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Dive into the research topics where C. Harvengt is active.

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Featured researches published by C. Harvengt.


European Journal of Clinical Pharmacology | 1983

Effects of clofibrate, bezafibrate, fenofibrate and probucol on plasma lipolytic enzymes in normolipaemic subjects

F. Heller; C. Harvengt

SummaryTen male, normolipaemic, non-obese subjects were given clofibrate 2g daily, fenofibrate 300 mg daily, bezafibrate 600mg daily and probucol 1g daily for eight days, in a crossover study with a wash-out period of 4–8 weeks between each drug regimen. Clofibrate, fenofibrate and bezafibrate caused a significant decrease in serum triglycerides, total cholesterol and LDL-cholesterol concentrations. Probucol caused a significant increase in serum LDL-cholesterol concentration. Serum HDL-cholesterol concentration was significantly increased by bezafibrate and significantly decreased by probucol. All drugs but probucol led to a significant rise in the activity of the plasma lipoprotein lipase; there was not a significant increase in the activity of plasma hepatic lipase after any drug. The activity of plasma lecithin: cholesterol acyltransferase was significantly increased by fenofibrate and probucol. Analysis of the correlations between serum lipids and plasma lipolytic enzymes suggests that the mechanism of the hypolipidaemic action of clofibrate and bezafibrate might be related to increased catabolism of triglyceride-rich particles; that of fenofibrate and probucol was less clear and might be multifactorial in origin.


The Journal of Clinical Pharmacology | 1976

Naproxen Plasma Levels in Volunteers After Single‐Dose Administration by Oral and Rectal Routes

Jean-Pierre Desager; M. Vanderbist; C. Harvengt

The bioavailability (plasma concentrations, AUC) of a rectal formulation (suppository) of naproxen was investigated in six healthy volunteers by comparison with an oral preparation (tablets). Plasma half-lives after both formulations were identical 10 hr 15 min+/-25 min (S.D.). Determined by the AUC the bioavailability of naproxen in the suppositories was 94.8%+/-6.3% of the bioavailability of naproxen in the tablets. This paper describes also a new gas-liquid chromatographic method for determining unchanged naproxen in human plasma which is quick, sensitive, and specific.


Clinical Pharmacology & Therapeutics | 1993

A pharmacokinetic evaluation of the second-generation H1-receptor antagonist cetirizine in very young children.

Jean-Pierre Desager; I. Dab; Yves Horsmans; C. Harvengt

The pharmacokinetics of the second‐generation H1‐receptor antagonist cetirizine was studied in eight children younger than 4 years of age who were treated with a single dose of cetirizine solution (5 mg). These children were hospitalized with suspected allergic respiratory problems or recurrent respiratory tract infections. Blood samples were collected at ½, 1, 1½, 2, 4, 6, 8, 12, and 24 hours, and a 24‐hour urine collection was performed in five of the samples. The findings obtained in children were compared with those obtained in 16 healthy young adults (mean ± SD, 24.6 ±4.1 years) who received a single 20 mg dose. Cetirizine was absorbed more slowly in children (p = 0.006; mean ± SD, 1.44 ± 1.12 hours) than in adults (0.62 ± 0.22 hours). The plasma elimination half‐life of cetirizine was significantly shorter in children (p < 0.001; 4.91 ± 0.6 hours) than in adults (8.6 ± 2.1 hours), and the clearance rate was significantly higher in children (p < 0.001; 1.48 ± 0.41 ml/min/kg) than in adults (0.80 ± 0.17 ml/min/kg). Urinary excretion of unchanged cetirizine was significantly lower in children (p < 0.001; 37.8% ± 5.2%; n = 5) than in adults (57.7% ± 11.8%). Therefore the metabolism of cetirizine is faster in young children than in adults. This effect must be taken into account in future pharmacodynamic studies in this age group.


Metabolism-clinical and Experimental | 1981

Plasma-lipid Concentrations and Lecithin - Cholesterol Acyltransferase Activity in Normolipidemic Subjects Given Fenofibrate and Colestipol

