Startseite Relationship between thiolactonase activity and hyperhomocysteinemia according to MTHFR gene polymorphism in Tunisian Behçet's disease patients
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Relationship between thiolactonase activity and hyperhomocysteinemia according to MTHFR gene polymorphism in Tunisian Behçet's disease patients

  • Nadia Koubaa , Sonia Hammami , Amel Nakbi , Khaldoun Ben Hamda , Sylvia Mahjoub , Testsuya Kosaka und Mohamed Hammami
Veröffentlicht/Copyright: 13. Dezember 2007
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Abstract

Background: Behçet's disease (BD) is a multisystemic immuno-inflammatory disorder. Inflammatory processes may cause lipid peroxidation, alteration of lipid profile and increase the risk of atherosclerosis. The aim of this study was to evaluate the association between thiolactonase (HTLase) activity and plasma homocysteine levels (tHcy) in a BD population and to investigate their association with methylenetetrahydrofolate reductase (MTHFR) 677C→T genotype.

Method: A total of 35 BD patients were compared to 39 healthy volunteers.

Results: Significantly higher tHcy levels associated with lower HTLase activities were found in BD patients as compared to healthy controls (p<0.001). These patients also exhibited lower values of triglycerides and high-density lipoprotein cholesterol (HDL-C). Homozygosity for the T allele of the MTHFR gene was more frequent in BD patients (14.3% vs. 7.7%). It was associated with significantly higher tHcy levels (16.9 μmol/L for n=17 vs. 13.1 μmol/L for n=18; p<0.05) and markedly lower HTLase activity (362.6±156.7 U/L vs. 414.2±180.2 U/L) for the (TT+CT) and CC genotypes, respectively. Moreover, HDL-C levels were inversely correlated with tHcy (r=–0.5; p=0.004) but positively associated with HTLase activity (r=0.374; p=0.038). These correlations were also present in several clinical manifestations, such as ocular, neurological involvement or thrombosis.

Conclusions: Homozygosity of the T allele of the MTHFR gene is prevalent in BD patients. High levels of tHcy associated with low HTLase activities may be one of the causes leading to thrombosis in BD patients.

Clin Chem Lab Med 2008;46:187–92.


Corresponding author: Professor M. Hammami, Faculty of Medicine, Laboratory of Biochemistry, UR “Human Nutrition and Metabolic Disorders”, Avicene st 5019, Monastir, Tunisia Phone: +216-73-462-200, Fax: +216-73-460-737

Received: 2007-8-2
Accepted: 2007-10-16
Published Online: 2007-12-13
Published in Print: 2008-02-01

©2008 by Walter de Gruyter Berlin New York

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