ApaI VDR Polymorphism as a Risk Factor of Treatment Failure in Chronic Hepatitis C Patients
ApaI VDR Polymorphism as a Risk Factor of Treatment Failure in Chronic Hepatitis C Patients
Noora Hassan Hezam Al-Aqmer1*, Zain Aamir2, Muhammad Farooq Hanif3, Soumble Zulfiqar4, Sibgha Zulfiqar1, Mateen Izhar5 and Abdul Rauf Shakoori4*
ABSTRACT
The objective of this study was to find out the association between ApaI vitamin D receptor (VDR) polymorphism and the response to hepatitis C directly acting antiviral treatment. This study which is a case control study included 66 hepatitis C patients (genotype 3) who responded to the directly acting antiviral treatment and achieved negative HCV-RNA three months after completing the treatment (sustained virologic response (SVR)) and 66 hepatitis C patients (genotype 3) who did not achieve SVR three months after completing the same treatment. Informed consent was taken from participants, demographic data was collected, and 5 mL of blood was drawn from each participant and used for DNA extraction, polymerase chain reaction and restriction fragment length polymorphism analysis. After restriction, samples were run on 2% agarose gel followed by visualization under UV light. Data analysis was done using IBM SPSS 24. We found that the distribution of ApaI genotypes was 28 (42.4%), 27 (40.9%), and 11 (16.7%) for the genotypes AA, Aa, and aa in responders and 22 (33.3%), 26 (39.4%), and 18 (27.3%) in non-responders. The allelic distribution was 83 (62.9%) and 49 (37.1%) for the “A” and “a” alleles in responders and 70 (53%) and 62 (47%) in non-responders. ApaI genotype ‘’aa’’ was found to be a significant predictor of treatment failure (p-value= .024, OR= 3.589, 95% CI= 1.181-10.911). There was no significant association between ApaI VDR genotypes and cirrhosis and ApaI VDR genotypes and gender (p-values ˂ .05). To conclude ApaI genotype aa could be used as a marker to predict treatment failure in hepatitis C patients receiving directly acting antiviral treatment.
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