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首页> 外文期刊>Clinical rheumatology >Angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism is not a risk factor for hypertension in SLE nephritis
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Angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism is not a risk factor for hypertension in SLE nephritis

机译:血管紧张素转换酶(ACE)基因插入/缺失多态性不是SLE肾炎高血压的危险因素

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摘要

SLE is a systemic autoimmune disease with high prevalence of hypertension. Around 40-75 % of SLE patients develop nephritis, a major cause of hypertension and mortality. Angiotensin-converting enzyme (ACE) maintains the blood pressure and blood volume homeostasis. An insertion/deletion (I/D) polymorphism in intron 16 of ACE gene was reported to influence the development of hypertension, nephritis, and cardiovascular diseases in different ethnic populations. Despite compelling evidence for the high prevalence of hypertension in individuals with SLE, underlying factors for its development are not well studied. With this background, we analyzed the influence of ACE insertion/deletion polymorphism on susceptibility to SLE, development of nephritis and hypertension, other clinical features and autoantibody phenotype in South Indian SLE patients. Three hundred patients with SLE and 460 age and sex similar ethnicity matched individuals were included as patients and healthy controls, respectively. The ACE gene insertion/deletion polymorphism was analyzed by PCR. Insertion (I) and deletion (D) alleles were observed to be equally distributed among patients (57 and 43 %) and controls (59 and 41 %), respectively. The mutant (D) allele did not confer significant risk for SLE (II vs. ID: p = 0.4, OR 1.15, 95 % CI 0.8-1.6; II vs. DD: p = 0.34, OR 1.22, 95 % CI 0.8-1.85). There was no association of the ACE genotype or the allele with development of lupus nephritis (II vs. ID: p = 0.19, OR 1.41, 95 % CI 0.84-2.36; II vs. DD: p = 0.41, OR 0.74, 95 % CI 0.38-1.41) or hypertension (II vs. ID: p = 0.85, OR 0.9, 95 % CI 0.43-1.8; II vs. DD: p = 0.66, OR 1.217, 95 % CI 0.5-2.8). The presence of mutant allele (D) was not found to influence any clinical features or autoantibody phenotype. The insertion/deletion polymorphism of the ACE gene is not a genetic risk factor for SLE and does not influence development of hypertension or lupus nephritis in South Indian Tamils.
机译:SLE是一种全身性自身免疫性疾病,高血压高发。大约40-75%的SLE患者发展为肾炎,这是高血压和死亡率的主要原因。血管紧张素转换酶(ACE)维持血压和血容量稳态。据报道,ACE基因内含子16的插入/缺失(I / D)多态性会影响不同族裔人群高血压,肾炎和心血管疾病的发展。尽管有充分的证据表明SLE患者中高血压的患病率很高,但对其发展的潜在因素尚未进行充分的研究。在此背景下,我们分析了ACE插入/缺失多态性对南印度SLE患者对SLE易感性,肾炎和高血压的发展,其他临床特征以及自身抗体表型的影响。将300例SLE患者和460名年龄和性别相似的种族相匹配的患者分别作为患者和健康对照组。通过PCR分析ACE基因的插入/缺失多态性。插入(I)和缺失(D)等位基因分别在患者(57%和43%)和对照(59%和41%)中平均分布。突变(D)等位基因未赋予SLE显着风险(II vs.ID:p = 0.4,OR 1.15,95%CI 0.8-1.6; II vs.DD:p = 0.34,OR 1.22,95%CI 0.8-1.6 1.85)。 ACE基因型或等位基因与狼疮性肾炎的发生没有关联(II vs.ID:p = 0.19,OR 1.41,95%CI 0.84-2.36; II vs. DD:p = 0.41,OR 0.74,95% CI 0.38-1.41)或高血压(II vs. ID:p = 0.85,OR 0.9,95%CI 0.43-1.8; II vs. DD:p = 0.66,OR 1.217,95%CI 0.5-2.8)。突变等位基因(D)的存在未发现影响任何临床特征或自身抗体表型。 ACE基因的插入/缺失多态性不是SLE的遗传风险因素,也不影响南印度泰米尔人的高血压或狼疮性肾炎的发展。

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