Objectives: to evaluate the value of APRI as a non-invasive indicator for hepatic fibro-inflammatory reaction and as a predictor for outcome of interferon therapy in chronic hepatitis C patients.
Patients & methods: data of 600 patients with chronic hepatitis C infection were collected from their files, including age, sex, body weight, complete blood count, platelets count, ESR, serum levels of AST, ALT, GGT, alkaline phosphatase, bilirubin, albumin, urea and creatinine; also ANAs, anti-Bilharzial antibody titers, PT, HCV antibodies and HCV 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. The 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 F0 had mean pretreatment APRI of 0.17, while those with F4 had mean pretreatment APRI of 3.16, and patients with HAI 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 was associated with significant fibrosis and lower APRI was associated with minimal or no fibrosis. In all treated patients, whether responders or non-responders, a gradual decline in mean APRI values was observed with progressing course of interferon therapy indicating gradual regression of hepatic fibro-inflammatory changes with progressing course of interferon therapy. Thos who respond to interferon therapy at treatment week 12 (i.e., early responders) had lower initial APRI (0.81 ± 0.23), lower stages of fibrosis (F0-F2), lower HAI grading (grade 0-8) and lower HCV RNA levels (69520 ± 13783 IU/mL) compared to those who respond at treatment week 24 and to non-responders. The response to interferon therapy was observed to be affected by pretreatment APRI value, where the response in those with pretreatment APRI ≤ 0.63 was 73.91%, in those with pretreatment APRI > 0.63 but < 1.19 was 60.37% and in those with pretreatment APRI > 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 cut-off values of 0.63 and 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 declining of APRI values during the course of interferon therapy indicates reduction of fibro-inflammatory reaction.
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