Fr. Heller; Jean-Pierre Desager; C. Harvengt

Plasma lipids and lipoprotein cholesterol concentrations and lecithin:cholesterol acyltransferase activity were measured in 7 normolipidemic subjects before, and 7 days after, the administration of fenofibrate (300 mg daily) and colestipol (15 g daily) taken separately or simultaneously. Fenofibrate provoked a significant decrease in the mean plasma triglycerides (26%) and cholesterol (10%) concentration; only plasma cholesterol concentrations were significantly lowered by colestipol (26%). The cholesterol lowering effects of the two drugs were additive as was observed when colestipol was added to fenofibrate. The mean plasma high density lipoprotein cholesterol (HDL-C) concentration was significantly increased by fenofibrate (10%) and when colestipol was added to fenofibrate (15%), but not by colestipol alone. Both fenofibrate and colestipol caused significant reduction of the mean plasma low density lipoprotein cholesterol (LDL-C) concentration and the mean plasma LDL-C/HDL-C ratio (13% and 18%, respectively, with fenofibrate, 44% and 52% with colestipol, and 53% and 62% with colestipol added to fenofibrate). The mean plasma fractional esterification rate was significantly increased by 25% and 12%, respectively, with fenofibrate and colestipol when taken separately, and still more (91%) when colestipol was added to fenofibrate. The mean plasma molar esterification rate was significantly lowered by colestipol, but remained unchanged with the other drug regimens. This study shows that fenofibrate and colestipol given to normolipidemic subjects can induce in a very short period of time (7 days) marked changes in lipoprotein metabolism. Interpretations of the findings in relation to lipoprotein metabolism are discussed.


The Journal of Clinical Pharmacology | 1993

Single‐Dose Pharmacokinetics of Cetirizine in Patients With Chronic Liver Disease

Yves Horsmans; Jean-Pierre Desager; R. Hulhoven; C. Harvengt

The pharmacokinetics of the H1‐receptor antagonist cetirizine were studied from 0 to 72 hours after a single dose of 20 mg in 5 patients with chronic hepatocellular liver disease (group A), in 5 patients with chronic cholestatic liver disease (group B), and in 16 healthy volunteers. The renal function of patients and volunteers was normal (creatinine clearance ≥ 70 mh/min). Cetirizine pharmacokinetics were similar in the two groups of patients. The elimination t1/2 was prolonged in patients (mean ± standard deviation; group A: 14.32 ± 2.30 hours; group B: 13.86 ± 3.14 hours) in comparison with the values observed in volunteers (9.42 ± 2.4 hours). A reduced apparent oral body clearance also was observed in patients (group A: .48 ± .23 mL/min/kg; group B: .41 ± .09 mL/min/kg) in comparison with volunteers (.74 ± .19 mL/min/kg). No differences were observed in the mean cumulative urinary excretion between patients (group A: 69 ± 15%; group B: 69 ± 13%) and volunteers (70.7 ± 7.8%).


Nephron | 1982

Effect of Hemodialysis On Plasma Kinetics of Fenofibrate in Chronic-renal-failure

Jean-Pierre Desager; Joseph Costermans; René Verberckmoes; C. Harvengt

The influence of hemodialysis on plasma fenofibric acid kinetics has been investigated in patients with chronic renal failure given 300 mg of fenofibrate in a single oral dose. A very pronounced lengthening of the fenofibric acid plasma decay was observed in both hemodialyzed (n = 6) and nonhemodialyzed (n = 9) patients. Hemodialysis did not modify the plasma levels and the ultrafiltrates contained very small amounts of fenofibric acid. The repeated daily administration of 100 mg of fenofibrate during 2 weeks in 5 renal patients on regular hemodialysis resulted in increasing plasma levels and led to progressive cumulation of fenofibric acid. Plasma fenofibric acid conjugates could not be detected. No particular clinical side effects or increase of CPK, GOT, GPT were be observed.


The Journal of Clinical Pharmacology | 1992

Effects of combined bezafibrate-simvastatin appraised in healthy subjects.

Yves Horsmans; Jean-Pierre Desager; C. Harvengt

The occurrence of clinical and biochemical side effects of bezafibrate (400 mg daily) or simvastatin (20 mg daily) alone or combined was appraised in 13 healthy male normolipidemic subjects according to a single blind design. Each period of 2 weeks of treatment with bezafibrate or simvastatin or bezafibrate plus simvastatin was followed by a period of placebo (1 week). No subjects experienced myalgia or muscle weakness. Plasma creatine kinase (CK) elevations, particularly skeletal muscle CK (CK‐MM), were observed in 6 subjects: 11 times during different placebo periods, 5 times on bezafibrate, 4 times on simvastatin, and 4 times on combined bezafibrate‐simvastatin, but never reached 1,600 IU/L. Only a trend to an increase of CK mean values on combined bezafibrate‐simvastatin was shown. The hepatic transaminase and gamma‐glutamyltransferase activities remained unmodified throughout the trial, unlike alkaline phosphatase activity, which fell on bezafibrate and on bezafibrate plus simvastatin. The low‐density lipoprotein cholesterol level was more reduced with simvastatin than with bezafibrate. The addition of bezafibrate to simvastatin did not decrease it further. Lecithin: cholesterol acyltransferase activity expressed as fractional esterification rate was enhanced only on simvastatin and bezafibrate‐simvastatin.


