Association of TNF-α polymorphism rs1800629 with multisomatoform disorder in a group of German patients and healthy controls: An explorative study

被引:9
作者
Harms, Katharina C. [1 ]
Kapitza, Karl P. [2 ,3 ]
Pahl, Lisa [1 ]
Anh-Thu Tran [2 ]
Volkmann, Lilly [2 ]
Buers, Dennis [2 ]
Karst, Matthias [2 ]
Stuhrmann, Manfred [1 ]
Bernateck, Michael [2 ]
机构
[1] Hannover Med Sch, Inst Human Genet, D-30625 Hannover, Germany
[2] Hannover Med Sch, Pain Clin, Dept Anesthesiol, D-30625 Hannover, Germany
[3] Med Univ Lubeck, Dept Psychiat & Psychotherapy, D-23538 Lubeck, Germany
关键词
MSD; Pain; Proinflammatory cytokines; TNF polymorphism; NECROSIS-FACTOR-ALPHA; PROMOTER POLYMORPHISM; RECEPTOR ANTAGONIST; GENE POLYMORPHISM; PAIN; CYTOKINES; HYPERALGESIA; INFLAMMATION; DISEASE; G-308A;
D O I
10.1016/j.cyto.2012.12.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Introduction: The etiology of multisomatoform disorder (MSD) is still largely unknown, but genetic factors seem to have an influence on pathogenesis. Pain is a major symptom of MSD and polymorphisms of different proinflammatory cytokines have been found associated with pain in former studies. Therefore, we presumed that cytokine polymorphisms could also be associated with MSD. Patients and methods: Groups of 148 MSD patients with pain as the leading clinical symptom and 149 age and gender matched healthy controls participated in this study. Nine cytokine polymorphisms were genotyped and statistically analyzed for associations with MSD. Results: Allelic and genotypic associations were found for rs16944 (interleukin 1 beta), rs1800629 (tumor necrosis factor) and rs909253 (lymphotoxin alpha). After correcting for multiple testing, the association of rs1800629 with MSD remained significant. The rare A-allele was correlated with MSD (p = 0.007). Discussion: Since the common G-allele of rs1800629 (TNF alpha) occurs much more often in the control group than in the MSD group it is assumed to be protective. Being carrier of the A-allele seems to be a risk factor for MSD. (c) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:389 / 393
页数:5
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