Aspartate Aminotransferase -To-Platelets Ratio Index (Apri) As Indicator For Hepatic Fibro-Inflammation And Predictor For Interferon Therapy Outcomes In Chronic Hepatitis C Patients
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Objectives: To evaluate the value of APRI as a non-invasive indicator for hepatic fibro-inflammatony reactions and as a predictor for outcomes of interferon therapy in chronic hepatitis C patients. Patients & Methods: Data of 600 patients with chronic hepatitis C infection were collected from their medical files, including age, sex, body weight, complete blood count, platelets count, ES!?, serum levels of AST, ALT, GGT, alkaline phosphatase, bilintbin, albumin, urea and creatinine ; also ANAs, anti-Bilharzial antibody titers; PT, HCV antibodies and FIC V RNA levels were collected at time of patients' presentation. Pretreatment APRI values were calculated using platelets count and serum AST levels at patients' presentation; also APRI values were calculated at certain times during interferon therapy using platelets count and AST levels at these times. The degree of hepatic fibrosis and HAI grading were evaluated via histopathologic examination of liver biopsies. Patients' response to interferon therapy was determined at treatment week 12, treatment week 24 and treatment week 48 based on presence or absence of HCV RNA in serum. Results: The advancing the degree of fibrosis and HAI grading was associated with a progressing increase in APRI values, where patients with FO had mean pretreatment APRI of 0.17, while those with F4 had mean pretreatment APRI of 3.16, and patients with HA! grade 1-4 had mean-pretreatment APRI of 0.79, while those with HAI grade 13-18 had mean APRI of 2.87. This indicated that higher APRI values were associated with significant fibrosis and lower APRI values were associated with minimal or no fibrosis. A gradual decline in mean APRI values was observed with progression of course of interferon therapy, indicating gradual regression of hepatic fibro-inflammatony changes with progression of therapy. Those who responded to interferon therapy at treatment week 12 (i.e., early responders) had lower pretreatment APRI (0.81 ± 0.23), lower stages of fibrosis (F0-F2), lower HAI grading (grade 0-8) and lower HCV RNA levels (69,520 ± 13,784 IU/mL) compared to those who responded at treatment week 24 and to non-responders. The response to interferon therawilms observed to be affected by pretreatment APRI values, where the response in those with pretreatment APIU 5 0.63 was 73.91%, in those with pretreatment APRI > 0.63 but < 1.19 was 60.37% and in those with pretreatment APR1> 1.19 was 40.77%. Conclusion: Estimation of APRI could be used as a non-invasive tool to differentiate between patients with no-to-mild hepatic fibrosis and patients with significant fibrosis, with a lower cut-off value of 0.63 and a higher cut-off value of 1.19, but we cannot depend on it for precise determination of individual stages of fibrosis. Higher pretreatment APRI values were associated with bad response to interferon therapy, and decline in APRI values during the course of interferon therapy indicated reduction of fibro-infiammatonj reactions.