急性关节炎患者的CD14和肿瘤坏死因子α启动子多态性。特别提及慢性脊柱关节病的发展。

CD14 and TNfa promoter polymorphisms in patients with acute arthritis. Special reference to development of chronic spondyloarthropathy.

作者信息

Repo Heikki, Anttonen Krista, Kilpinen Sami K, Palotie Aarno, Salven Petri, Orpana Arto, Leirisalo-Repo Marjatta

机构信息

Department of Medicine, Division of Infectious Diseases, Helsinki University Central Hospital, Haartman Institute, University of Helsinki, Finland.

出版信息

Scand J Rheumatol. 2002;31(6):355-61. doi: 10.1080/030097402320817086.

DOI:10.1080/030097402320817086

PMID:12492251

Abstract

OBJECTIVE

To examine CD14 and TNFalpha gene polymorphisms in early arthritis in relation to clinical outcome.

METHODS

We studied 141 Caucasians who had had early arthritis 10 to 38 years earlier. We analysed CD14 (-159) and TNFalpha (-238, -308, -376) polymorphisms using a novel cycle minisequencing method. DNA pools from 370 Caucasian blood donors served as controls.

RESULTS

CD14 (-159)C-->T allele frequencies were comparable among patients and controls (39% vs 40%). Fifty men and 42 women had recovered while 24 men and six women had chronic spondyloarthropathy (SpA). Mutant T allele frequency was higher in the chronic SpA group than in the recovered group in women (75% vs 32%, relative risk 1.3, 95% confidence limit 1.1 to 1.6, P = 0.011), but not in men (38% vs 44%). All female patients with chronic SpA had CD14 (-159)T allele and none had a possibly protective TNFalpha (-308)G-->A allele.

CONCLUSIONS

Possession of CD14 (-159)T allele does not increase risk of ReA but may increase susceptibility of female patients to development of chronic SpA.

摘要

目的

研究早期关节炎中CD14和肿瘤坏死因子α（TNFα）基因多态性与临床结局的关系。

方法

我们研究了141名10至38年前患早期关节炎的白种人。我们使用一种新型循环微测序方法分析了CD14（-159）和TNFα（-238、-308、-376）基因多态性。来自370名白种人献血者的DNA池作为对照。

结果

患者和对照中CD14（-159）C→T等位基因频率相当（39%对40%）。50名男性和42名女性病情已恢复，而24名男性和6名女性患有慢性脊柱关节病（SpA）。在女性中，慢性SpA组的突变T等位基因频率高于病情已恢复组（75%对32%，相对风险1.3，95%置信区间1.1至1.6，P = 0.011），但在男性中并非如此（38%对44%）。所有患有慢性SpA的女性患者均有CD14（-159）T等位基因，且无一例具有可能具有保护作用的TNFα（-308）G→A等位基因。