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J-L Reny

Publications and source records attributed to J-L Reny.

5 recordsLinked to original sources
PubMed2006

[Medical treatment in peripheral arterial disease: a professional practice study in 262 patients].

PURPOSE: Antiplatelet agents (APA), statins and angiotensin converting enzyme inhibitors (ACEI) are effective to reduce the risk of cardio-vascular events in patients with peripheral arterial disease (PAD). Few data are available on the actual prescription of these drugs in outpatients and on the effect of hospital care on the level of prescription. METHODS: Retrospective study of patients hospitalized with a confirmed diagnosis of PAD over a one-year period. Comparison of medical treatments on admission and on discharge. RESULTS: 262 patients were included. Mean age was 73 +/- 11 years, and 29% of the patients were women. APA were present in 64% on admission and in 83% when discharged (P < 0.0001). A statin was present in 29% on admission and in 38% when discharged (P = 0.001). ACEI were present in 27% on admission and in 32% when discharged (P= 0.02). A vasodilator was present in 47% on admission and 52% when discharged (P = 0.1). 35% of the patients had isolated PAD. Compared to the patients with associated clinical coronary or cerebro-vascular disease, they were less frequently discharged on statins (respectively 26 and 45%, p = 0.003) and on ACEI (respectively 23 et 38%, P = 0.016) whereas APA were equally prescribed (respectively 82 and 84%, P= 0.7). CONCLUSION: APA were prescribed to a majority of outpatients and the level of prescription was further improved when patients were discharged from the hospital. Statins and ACEI were insufficiently prescribed. On the other hand, vasodilator therapy remained still largely prescribed, despite the lack of any strong effect on morbidity and survival.

Aged↗
PubMed2005

[Pharmacogenetics and antiplatelet drugs].

PURPOSE: The observation of inherited drug response variability gave rise to the field of pharmacogenetics. Pharmacogenetic research on drug targets, particularly platelet enzymes and receptors, is more recent and is becoming an emerging field. CURRENT KNOWLEDGE AND KEY POINTS: In the Framingham study, the heritability of platelet aggregation response ranges from 44 to 62%, depending on the agonists used. The gene coding for GPIIIa, a sub-unit of the fibrinogen receptor GPIIbIIIa, is one of the most extensively studied gene in relation with aggregation tests and antiplatelet drugs. The GPIIIa PLA1/PLA2 polymorphism has been associated with clopidogrel and orbofiban platelet response. However, data are more controversial concerning the association with aspirin response. Recently, Cox-1 and GPIa (part of the GPIaIIa collagen receptor) genetic variations have also been pointed out as possible candidates to explain part of the variability of the response to antiplatelet agents. Finally, the H1/H2 polymorphism of the platelet ADP receptor P2Y12 gene has been associated with ADP-induced platelet aggregation response and peripheral arterial disease. This polymorphism may modulate the effect of P2Y12 antagonists like clopidogrel and its clinical implication is currently under study. FUTURE PROSPECTS AND PROJECTS: Gene-expression profiling and proteomics may allow the identification of new candidate genes whose variations may be associated with the heritability of platelet aggregation response. In the next future, phenotypic or genotypic studies could be available to tailor the prescription of antiplatelet drugs.

Gene Expression Profiling↗
PubMed2005

The specific thromboxane receptor antagonist S18886: pharmacokinetic and pharmacodynamic studies.

OBJECTIVES AND PATIENTS: We conducted a multicenter double-blind pharmacokinetic/pharmacodynamic (PK/PD) study of the new oral thromboxane receptor antagonist S18886 in 30 patients with peripheral artery disease, who were randomized to receive five different oral dosages of S18886 (1, 2.5, 5, 10 or 30 mg) for 12 weeks (83 days). Primary objective was to determine the effect of S18886 on platelet aggregation ex vivo. RESULTS: Pharmacokinetics of S18886 was linear, with peak plasma levels being reached between 30 min and 2 h and a terminal half-life of 5.8-10 h. No significant accumulation of S18886 in plasma was observed after repeated dosing. The relationship between the S18886 concentration and platelet inhibition was examined in terms of U46619-induced platelet aggregation. Over the range of doses studied, there was a predictable relation between the plasma drug concentration and the degree of platelet inhibition at each dose. Maximal inhibition of U46619-induced platelet aggregation was achieved within 1 h with all oral doses of S18886, and this effect was maintained for at least 12 h. The PK/PD relationship was direct, and U46619-induced platelet aggregation was strongly inhibited by S18886 plasma concentrations above 10 ng mL(-1). This concentration was thus the minimal effective antiplatelet level in this population, and was maintained only by the dosages of 10 and 30 mg. The safety profile of S18886 was excellent, whatever the unit dose, with no attributable adverse events. CONCLUSION: The results of this study, which included modeling and simulation, help identify the minimal effective plasma concentration of S18886 required for potent antiplatelet efficacy in patients with stable peripheral arterial disease.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