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8. Plasma homocysteine as a risk factor for vascular disease. The European Concerted Action Project

Author

Graham, I., Leslie, E., Daly, L.E., Refsum, H., Robinson, K., Brattström, L.E., Ueland, P.M., Palma-Reis, R.J., Boers, G.H.J., Sheahan, R.G., Israelsson, B., Cuna, S., Uiterwaal, C.S., Meleady, R., McMaster, D., Verhoef, P., Witteman, J., Rubba, P., Bellet, H., Wautrecht, J.C., Valk, H.W. de, Sales Luis, A.C., Parrot-Roulaud, F.M., Tan, K.S., Higgins, I., Garcon, D., Medrano, M.J., Candito, M., Evans, A.E., and Andria, G.

Subjects
GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries)
Abstract

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Published
1997

14. Mesure de l'épaisseur intima-média carotidienne, marqueur du risque d'athérosclérose, chez les patients infectés par le VIH-1

Author

Mercié, P., primary, Thiébaut, R., additional, Lavignolle, V., additional, Pellegrin, J.L., additional, Yvorra-Vives, M.C., additional, Morlat, P., additional, Ragnaud, J.M., additional, Dupon, M., additional, Malvy, D., additional, Bellet, H., additional, Lawson-Ayayi, S., additional, Roudaut, R., additional, and Dabis, F., additional

Published
2001
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17. Vitamine B6 et maladie thromboembolique veineuse

Author

Quéré, I., primary, de Moerloose, P., additional, Bounameaux, H., additional, Bellet, H., additional, Zittoun, J., additional, Leger, P., additional, Mercier, P., additional, Berrut, G., additional, Pinède, L., additional, Gris, J.C., additional, Dupuy, E., additional, Ninet, J., additional, Boccalon, H., additional, Boneu, B., additional, Conri, C., additional, Schved, J.F., additional, and Janbon, C., additional

Published
1999
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18. Homocystéine, folates et maladie thromboembolique veineuse

Author

Quéré, I., primary, de Moerloose, P., additional, Bounameaux, H., additional, Bellet, H., additional, Zittoun, J., additional, Leger, P., additional, Mercier, P., additional, Berrut, G., additional, Pinède, L., additional, Gris, J.C., additional, Dupuy, E., additional, Ninet, J., additional, Boccalon, H., additional, Boneu, B., additional, Conri, C., additional, Schved, J.F., additional, and Janbon, C., additional

Published
1999
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19. Maladie thromboembolique veineuse et facteurs de risque artériels

Author

Quéré, I., primary, de Moerloose, P., additional, Bounameaux, H., additional, Bellet, H., additional, Zittoun, J., additional, Leger, P., additional, Mercier, P., additional, Berrut, G., additional, Pinède, L., additional, Gris, J.C., additional, Dupuy, E., additional, Ninet, J., additional, Boccalon, H., additional, Boneu, B., additional, Conri, C., additional, Schved, J.F., additional, and Janbon, C., additional

Published
1999
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20. 050 Ischaemic arterial strokes in childhood: Importance of idiopathic forms

Author

Rivier, F., primary, Biron-Andréani, C., additional, Dauvilliers, Y., additional, Bellet, H., additional, Martinez, P.A., additional, Eliaou, J.F., additional, Semprino, M., additional, Azias, M., additional, Mercier, M., additional, Humbertclaude, V., additional, Roubertie, A., additional, Cheminal, R., additional, and Echenne, B., additional

Published
1999
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22. Plasma Homocysteine as a Risk Factor for Vascular Disease

