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  • The present study involved LCPD

    2020-08-06

    The present study involved LCPD patients with age matched healthy controls from an Iranian genetically homogenous population. Our results suggest that the two eNOS 894G > T and −786T > C polymorphisms are associated with increased risk of LCPD. The few available studies supporting this evidence include a recent study conducted by Zhao et al. in Chinese population. Regarding to the rifampicin sale functional role of NO in regulating angiogenesis in human, it is possible that eNOS 894G > T and −786T > C polymorphisms might be positively correlated with development LCPD by affecting NO synthesis. Over the last few years several polymorphisms of the eNOS gene have been identified, and their association with orthopedic disease has been explored. Several studies revealed a statistically significant correlation of eNOS −786T > C polymorphism with neuralgia-inducing cavitational osteonecrosis, osteoporosis, idiopathic as well as secondary multifocal idiopathic osteonecrosis of the head of the femur., To the best of our knowledge this is the first study analyzing eNOS −786T > C polymorphism with LCPD. This study revealed a significantly higher percentage of homozygote mutant rifampicin sale (CC) of the eNOS −786T > C polymorphism in LCPD as compared with controls, indicating that T786C polymorphism is associated with susceptibility to LCPD patients in Iranian children. The −786T > C polymorphism in the promoter region of eNOS gene is associated with the reduction of eNOS promoter transcription rate and significantly reduced promoter activity, leading to endothelial dysfunction and reduced NO production in the vascular endothelium. It seems an impairment of NO production by eNOS −786T > C polymorphism may play in the development of LCPD. The eNOS 894G > T polymorphism, located at exon 7, leads to an amino acid substitution and subsequently leading an immature protein, in which a G > T substitution at exon 7 leads to Glu > Asp substitution at position 298. The eNOS 894G > T polymorphism can lead to low expression levels and activity of eNOS. Therefore, the TT genotype of eNOS 894G > T polymorphism caused a diminished and slower aggregation of erythrocytes, as this genotype has been shown to blunt endothelium-mediated vasodilatation and implicated as a risk factor in numerous cardiovascular conditions hypertension, coronary spasm, myocardial infarction, and coronary artery disease. We have found that the heterozygous GA genotype of eNOS 894G > T was significantly associated increased risk of LCPD (OR = 3.347, 95% CI 1.440–7.778, P = 0.005), compared with the homozygous mutant TT genotype (OR = 2.512, 95% CI 0.220–28.634, P = 0.458). Similar results for the associations of the GA genotype of eNOS 894G > T and LCPD risk were reported in a Chinese population. The eNOS 27-bp VNTR polymorphism has been found to be associated with altered plasma NO levels. This polymorphism also has been associated with many vascular diseases including hypertension, diabetic retinopathy, and diabetic nephropathy in various populations. Notably, our results were different from a previous study by Zhao et al., which revealed that no significant association between eNOS 27-bp VNTR polymorphism and LCPD risk. Moreover, in the present study, frequency of 27-bp VNTR polymorphism genotypes was not significantly higher in control group than LCPD patients. Therefore, we suggest that the eNOS 27-bp VNTR polymorphism may not function as a protective factor LCPD risk.