore, there was no atherogenic plasma lipoprotein alteration: LDL were not increased and the possibly antiatherogenic HDL were even significantly increased after the four weeks' study period. Again, HTGL activity remained unchanged but that of LPL reached its maximum after 4 weeks. It is therefore suggested that regular alcohol intake may increase LPL activity and hence may lead to a more rapid catabolism of triglyceride-rich lipoproteins in plasma.

Adult↗
PubMed1982

Serum lipoproteins in patients with mild renal disease treated with the diuretic muzolimine.

Patients with renal functional impairment are prone to develop hypertension and hyperlipidemia, and both abnormalities tend to occur already at an early stage of kidney disease. In 18 patients with mild renal disease (glomerular filtration rate 65 +/- 5 ml/min) and hypertension (mean blood pressure 126 +/- 4 mm Hg), the effect of six weeks of treatment with the loop-diuretic muzolimine on serum lipoproteins was assessed. Compared to placebo values, the diuretic significantly increased serum low-density lipoprotein cholesterol (LDL-C) and apoprotein B (+ 18 and 11%, respectively, P less than 0.005) in 13 men or postmenopausal women, but not in 5 premenopausal women. Serum high-density lipoprotein cholesterol (HDL-C), and total triglycerides or lipoprotein triglyceride fractions were not consistently changed in both subgroups. Thus, the ratio LDL-C/HDL-C was increased from 3.2 +/- 0.3 to 3.9 +/- 0.3 (P less than 0.05) in the men or postmenopausal women, while no such tendency occurred in the premenopausal women (4.1 +/- 0.6 to 3.7 +/- 0.6). Changes in serum LDL-C were not associated with hemoconcentration or alterations in carbohydrate metabolism and were not related to variations in serum potassium or blood pressure. Increased serum levels of the atherogenic LDL-C fraction during diuretic treatment in men or postmenopausal women with renal disease may represent a potentially undesirable effect, particularly since such patients may tend to have hyperlipidemia in the untreated state.

Female↗
PubMed1982

[Changes in serum lipoproteins in kidney diseases].

Secondary hyperlipoproteinemias frequently occur in patients with conservatively treated chronic uremia, under hemodialysis, after renal transplantation and notably in patients with the nephrotic syndrome. In chronic uremia patients conservatively treated or under hemodialysis, hypertriglyceridemia (type IV-pattern) is predominant whereas after renal transplantation and in the nephrotic syndrome hypercholesterolemia (type II-pattern) is more frequent. With the exception of hyperlipoproteinemia in the nephrotic syndrome, these hyperlipoproteinemias are associated with markedly reduced levels of the protective HDL. They therefore represent a relevant atherogenic risk. Lipoprotein disorders in chronic uremia are mainly due to disturbed catabolism of triglyceride-rich lipoproteins; treatment with corticosteroids may be the major underlying pathogenic mechanism of hyperlipoproteinemia after renal transplantation, whereas in the nephrotic syndrome increased hepatic lipoprotein production is observed.

Arteriosclerosis↗
PubMed1982

Effects of estrogens and progestogens on lipid metabolism.

Because the incidence of venous thromboembolism, coronary heart disease, and stroke is increased in users of oral contraceptives (OCs), the possible causal metabolic side effects of OCs have been widely investigated. In this article we present epidemiologic data associated with OC use. Total plasma triglycerides and cholesterol levels were elevated in OC users while high-density lipoprotein cholesterol levels were lowered. Another section discusses some hormone-dependent physiologic and pathophysiologic aspects of lipid metabolism. Finally, we report on the isolated influence of estrogens and progestogens and their interrelation, including some recent findings about the effects of different progestogens on lipoproteins.

Adolescent↗
PubMed1982

[Behavior of high-density lipoproteins in drug lipid-lowering treatment].