Author

GRAHAM, IAN M., primary, DALY, LESLIE E., additional, REFSUM, HELGA M., additional, ROBINSON, KILLIAN, additional, BRATTSTR??M, LARS E., additional, UELAND, PER M., additional, PALMA-REIS, ROBERTO J., additional, BOERS, GODFRIED H.J., additional, SHEAHAN, RICHARD G., additional, ISRAELSSON, B O, additional, UITERWAAL, CUNO S., additional, MELEADY, RAYMOND, additional, McMASTER, DOROTHY, additional, VERHOFF, PETRA, additional, WITTEMAN, JACQUELINE, additional, RUBBA, PAOLO, additional, BELLET, H??L??NE, additional, WAUTRECHT, JAN C., additional, DE VALK, HAROLD W., additional, SALES LUIS, ARMANDO C., additional, PARROT-ROULAUD, FRANCOISE M., additional, TAN, KOK SOON, additional, HIGGINS, ISABELLA, additional, GARCON, DANIELLE, additional, MEDRANO, MARIA JOS??, additional, CANDITO, MIRANDE, additional, EVANS, ALUN E., additional, and ANDRIA, GENEROSO, additional

Published
1998
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28. Benign infantile familial convulsions are not an allelic form of the benign familial neonatal convulsions gene

Author

Malafosse, A., primary, Beck, C., additional, Bellet, H., additional, Di Capua, M., additional, Dulac, O., additional, Echenne, B., additional, Fusco, L., additional, Lucchini, P., additional, Ricci, S., additional, Sebastianelli, R., additional, Feingold, J., additional, Baldy-Moulinier, M., additional, and Vigevano, F., additional

Published
1994
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29. Plasma Homocysteine as a Risk Factor for Vascular Disease

Author

Richard G. Sheahan, Jacqueline C.M. Witteman, Sales Lúis Ac, Helga Refsum, I.M. Higgins, Paolo Rubba, Israelsson B, Parrot-Rouland Fm, Generoso Andria, Roberto Palma-Reis, Per Magne Ueland, Godfried H.J. Boers, Leslie Daly, Dorothy McMaster, Petra Verhoef, Cuno S.P.M. Uiterwaal, Bellet H, Lars Brattström, Danielle Garcon, de Valk Hw, Killian Robinson, Graham Im, K.S. Tan, Jan C. Wautrecht, and Raymond Meleady

Subjects
Adult, Male, medicine.medical_specialty, Homocysteine, Arteriosclerosis, Hypercholesterolemia, Lower risk, Cobalamin, chemistry.chemical_compound, Methionine, Risk Factors, Internal medicine, Blood plasma, Humans, Medicine, Vascular Diseases, Risk factor, business.industry, Vascular disease, Smoking, Case-control study, Fasting, General Medicine, Middle Aged, medicine.disease, Logistic Models, Endocrinology, chemistry, Case-Control Studies, Relative risk, Hypertension, Female, business, Blood Chemical Analysis
Abstract

Context. —Elevated plasma homocysteine is a known risk factor for atherosclerotic vascular disease, but the strength of the relationship and the interaction of plasma homocysteine with other risk factors are unclear. Objective. —To establish the magnitude of the vascular disease risk associated with an increased plasma homocysteine level and to examine interaction effects between elevated plasma homocysteine level and conventional risk factors. Design. —Case-control study. Setting. —Nineteen centers in 9 European countries. Patients. —A total of 750 cases of atherosclerotic vascular disease (cardiac, cerebral, and peripheral) and 800 controls of both sexes younger than 60 years. Measurements. —Plasma total homocysteine was measured while subjects were fasting and after a standardized methionine-loading test, which involves the administration of 100 mg of methionine per kilogram and stresses the metabolic pathway responsible for the irreversible degradation of homocysteine. Plasma cobalamin, pyridoxal 5'-phosphate, red blood cell folate, serum cholesterol, smoking, and blood pressure were also measured. Results. —The relative risk for vascular disease in the top fifth compared with the bottom four fifths of the control fasting total homocysteine distribution was 2.2 (95% confidence interval, 1.6-2.9). Methionine loading identified an additional 27% of atrisk cases. A dose-response effect was noted between total homocysteine level and risk. The risk was similar to and independent of that of other risk factors, but interaction effects were noted between homocysteine and these risk factors; for both sexes combined, an increased fasting homocysteine level showed a more than multiplicative effect on risk in smokers and in hypertensive subjects. Red blood cell folate, cobalamin, and pyridoxal phosphate, all of which modulate homocysteine metabolism, were inversely related to total homocysteine levels. Compared with nonusers of vitamin supplements, the small number of subjects taking such vitamins appeared to have a substantially lower risk of vascular disease, a proportion of which was attributable to lower plasma homocysteine levels. Conclusions. —An increased plasma total homocysteine level confers an independent risk of vascular disease similar to that of smoking or hyperlipidemia. It powerfully increases the risk associated with smoking and hypertension. It is time to undertake randomized controlled trials of the effect of vitamins that reduce plasma homocysteine levels on vascular disease risk.