The Journal of Clinical Pharmacology | 1987

Short‐Term Effects of Beta Blockers Atenolol, Nadolol, Pindolol, and Propranolol on Lipoprotein Metabolism in Normolipemic Subjects

C. Harvengt; F. Heller; Philippe Martiat; Y van Nieuwenhuyze

The short‐term effect of the blockade of the beta‐adrenergic receptors on serum lipoproteins and the plasma activities of the enzymes involved in the metabolism of the serum lipoproteins: lipoprotein lipase (LPL), hepatic lipase (HL) and lecithin: cholesterol acyltransferase (LCAT) was evaluated in ten healthy normolipemic and normotensive subjects. In the first part of the study, the first three‐day period of placebo was followed by another three‐day period during which propranolol (120 mg/d) was given. In the second, third, and fourth part of the study, the same schedule was used but pindolol (15 mg/d), nadolol (160 mg/d), atenolol (100 mg/d) were given respectively instead of propranolol. The four drugs induced a significant blockade of the beta‐adrenergic receptors as evaluated by the measurement of the double two‐step test of Master (‐45%). Despite similar blockade, the effect on serum lipid concentrations depended on the type of drug: propranolol induced an increase in triglycerides and apoprotein B‐concentrations and a decrease in serum high density lipoprotein cholesterol (HDL‐C) and apoprotein AI‐concentrations. Pindolol provoked only a slight decrease of serum HDL‐C concentration. Nadolol and atenolol elicited a lowering of the same magnitude in HDL‐C. Except for a possible slight increase in plasma LCAT activity on propranolol, there was no significant change in the plasma activities of LPL, HL, and LCAT during the blockade of the beta‐adrenergic receptors with the drugs used. It is difficult to draw firm conclusions in regard to the mechanism by which beta blockers given to patients for much longer periods of time alter lipoprotein metabolism from results obtained in normolipemic subjects receiving beta blockers for only three days. It seems that pindolol modifies the serum lipoprotein pattern less likely than propranolol, nadolol, or atenolol. This difference could be attributed to the intrinsic sympathomimetic activity of pindolol of which the other beta blocking drugs that were used are devoid. The mechanism by which the serum lipid changes can be induced by beta blockade does not involve a lower activity of any of the plasma enzymes regulating the intravascular metabolism of lipoproteins.


European Journal of Clinical Pharmacology | 1980

Lack of Pharmacokinetic Interaction of Colestipol and Fenofibrate in Volunteers

C. Harvengt; Jean-Pierre Desager

SummaryThe possibility of a pharmacokinetic interaction between two hypolipidemic drugs, colestipol, an ion exchange resin, and fenofibrate, a phenoxyacid derivative, was studied in 6 male volunteers. The investigation followed a four-step protocol during 18 days, and relied on determination of plasma and urinary levels of fenofibric acid, the active metabolite of fenofibrate. The kinetics of a single dose of fenofibrate 300 mg was established over 3 days. Thereafter, from Days 4 to 9 fenofibrate was given daily as 200 mg in the morning and 100 mg in the evening; the plasma fenofibric acid level reached about 10 µg/ml. From Days 9 to 15 the same dose of fenofibrate was administered together with colestipol 10 g in the morning and 5 g in the evening. Plasma fenofibric acid concentrations remained unchanged and the 24 h urinary excretion of fenofibric acid did not fall. On Day 15, a last single dose of fenofibrate 300 mg was given with colestipol 15 g. The pharmacokinetic pattern of fenofibric acid on Days 15 to 18 did not differ significantly from that found previously (Days 1 to 3). From these results, it is likely that there is no pharmacokinetic interaction between the two hypolipidemic drugs.


Clinical Pharmacology & Therapeutics | 1976

Colestipol in familial type II hyperlipoproteinemia: A three‐year trial

C. Harvengt; Jean-Pierre Desager

Colestipol. a new bile acid sequestrant polymer. has been shown to lower the serum cholesterol level more than 30% in 13 patients with familial type 11 hyperlipoproteinemia. Placebo for 6 wk was followed by colestipol for periods up to 36 mo. A slight but not significant increase of serum triglyceride concentrations was observed during the first 18 mo. but they returned to values under the baseline level thereafter. No signs of impaired intestinal fat resorption were noted. Side effects were primarily gastrointestinal (mild and transient constipation). Colestipol seems to be an effective and safe drug in the treatment of the familial type 11 hyperlipoproteinemia. without escape phenomenon.

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Jean-Pierre Desager

Université catholique de Louvain

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F. Heller

Université catholique de Louvain

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R. Hulhoven

Université catholique de Louvain

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Yves Horsmans

Université catholique de Louvain

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Michel Sclavons

Université catholique de Louvain

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E. Dumont

Université catholique de Louvain

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M. Vanderbist

Université catholique de Louvain

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Pierre Mailleux

Université catholique de Louvain

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Joseph Costermans

Université catholique de Louvain

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L. Vanderlinden

Université catholique de Louvain

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