Changes in serum lipids, the individual lipoprotein fractions after ultracentrifugation and the apoproteins B, A1 and A2 were studied in 66 patients with primary hypercholesterolemia under treatment with different lipid-lowering agents. After 3 months with dietary treatment alone and a 4-week placebo period the patients were given bezafibrate (3 X 200 mg daily), colestipol (2 X 10 g per day) or probucol (2 X 500 mg daily) for 12 months, followed by another 4-week placebo period at the end of the study. Colestipol showed the best lipid-lowering effect (total and LDL cholesterol were decreased by 20% and 23% respectively) but satisfactory total and LDL cholesterol lowering results were also obtained with the other substances. However, the changes in HDL differed widely among the three substances: bezafibrate increased HDL cholesterol and the HDL apoproteins A1 and A2 significantly, colestipol did not alter these parameters, while probucol treatment was followed by a significant decrease in both HDL-cholesterol and the apoproteins A1 and A2.

Adult↗
PubMed1982

Reversal or prevention of diuretic-induced alterations in serum lipoproteins with betablockers.

In 18 patients with essential hypertension serum low density lipoprotein cholesterol (LDL-C) was significantly (P less than 0.001) increased following short-term chlorthalidone therapy, but not during combination therapy with chlorthalidone and a betablocker. This tendency was similar in two subgroups which were studied with an inverse sequence of drug administration. In Group I (11 men), a 22% increase (P less than 0.01) in LDL-C during chlorthalidone monotherapy was restored to normal 6 weeks after addition to a betablocker to the diuretic; in Group II (5 men, 2 postmenopausal women) LDL-C levels were increased by 41% (P less than 0.05) 6 weeks after withdrawal of the betablocker from the combination therapy. No significant changes occurred during either the treatment phase in high density lipoprotein cholesterol or apoprotein B levels. It is concluded that combination therapy with a betablocker may prevent or reverse an increase in serum LDL-C associated with short-term chlorthalidone monotherapy.

Adolescent↗
PubMed1982

Reversal of diuretic-induced increases in serum low-density-lipoprotein cholesterol by the betablocker pindolol.

Seventeen patients with mild to moderate essential hypertension received during three consecutive 4 wk periods a matched placebo, the thiazide-like diuretic, clopamide in a low dosage of 5 mg/day, or this diuretic combined with the betablocker, pindolol in a low dosage of 10 mg/day. Compared to placebo conditions, clopamide monotherapy significantly increased serum low-density lipoprotein cholesterol (LDL-C) by 13% (p less than 0.025). Following addition of pindolol, serum LDL-C was restored to control values. These variations in serum LDL-C were unrelated to concomitant changes in blood pressure, plasma potassium, renin activity or aldosterone levels. Blood pressure in the supine position was reduced from 152/99 +/- 13/9 mm Hg (+ SD) to 141/93 +/- 15/7 mm Hg following diuretic-monotherapy and to 139/90 +/- 12/9 mm Hg following diuretic-betablocker combination treatment. These findings suggest that antihypertensive combination treatment with low doses of clopamide and pindolol is not only effective and well tolerated, but may also avoid the increase in serum LDL-C levels occurring when the thiazide-like diuretic is given alone.

Adult↗
PubMed1982

Menopause-dependent plasma lipoprotein alterations in diuretic-treated women.

The effects of chlorthalidone, 100 mg/d given for 6 weeks, on serum lipids and lipoproteins were assessed in 22 premenopausal and 18 postmenopausal women. In the latter, chlorthalidone significantly increased total serum cholesterol (13%, p less than 0.001), low-density-lipoprotein (LDL) cholesterol (21%, p less than 0.001) and apoprotein B (16%, p less than 0.05). In contrast, these values were not altered in the premenopausal group. Levels of LDL cholesterol, high-density-lipoprotein cholesterol, total and very-low-density triglycerides, apoproteins A1 and A2, and plasma volume, plasma glucose, insulin, epinephrine, estradiol, and free fatty acids were unchanged in both groups. Chlorthalidone-induced changes in levels of LDL cholesterol did not correlate significantly with variations in blood pressure, plasma potassium, uric acid, renin, aldosterone, or norepinephrine levels. These findings indicate that the thiazide-like diuretic chlorthalidone increases serum LDL cholesterol in postmenopausal but not in premenopausal women.

Adult↗