Introduction: Prior to the 1990s, the most common sources of HCV infections were blood transfusions, unsafe injections and I.V drug use. Screening of blood products for HCV has eradicated transfusion-transmitted hepatitis C in most countries since 1992-in Bosnia and Herzegovina, however, since 1995, due to the war.
Aim: To investigate the impact of the source of HCV infection on the therapeutic response in patients treated for chronic HCV infection with dual combined therapy.
Methods: We diagnosed chronic HCV infections amongst 246 patients over a period of five years and selected them according to the reported source of infection. Pegylated interferon alfa 2a or alfa 2b with ribavirin was administered during the time that was genotype-dependent. HCV RNA levels in sera were measured by real time PCR. Liver histology was evaluated in accordance with the level of necroinflammation activity and the stadium of fibrosis.
Results: Regardless of the genotype of the virus and the source of infection, SVR was achieved in 67% of the patients. Therapeutic response (ETR) was not achieved in 25% of the patients who were infected with an untested blood transfusion and 6% of the patients who had had wartime surgery. Amongst the different sources of infections, patients with a war-surgery source of infection responded better to therapy than those with a blood transfusion source of infection (p = 0.023). A blood transfusion source of infection implies a larger fibrosis stage than in blood donors; (g = 1.177; s2 = 0.577). A blood transfusion source of infection implies a significantly larger necroinflammatory activity than in blood donors; (g = 1.456; s2 = 0.618).
Conclusions: An untested blood transfusion was a significant risk factor for more advanced liver diseases in regards to necroinflammatory activity and the fibrosis stage. This source of infection was also a risk factor for low responses to antiviral therapy. At the same time, I.V. drug users had more progressive necroinflammatory activity, but a high therapeutic response to antiviral therapy.
Keywords: blood transfusion; therapy response; viral hepatitis C.