Srivastava Daya Shankar Lal, Jain Vijay K, Verma Poonam, Yadav Jaya P
Department of Biotechnology and Molecular Medicine, Pt. B.D. Sharma PGIMS, Rohtak, Haryana, India.
Department of Skin and VD, Pt. B.D. Sharma PGIMS, Rohtak, Haryana, India.
Indian J Dermatol Venereol Leprol. 2018 Jan-Feb;84(1):39-44. doi: 10.4103/ijdvl.IJDVL_1128_16.
Increased oxidative stress and resulting inflammation has been emphasized as a factor in the pathogenesis of many diseases including psoriasis. Glutathione S-transferases (GSTs) protect against oxidative stress, inflammation, and genotoxicity. Polymorphisms in the GST genes may lead to an imbalance in pro- and antioxidant systems resulting in the increased production of reactive oxygen species that could influence the pathogenesis of psoriasis.
The aim of this study was to investigate the association between GSTs (GSTM1 and GSTT1) gene polymorphism in patients with chronic plaque psoriasis as a factor in the susceptibility and development of psoriasis.
We assessed 128 patients with psoriasis and 250 age- and sex-matched healthy controls. Genomic DNA was extracted from peripheral blood by the phenol chloroform method. The null GSTT1 and GSTM1 genotypes were identified by multiplex polymerase chain reaction (PCR) method.
The null genotype of GSTM1 and GSTT1 was seen in 45.3% and 40.6% in psoriasis patients whereas in the controls it was 34.4% and 20.0%, respectively. A significant association was seen between the null alleles of the GSTT1 (OR = 2.74) and GSTM1 (OR = 1.58) alone or in combination with tobacco use (P < 0.001) and psoriasis risk. The presence of both null genotypes of GSTM1 and GSTT1 further increased the risk of psoriasis (OR = 3.52) when compared with the positive genotypes of GSTM1 and GSTT1.
A major limitation of this study was the small sample size. A large epidemiological study is necessary to confirm these findings.
The null genotype of GSTT1 is a strong predisposing factor for psoriasis in North India.
氧化应激增加及由此引发的炎症已被视为包括银屑病在内的多种疾病发病机制中的一个因素。谷胱甘肽S-转移酶（GSTs）可抵御氧化应激、炎症和基因毒性。GST基因的多态性可能导致促氧化和抗氧化系统失衡，从而增加活性氧的产生，这可能影响银屑病的发病机制。
本研究旨在探讨慢性斑块状银屑病患者中GSTs（GSTM1和GSTT1）基因多态性与银屑病易感性及病情发展之间的关联。
我们评估了128例银屑病患者以及250例年龄和性别匹配的健康对照者。采用酚氯仿法从外周血中提取基因组DNA。通过多重聚合酶链反应（PCR）法鉴定GSTT1和GSTM1的无效基因型。
银屑病患者中GSTM1和GSTT1的无效基因型分别为45.3%和40.6%，而在对照组中分别为34.4%和20.0%。单独或与吸烟联合时，GSTT1（OR = 2.74）和GSTM1（OR = 1.58）的无效等位基因与银屑病风险之间存在显著关联（P < 0.001）。与GSTM1和GSTT1的阳性基因型相比，GSTM1和GSTT1两种无效基因型的存在进一步增加了银屑病风险（OR = 3.52）。
本研究的一个主要局限性是样本量小。需要进行大规模的流行病学研究来证实这些发现。
在印度北部，GSTT1的无效基因型是银屑病的一个强有力的易感因素。
