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血管紧张素转换酶基因多态性对白癜风患者的有害影响。

Deleterious effect of angiotensin-converting enzyme gene polymorphism in vitiligo patients.

作者信息

Basher Nosiba Suliman, Malik Abdul, Aldakheel Fahad, Chaudhary Anis Ahmad, Rudayni Hassan Ahmad, Alkholief Musaed, Alshamsan Aws

机构信息

Department of Biology, College of Science, Imam Mohammad Ibn Saud Islamic University, Riyadh, Saudi Arabia.

Nanobiotechnology Unit, Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.

出版信息

Saudi J Biol Sci. 2021 Aug;28(8):4478-4483. doi: 10.1016/j.sjbs.2021.04.045. Epub 2021 Apr 24.

DOI:10.1016/j.sjbs.2021.04.045
PMID:34354433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8324959/
Abstract

Vitiligo is a rare skin condition caused by an immune reaction. Vitiligo can occur anywhere on the body. This proposed explanation of vitiligo makes it clear that vitiligo is not linked to any other autoimmune diseases. The polymorphisms of some genes present in the immune system play a major function in susceptibility of vitiligo. Meta-analysis studies have shown that the Angiotensin converting enzyme (ACE) gene insertion and deletion polymorphism is closely associated with vitiligo in many ethnicities. The connection between gene and vitiligo is connected through the auto immune diseases and there are no genetic polymorphism studies have been carried out with ACE gene with vitiligo in the Saudi population. Previous studies show that vitiligo patients are more likely to also have an autoimmune disorder. The current study aims to investigate the I/D polymorphism in the ACE gene with diagnosed patients with vitiligo subjects. This is a case-control study carried out in the Saudi population with 100 vitiligo cases and 100 healthy controls. Genotyping was performed through polymerase chain reaction followed by 3% agarose gel electrophoresis. Genotype and allele frequencies were carried out with genetic mode of inheritances. Statistical analysis was performed considering p < 0.05 as significant association. There was a substantial difference in allele frequency distribution between vitiligo patients and healthy controls (OR-1.70 (95%CI: 1.14-2.53); p = 0.008). Additionally, DD genotype (OR-4.71 (95%CI: 1.42-15.61); p = 0.008) and recessive model (OR-2.66 (95%CI: 1.41-5.02); p = 0.002) was strongly associated. Both dominant and co-dominant showed the negative association (p > 0.05) when compared between the vitiligo cases and controls. The correlation between age and genotyping was performed with Anova analysis and current study results confirmed the substantial link between 11 and 20 years (p = 0.01) and 31-40 years (p = 0.04) with the defined age groups. In conclusion, in Saudi populations, the gene I/D polymorphism was identified as being correlated with vitiligo. This is the first study in Saudi Arabia to report the risk factors of vitiligo with the gene polymorphism.

摘要

白癜风是一种由免疫反应引起的罕见皮肤病。白癜风可发生于身体的任何部位。这种对白癜风的解释表明,白癜风与任何其他自身免疫性疾病无关。免疫系统中某些基因的多态性在白癜风易感性中起主要作用。荟萃分析研究表明,血管紧张素转换酶(ACE)基因插入/缺失多态性在许多种族中与白癜风密切相关。基因与白癜风之间的联系是通过自身免疫性疾病建立的,在沙特人群中尚未对白癜风患者进行ACE基因的遗传多态性研究。先前的研究表明,白癜风患者更有可能同时患有自身免疫性疾病。本研究旨在调查确诊为白癜风患者的ACE基因插入/缺失多态性。这是一项在沙特人群中进行的病例对照研究,有100例白癜风患者和100名健康对照。通过聚合酶链反应进行基因分型,随后进行3%琼脂糖凝胶电泳。根据遗传遗传模式计算基因型和等位基因频率。以p<0.05为显著关联进行统计分析。白癜风患者和健康对照之间的等位基因频率分布存在显著差异(OR = 1.70(95%CI:1.14 - 2.53);p = 0.008)。此外,DD基因型(OR = 4.71(95%CI:1.42 - 15.61);p = 0.008)和隐性模型(OR = 2.66(95%CI:1.41 - 5.02);p = 0.002)与白癜风显著相关。在白癜风病例与对照之间比较时,显性和共显性均显示出负相关(p>0.05)。通过方差分析对年龄与基因分型之间的相关性进行了分析,本研究结果证实了11至20岁(p = 0.01)和31至40岁(p = 0.04)与特定年龄组之间存在显著关联。总之,在沙特人群中,ACE基因插入/缺失多态性被确定与白癜风相关。这是沙特阿拉伯第一项报道白癜风与ACE基因多态性相关危险因素的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d1b/8324959/a7e2d5f109c2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d1b/8324959/3231f6ced7f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d1b/8324959/af574fc83781/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d1b/8324959/a7e2d5f109c2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d1b/8324959/3231f6ced7f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d1b/8324959/af574fc83781/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d1b/8324959/a7e2d5f109c2/gr3.jpg

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