RESUMO
BACKGROUND AND PURPOSE: Current views on B-cell lymphoma genesis suggest that several exogenous factors, acting in a multistep fashion upon a predisposing condition, may be involved in B-cell clonal expansion, a potentially prelymphomatous stage. This study was done to investigate the extrahepatic localization of Hepatitis C virus (HCV)in the gastric mucosa and the possibility of its involvement besides Helicobacter pylori (H. pylori) as possible predisposing factors that might play a role in the occurrence of gastric dysplasia or lymphoproliferation following gastritis and may end in carcinogenesis. PATIENTS AND METHODS: A well characterized series of 45 patients with chronic liver disease complaining of gastric dyspepsia were subjected to Upper Gastrointestinal Endoscopy and histological examination of gastric biopsy with studying the prevalence of serologic and molecular markers of HCV and H. pylori in the patients' serum and their gastric tissue. HCV-RNA detection in gastric tissue was done only for those who showed gastric dysplasia. RESULTS: Histopathological examination of the gastric biopsies revealed that 20 patients (44.4%) had chronic active gastritis, 15 patients (33.4%) had chronic gastritis and 10 patients (22.2%) had gastric dysplasia with chronic gastritis. As for hepatitis C virus, 38 patients (84.4%) were reactive for serum antibodies (HCV-Abs) and 18 patients (40%) showed Polymerase Chain Reaction (PCR) positivity. Helicobacter pylori antibody reactivity was detected in 37 patients (82.2%) while PCR positivity was detected in 24 patients (53.3%) both in their serum as well as in gastric tissues. Seventeen out of twenty cases showing chronic active gastritis were serologically positive for both H. pylori and HCV. Patients who showed dysplasia on pathological examination (n=10) were all HCV-Abs positive (p-value = 0.32), seven patients were serum HCV-RNA positive (p-value = 0.083) and 3 of them showed HCV-RNA positivity in their gastric tissue. Nine out of the patients with gastric dysplastic changes proved positive for H. pylori DNA both in serum (p-value= 0.027) and tissue (p-value= 0.029). CONCLUSIONS: We suggest that Hepatitis C virus may be considered, in addition to Helicobacter pylori, as another potential infectious co-factor in the occurrence of gastric mucosal dysplasia and thus might be associated in the multistep hypothesis of carcinogenesis.