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Atherosclerosis | 2003

Serum uric acid in hypertensive patients with and without peripheral arterial disease

Michel Langlois; Dirk De Bacquer; Daniel Duprez; Marc L. De Buyzere; Joris Delanghe; Victor Blaton

BACKGROUND Uric acid is frequently elevated in hypertension. In addition to renal and metabolic disturbances, lower limb ischemia might contribute to hyperuricemia among hypertensives complicated by peripheral arterial disease (PAD). OBJECTIVE To test the hypothesis that uric acid status is related to lower limb function in hypertensives with PAD. METHODS Serum and 24-h urine uric acid levels and other risk factors were examined in 145 hypertensives free of PAD and 166 hypertensives with PAD. Ankle/brachial index (ABI) and absolute claudication distance (in PAD) on a treadmill test (ACD) were assessed. RESULTS In multiple regression analysis for serum uric acid in the total group, PAD emerged as an independent determinant (P=0.03) next to age (P=0.005), triglycerides (P=0.04), and insulin (P=0.02). Serum uric acid concentrations were higher in hypertensives with PAD (404+/-101 vs. 347+/-80 micromol/l, P<0.001) independent of components of the metabolic syndrome (body mass index, triglycerides, insulin) and of age, gender, diabetes mellitus, pulse pressure, cholesterol, C-reactive protein, and treatment. After adjustment for kidney function by uric acid/creatinine ratio, values remained higher in hypertensives with PAD (P=0.01). Uric acid excretion was higher in the PAD group (P<0.001), whereas uric acid clearance was comparable between both groups. In multiple regression analysis for ACD (357+/-183 m) in the PAD group, serum uric acid (P=0.02), C-reactive protein (P<0.0001), age (P=0.02), and smoking (P=0.004) were independently associated. ABI (0.62+/-0.17) was not related to uric acid in PAD patients. CONCLUSION Hyperuricemia is more pronounced in hypertensives complicated by PAD and is associated with worse functional status of the peripheral circulation.


Archive | 1998

METHOD AND KIT FOR DETERMINING THE PHENOTYPE OF A HAPTOGLOBIN AND USE THEREOF

Joris Delanghe; Michel Langlois; Buyzere Marc L De


Archive | 2012

SCREENING AND IDENTIFICATION Carbohydrate Deficient Transferrin in a Driver's License Regranting Program

Thomas M. Maenhout; Guido Baten; Marc De Buyzere; Joris Delanghe


Journal of Biomedical chromatography | 1998

Application of western-blotting technique with chemiluminisence imaging to the study of haptoglobin type and haptoglobin complexes

Jin Ouyang; Joris Delanghe; Willy Baeyens; Michel Langlois


European Journal of Laboratory Medicine , 4 pp. 55-59. (1996) | 1996

Pseudohypertriglyceridemia due to benign glycerol kinase deficiency

Joris Delanghe; Jp Deslypere; Marc De Buyzere; S De Biscop; P Willems; A Walker


Biologie prospective -Comptes rendus du 9e colloque de Pont-à-Mousson. John Libbey Eurotext, Paris 1997 | 1997

Haptoglobin polymorphism as a risk factor in cardiovascular disease

Joris Delanghe; Michel Langlois; Marc De Buyzere; Daniel Duprez


Advances in critical care testing (List WF, Mueller MM, McQueeen MJ, eds). Springer Verlag, Berlin-Heidelberg-New York 1997:p. 86-87 | 1997

Evolution of haptoglobin concentration in serum during the early phase of acute myocardial infaction

Dirk Bernard; Michel Langlois; Marc De Buyzere; Joris Delanghe


Archive | 1996

Table 1. Serum concentrationsof Hp, CRP, and immunoglobullns accordIngto Hp type.

Michel Langlois; Joris Delanghe; Marc Dc Buyzere


Pathobiochemie, Molekularbiologie und moderne Diagnostik kardiovaskulärer Erkrankungen' Springer Verlag, Berlin-Heidelberg | 1994

Creaün als fruehzeitiger Merker fuer die Myokardinfarktdiagnostik

Joris Delanghe; Marc De Buyzere


ISSN: 0009-7322 | 1994

MN blood group phenotype, a genetic risk factor for early onset of essential arterial hypertension

Marc De Buyzere; D Robbrecht; Joris Delanghe; Daniel Duprez; Denis Clement

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Michel Langlois

Ghent University Hospital

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Jin Ouyang

Beijing Normal University

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Dirk Bernard

Ghent University Hospital

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