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寻常型银屑病的风险和严重程度与血管紧张素II 1型受体基因多态性及代谢综合征的关系

Risk and severity of psoriasis vulgaris in relation to angiotensin II type 1 receptor gene polymorphism and metabolic syndrome.

作者信息

ElGhareeb Mohamed Ibrahim, Khater Mohamed Hamed, Fakhr Ahmed, Khedr Hanaa Abd-Elftah

机构信息

Dermatology and Venereology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.

Microbiology, Molecular Biology and Immunology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.

出版信息

Clin Cosmet Investig Dermatol. 2019 Sep 12;12:683-690. doi: 10.2147/CCID.S212781. eCollection 2019.

DOI:10.2147/CCID.S212781
PMID:31571968
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6749980/
Abstract

BACKGROUND

Psoriasis vulgaris is a chronic inflammatory and proliferative skin disease, characterized by the formation of itchy, erythematous skin patches or plaques. Patients with psoriasis are at an increased risk of developing metabolic syndrome, including obesity, hypertension, diabetes, and atherosclerosis. Recently, angiotensin II (Ang II) has been reported to be associated with the development of psoriasis. Ang II not only increases the blood pressure but is also a potent proinflammatory modulator and functions through interaction with angiotensin II type 1 receptor (AT1R). Moreover, it is hypothesized that the AT1R gene expression could be correlated with the severity of psoriasis and/or metabolic syndrome.

AIM

We examined the association of Ang II type 1 receptor (AT1R) A1166C gene polymorphisms and metabolic syndrome with the severity of psoriasis.

PATIENTS AND METHODS

The present case-control study included 25 patients with psoriasis vulgaris and 25 healthy subjects in Egypt. The psoriasis lesions in the patient group were assessed using the psoriasis area and severity index (PASI) score. The AT1R polymorphism A1166C (rs5186) was studied using restriction fragment length polymorphism (RFLP) and polymerase chain reaction (PCR) amplification of the gene from the whole blood sample in both groups. Serum lipid profile and blood sugar levels were assessed post 12 h and 8 h fasting, respectively, in both groups. The severity of metabolic syndrome was evaluated using the severity score.

RESULTS

The results of the present study demonstrated that the AT1R A1166C gene polymorphisms increased the risk of developing psoriasis in the Egyptian population. We found that 70% of patients with AC genotype and 100% of patients CC genotype reported a PASI score >20 and were considered to be severe cases with a statistically significant difference as compared with patients with AA genotype (=0.003). In addition, a high statistically significant difference (=0.001) existed among AT1R genotypes with respect to the percentage of metabolic syndrome in psoriasis patients. Similarly, a statistically significant difference (=0.004) among AT1R genotypes with respect to metabolic score was found, with the highest level of score and percentage observed in patients with CC genotype than in patients with AC genotype. The lowest level was present among those with AA genotype.

CONCLUSION

Patients with psoriasis expressing the C allele of AT1R1166 are susceptible to developing metabolic syndrome and have higher PASI scores as compared with patients carrying the A allele.

摘要

背景

寻常型银屑病是一种慢性炎症性增殖性皮肤病,其特征为形成瘙痒性红斑皮肤斑块或斑片。银屑病患者发生代谢综合征(包括肥胖、高血压、糖尿病和动脉粥样硬化)的风险增加。最近,有报道称血管紧张素II(Ang II)与银屑病的发生有关。Ang II不仅会升高血压,还是一种强效促炎调节剂,通过与血管紧张素II 1型受体(AT1R)相互作用发挥作用。此外,据推测AT1R基因表达可能与银屑病和/或代谢综合征的严重程度相关。

目的

我们研究了血管紧张素II 1型受体(AT1R)A1166C基因多态性及代谢综合征与银屑病严重程度之间的关联。

患者与方法

本病例对照研究纳入了埃及的25例寻常型银屑病患者和25名健康受试者。使用银屑病面积和严重程度指数(PASI)评分评估患者组的银屑病皮损情况。通过限制性片段长度多态性(RFLP)和聚合酶链反应(PCR)扩增两组全血样本中的基因,研究AT1R多态性A1166C(rs5186)。两组分别在禁食12小时和8小时后评估血脂谱和血糖水平。使用严重程度评分评估代谢综合征的严重程度。

结果

本研究结果表明,AT1R A1166C基因多态性增加了埃及人群患银屑病的风险。我们发现,70%的AC基因型患者和100%的CC基因型患者PASI评分>20,被认为是重症病例,与AA基因型患者相比差异有统计学意义(=0.003)。此外,银屑病患者中AT1R基因型在代谢综合征百分比方面存在高度统计学差异(=0.001)。同样,在AT1R基因型之间,代谢评分也存在统计学差异(=0.004),CC基因型患者的评分和百分比最高,高于AC基因型患者。AA基因型患者的水平最低。

结论

与携带A等位基因的患者相比,表达AT1R1166 C等位基因的银屑病患者易患代谢综合征且PASI评分更高。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/501f/6749980/5b1b10f41fcc/CCID-12-683-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/501f/6749980/5b1b10f41fcc/CCID-12-683-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/501f/6749980/5b1b10f41fcc/CCID-12-683-g0001.jpg

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