Published
1997
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30. Does oxidative stress alter quadriceps endurance in chronic obstructive pulmonary disease?

Author

Koechlin C, Couillard A, Simar D, Cristol JP, Bellet H, Hayot M, and Prefaut C

Abstract

The role of exercise-induced oxidative stress in the reduced quadriceps endurance of chronic obstructive pulmonary disease (COPD) patients has never been shown. We conducted a randomized, double-blind, and crossover study in which nine severe patients performed localized dynamic quadriceps endurance tests at 40% of maximal strength after oral treatment with the antioxidant, N-acetylcysteine (NAC), and placebo. Venous blood was sampled before, immediately after exercise, and 6 hours later. Endurance time improved by 25% after NAC treatment compared with placebo (p < 0.05). Superoxide anion (oxidant) release by stimulated phagocytes decreased after treatment (p < 0.05). No change in the antioxidant system was observed. Lipid peroxidation, an index of oxidative stress, was significantly increased 6 hours after exercise in the placebo condition (p < 0.05) but not after treatment. Advanced oxidized protein products, another index of oxidative stress, were also increased 6 hours after exercise by 139 +/- 27% in the placebo condition but only by 54 +/- 19% after treatment (p < 0.05). This study shows that NAC treatment in COPD reduced basal disturbance in the prooxidant system, improved endurance time, and prevented exercise-induced oxidative stress. Oxidative stress thus seems to be implicated in the reduced quadriceps endurance of patients with COPD. [ABSTRACT FROM AUTHOR]

Published
2004
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31. Urinary excretion of free cysteine in critically ill neonates.

Author

Cambonie, G, Bellet, H, Houdon, L, Vallat, C, El Younsi, M, and Vergnes, C

Subjects
*NEONATAL diseases, *CYSTEINE proteinases, *CYSTEINE, *NEUROLOGICAL disorders, *HEALTH outcome assessment, *GESTATIONAL age, *CATASTROPHIC illness, *SEVERITY of illness index, *SULFITES, *ASPHYXIA neonatorum, *APGAR score, *SEPTIC shock, *DISEASE complications
Abstract

Unlabelled: In preliminary observations, significant amounts of free cysteine, a neurotoxic amino acid, were noted in the urine of asphyxiated or septic-shocked neonates. The present study was conducted to determine whether free urinary cysteine was elevated in these critically ill neonates compared with a control group, and to assess the clinical significance of this generation. Free cysteine was measured in the urine of newborn infants with perinatal asphyxia (n = 16) or neonatal sepsis (n = 14) and the urine of a control group (n = 10) by ion-exchange chromatography. Relationships between cysteine levels and the clinical severity, sulfite supply and neurological outcome of the patients were then studied. Urinary cysteine was 27.6 (15-49) mmol mol(-1) creatinine for the patients but was not detectable in the control group. Cysteine levels were correlated with the severity of neonatal septic shock but not with the grade of perinatal asphyxia and did not have a specific influence on the neurological outcome of these patients. The correlation between cysteine level and the severity of neonatal septic shock was indirect and probably linked to higher sulfite administration in this population.Conclusion: The mean daily supply of sulfites is high in critically ill neonates, mainly originating from dopamine and generating significant amounts of cysteine. Although a worsening effect attributable to cysteine on the neurological outcome of the patients could not be demonstrated, the appropriateness of cryptic administration of sulfites by way of drug excipients is called into question. [ABSTRACT FROM AUTHOR]

Published
2001
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