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Article Type

Original Study

Abstract

Objectives The aim of the study was to investigate the role of protein tyrosine phosphatase-1B (PTP-1B) gene polymorphism in essential hypertension and dyslipidemia. Background Essential hypertension is the most common chronic disease and an important risk factor for major health problems. PTP-1B has been recognized as a key modulator of several important physiological pathways. Multiple SNPs of PTP-1B have been shown to be associated with diseases accompanying insulin resistance, such as dyslipidemia and hypertension. Participants and methods The study included 57 individuals divided into two groups: group I comprised 37 hypertensive patients and group II comprised 20 healthy individuals as controls. The participants were subjected to the following: history taking and clinical examination, assessment of weight, height, and BMI, fasting blood sugar, lipid profile, renal function tests, and PCR-RFLP for determination of genotype and allele frequencies of the g54281T > A polymorphism of the PTP-1B gene. Results Group I had statistically higher fasting blood sugar, weight, BMI, and TG. The TT genotype recorded higher frequency in group II than in group I (70%, 43.2%, respectively). While, AA genotype showed higher frequency in group I than in group II (29.7%, 5%, respectively) and TA genotype was higher in group I than in group II (27%, 25%, respectively). However, the differences were without statistical significance. The T allele was more prevalent in group II (82.5%) than in group I (56.8) and the A allele was more prevalent in group I (43.2%) than in group II (17.5%). TA carried a 1.75-fold higher risk than TT [confidence interval (CI): 0.48-6.36], whereas AA carried a 9.63-fold higher risk than TT (CI: 1.10-84.23). The A allele carried a 3.59-fold higher risk than the T allele (CI: 1.41-9.16). In group I, AA genotype was higher in BMI than TT, also TA and AA genotypes were higher in TG than TT. Conclusion The g54281T > A polymorphism of the PTP-1B gene can be implicated in the pathogenesis of essential hypertension.

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