Influence of Schistosomiasis on Fibrosis Evolution After Interferon-Induced SVR in Chronic HCV Over a 12-Year Biopsy-Based Study.

Schistosomiasis ranks as the second most significant parasitic illness in terms of socioeconomic impact, after malaria. The hepatitis C virus (HCV) is a primary cause of serious liver disease, such as chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Schistosomiasis increases the probability of HCV co-infection, exacerbates liver damage, and reduces the efficacy of antiviral treatments. The study aimed to compare the prognostic significance of serologically identified versus biopsy-confirmed hepatic schistosomiasis (bilharzial hepatic granuloma) in chronic HCV patients treated with interferon-based therapy. A cohort of 453 patients with chronic HCV who received interferon-based therapy was followed over 12 years. Baseline assessments included clinical and laboratory tests, transient elastography, indirect hemagglutination assay (IHA) for Schistosoma antibodies, and liver biopsy. Outcomes were monitored through periodic clinical, laboratory, and elastography evaluations. fibrosis progression occurred in 50% (4/8) of patients with hepatic granulomas, while 50% demonstrated a stable course; no regression was observed. Fibrosis outcomes did not differ significantly between patients with low versus high indirect hemagglutination assay (IHA) titers. No mortality or episodes of hepatic decompensation were recorded in either group. Notably, HCC developed exclusively in the high IHA titer group (incidence rate: 0.08 per 100 person-years). Liver Biopsy-confirmed schistosomiasis granuloma exacerbates fibrosis outcomes in interferon-treated chronic HCV patients. Additionally, a high Schistosoma antibody titer (IHA) is linked to increased HCC incidence, underscoring the prognostic value of both biopsy and serologic evaluation in this population.