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Titolo:
CYP2D6 polymorphism in systemic lupus erythematosus patients
Autore:
Kortunay, S; Bozkurt, A; Bathum, L; Basci, NE; Calguneri, M; Brosen, K; Kayaalp, SO;
Indirizzi:
Hacettepe Univ, Fac Med, Dept Pharmacol, TR-06100 Altindag Ankara, Turkey Hacettepe Univ Altindag Ankara Turkey TR-06100 0 Altindag Ankara, Turkey Odense Univ Hosp, Dept Clin Chem, DK-5000 Odense, Denmark Odense Univ Hosp Odense Denmark DK-5000 in Chem, DK-5000 Odense, Denmark Hacettepe Univ, Fac Med, Dept Rheumatol, TR-06100 Ankara, Turkey HacettepeUniv Ankara Turkey TR-06100 Rheumatol, TR-06100 Ankara, Turkey Odense Univ, Inst Med Biol, Dept Clin Pharmacol, Odense, Denmark Odense Univ Odense Denmark d Biol, Dept Clin Pharmacol, Odense, Denmark
Titolo Testata:
EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY
fascicolo: 1, volume: 55, anno: 1999,
pagine: 21 - 25
SICI:
0031-6970(199903)55:1<21:CPISLE>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEBRISOQUINE OXIDATION; POOR METABOLIZERS; DRUG-METABOLISM; CYTOCHROME-P450 CYP2D6; RHEUMATOID-ARTHRITIS; HYDROXYLATION; GENE; POPULATION; SPARTEINE; PHENOTYPE;
Keywords:
cytochrome P450; systemic lupus erythematosus; debrisoquine and genetic polymorphism;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Kortunay, S Hacettependagv, Fac Med, Dept Pharmacol, Asistan Lojmani 120, TR-06100 Alti Hacettepe Univ Asistan Lojmani 120 Altindag Ankara Turkey TR-06100
Citazione:
S. Kortunay et al., "CYP2D6 polymorphism in systemic lupus erythematosus patients", EUR J CL PH, 55(1), 1999, pp. 21-25

Abstract

Objectives: To determine whether patients with idiopathic systemic lupus erythematosus (SLE) are associated with impaired CYP2D6 activity and to gaininsight into whether there is an association between particular CYP2D6 genotypes and susceptibility to SLE, and whether CYP2D6 polymorphism is linkedto any specific clinical features of SLE. Methods: Debrisoquine sulfate (10 mg p.o.) was given to 159 healthy volunteers and 39 idiopathic SLE patients. Genotypic assay was carried out in 80 healthy volunteers and 32 patients. A 10-ml blood sample was drawn for genotypic assay. Debrisoquine and 4-hydroxydebrisoquine were determined in 8-h urine samples. Blood samples were analysed for the presence of mutations inthe CYP2D6 gene, by using polymerase chain reaction (PCR) specific for CYP2D6*3 and CYP2D6*4 alleles. Results: The metabolic ratio of debrisoquine to 4-hydroxydebrisoquine ranged from 0.01 to 86.98 in healthy subjects and from 0.02 to 96 in SLE patients. We observed the poor metabolizer(Phl) debrisoquine phenotype in three of 39 patients with idiopathic SLE (7.6%) and five of 159 healthy subjects (3.1%). There was no significant difference in the frequency of PM phenotypes between idiopathic SLE and healthy subjects (Fisher's exact test, P = 0.19). No significant difference in the distribution of overall genotypes and allele frequencies were observed between the two groups. No significant relationships were found between specific clinical features and the overall genotype. Conclusion: The results of this study confirm that CYP2D6 activity is not impaired in SLE and that there is no association between SLE and phenotypicCYP2D6 status. The results also showed that there was no difference in thefrequency of CYP2D6A and CYP2D6B alleles between controls and patients with SLE.

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Documento generato il 25/01/20 alle ore 18:50:55