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TITLE:

A STUDY ON INTERFERON APLHA RECEPTORS AND STAT1 AS THERAPY PREDICTORS IN HEPATITIS INFECTION

AUTHORS:

Dr Muhammad Aatir Bhatti, Dr Muhammad Adnan Yousaf, Dr Faizan Bin Shabbir

ABSTRACT:

Introduction: Liver is a pivotal organ of the body and play very important role in the metabolism. If there is any problem in the liver then the herbs or different plants play an important role for the treatment of liver disorders. Objective of the study: The main objective of the study is to analyze the interferon aplha receptors and STAT1 as therapy predictors in hepatitis infection. Methodology of the study: This cross sectional study was conducted in hospital of Sialkot during September 2018 to January 2018. The purpose and benefits of the study were explained to each participant and informed written consent was obtained. By using non-probability convenience sampling, we enrolled treatment-naïve HCV mono-infected and HCV/HBV co-infected patients along with healthy controls. Out of the eligible patients, some were also positive with hepatitis B surface antigen (HbsAg) along with serum HBV-deoxyribonucleic acid (DNA) level. Results: The demographic values of patient group and control group shows a significant difference. The data suggest clearly that CD4 count decreases in abnormal liver function. There were non-significant relationship present in diseased group treated with different therapies like interferon and glutathione as as p<0.05. The level of micronutrients become decreases in diseased group. Of the eligible 171(88%) patients, 86(50.3%) were also positive with HbsAg. The final study sample had 191 subjects. Of them, there were 20(10.5%) in group-1a, 35(18.3%) in group-2a, 65(34%) in group-1b and 51(26.7%) in group-2b. Conclusion: It is concluded that hepatitis directly increase the liver enzymes even after receiving medication and other therapies. Expression rate of IFNAR-1 mRNA maybe useful index for predicting long-term efficacy of IFN therapy compared to STAT-1 and IFNAR-2. Replication of HBV-DNA is not the main factor leading to down-regulation of IFN- receptors or STAT-1.

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