OBJECTIVE: Mucosa-associated lymphoid tissue, which has a follicular structure closely resembling Peyer patches, is absent in the normal gastric mucosa, but it can develop in several chronic conditions. Since we recently detected hepatitis C virus-RNA in gastric mucosa-associated lymphoid tissue of patients with chronic hepatitis C, we tried to treat hepatitis C virus infection to evaluate the effect of antiviral therapy on gastric mucosa-associated lymphoid tissue. METHODS: Eighteen patients (12 men and 6 women; mean age: 52 years, range: 33-71 years) affected by chronic hepatitis C virus and with gastric mucosa-associated lymphoid tissue were enrolled. We enrolled only patients hepatitis C virus-positive, mucosa-associated lymphoid tissue-positive, and Helicobacter pylori-negative (8 patients) or hepatitis C virus-positive patients in whom anti-H. pylori therapy did not obtain disappearance of gastric mucosa-associated lymphoid tissue (10 patients). Hepatitis C virus was evaluated by hepatic biopsy with histologic evaluation and serologic examination; Gastric mucosa-associated lymphoid tissue was scored using Wotherspoon score. All patients were treated with recombinant leukocyte interferon-alpha-2b plus oral ribavirin for 6 months. The hepatitis C virus RNA was assayed at entry and at 3 months after stopping treatment. Virologic response was defined as undetectable levels of serum hepatitis C virus RNA 3 months after stopping treatment; esophagogastroduodenoscopy was repeated at this time to evaluate the effect of anti-hepatitis C virus therapy on acquired gastric mucosa-associated lymphoid tissue. RESULTS: Two (11.11%) patients were withdrawn from the study. Hepatitis C virus cure was obtained in 11/16 patients (68.75%), and in all of them we obtained disappearance of gastric mucosa-associated lymphoid tissue (P < 0.01). Hepatitis C virus infection persisted, but with very lower levels, in 5 of 16 patients (31.25%): in 3 patients gastric mucosa-associated lymphoid tissue persisted (but in 2 it decreased from grade 3 to grade 2), while in 2 it disappeared. CONCLUSIONS: We showed clearly that there is a strict correlation between hepatitis C virus infection and acquired MALT, obtaining the disappearance of this acquired immunologic acquired gastric tissue curing hepatitis C virus infection. However, further studies are needed to clarify there is the same correlation between hepatitis C virus infection and gastric mucosa-associated lymphoid tissue lymphomas in hepatitis C virus-positive patients.
OBJECTIVE: Mucosa-associated lymphoid tissue, which has a follicular structure closely resembling Peyer patches, is absent in the normal gastric mucosa, but it can develop in several chronic conditions. Since we recently detected hepatitis C virus-RNA in gastric mucosa-associated lymphoid tissue of patients with chronic hepatitis C, we tried to treat hepatitis C virus infection to evaluate the effect of antiviral therapy on gastric mucosa-associated lymphoid tissue. METHODS: Eighteen patients (12 men and 6 women; mean age: 52 years, range: 33-71 years) affected by chronic hepatitis C virus and with gastric mucosa-associated lymphoid tissue were enrolled. We enrolled only patientshepatitis C virus-positive, mucosa-associated lymphoid tissue-positive, and Helicobacter pylori-negative (8 patients) or hepatitis C virus-positive patients in whom anti-H. pylori therapy did not obtain disappearance of gastric mucosa-associated lymphoid tissue (10 patients). Hepatitis C virus was evaluated by hepatic biopsy with histologic evaluation and serologic examination; Gastric mucosa-associated lymphoid tissue was scored using Wotherspoon score. All patients were treated with recombinant leukocyte interferon-alpha-2b plus oral ribavirin for 6 months. The hepatitis C virus RNA was assayed at entry and at 3 months after stopping treatment. Virologic response was defined as undetectable levels of serum hepatitis C virus RNA 3 months after stopping treatment; esophagogastroduodenoscopy was repeated at this time to evaluate the effect of anti-hepatitis C virus therapy on acquired gastric mucosa-associated lymphoid tissue. RESULTS: Two (11.11%) patients were withdrawn from the study. Hepatitis C virus cure was obtained in 11/16 patients (68.75%), and in all of them we obtained disappearance of gastric mucosa-associated lymphoid tissue (P < 0.01). Hepatitis C virus infection persisted, but with very lower levels, in 5 of 16 patients (31.25%): in 3 patients gastric mucosa-associated lymphoid tissue persisted (but in 2 it decreased from grade 3 to grade 2), while in 2 it disappeared. CONCLUSIONS: We showed clearly that there is a strict correlation between hepatitis C virus infection and acquired MALT, obtaining the disappearance of this acquired immunologic acquired gastric tissue curing hepatitis C virus infection. However, further studies are needed to clarify there is the same correlation between hepatitis C virus infection and gastric mucosa-associated lymphoid tissue lymphomas in hepatitis C virus-positive patients.