Background: Gastric cancer screening using the pepsinogen filter test is receiving wide recognition in Japan owing to convenience, freedom from discomfort or risk, efficiency, and economy. Because the long-term outcomes of cancer development in extensive atrophic gastritis detected by pepsinogen test are unclear, testpositive and test-negative subjects were investigated in a longitudinal cohort study. Methods: Subjects comprised 5,209 middle-aged men with measured serum pepsinogen levels who were followed for 10 years. Cancer development based on ''atrophy-positive'' and ''atrophy-negative'' criteria used for cancer screening was investigated. Results: During the study, 63 cases of cancer developed in the cohort, representing an incidence rate of 125 per 100,000 person-years. Pepsinogen test screening using the most widely used atrophy-positive criterion (pepsinogen I, V70 ng/mL; pepsinogen I/II ratio, V3.0) displayed 58.7% sensitivity, 73.4% specificity, and 2.6% positive predictive value. Cancer inci-

A total of 5,209 asymptomatic, middle-aged subjects, whose serum pepsinogen (PG) and Helicobacter pylori antibody levels had been assessed, were followed for 10 years. Subjects with positive serum H. pylori antibodies (>50 U/mL) had an increased cancer risk (HR 5 3.48, 95% CI 5 1.26-9.64). Risk of gastric cancer increased as the antibody level increased; the H. pylori-positive group with antibody levels >500 U/mL had the highest incidence rate (325/100,000 person-years). Cancer development also increased with a reduced serum PG I level or a reduced PG I/II ratio; the risk was significantly elevated with serum PG I level ≤30 ng/mL (HR 5 3.54, 95% CI 5 1.95-6.40) or PG I/II ratio ≤3.0 (HR 5 4.25, 95% CI 5 2.47-7.32). Furthermore, the risk of diffuse-type cancer increased as PG II level increased; it was significantly elevated with PG II level ≥30 ng/mL (HR 5 3.81, 95% CI 5 1.10-13.21). Using H. pylori antibody and PG levels, subgroups with an especially high or low cancer incidence rate could be identified. H. pylori-negative or indeterminate subjects with low PG level (PG I ≤30 ng/mL or PG I/II ratio ≤2.0) or H. pylori-positive subjects with antibody levels >500 U/mL and a low PG level were among the subgroups with a high cancer incidence rate (over 400/100,000 person-years). In contrast, H. pylorinegative subjects with a PG I level >70 ng/mL or a PG I/II ratio >3.0 had the lowest risk; none of these subjects developed cancer. Thus, serum PG levels and/or H. pylori antibody levels can be used to predict the risk of cancer in individuals with H. pylorirelated gastritis from the general population. ' 2008 Wiley-Liss, Inc.Key words: gastric cancer; pepsinogen; Helicobacter pylori; chronic atrophic gastritis; intestinal metaplasia Stomach carcinogenesis in high-risk populations, including the Japanese population, is believed to begin with chronic active inflammation of the stomach mucosa, proceeding to extensive atrophy together with intestinal metaplasia, then to dysplasia, and finally to cancer. 1 Currently, Helicobacter pylori (H. pylori) is considered a major factor in the establishment of the carcinogenic sequence in the stomach. 2-12 H. pylori-related gastritis usually starts in the antrum and expands proximally towards the body of the stomach. [13][14][15] During this process, both multifocal atrophy and intestinal metaplasia develop, eventually leading to chronic atrophic gastritis (CAG) with extensive intestinal metaplasia. Several studies dealing with endoscopic biopsies or chromoendoscopic testing found that the progression of CAG increases the risk for cancer. 12,[16][17][18][19][20] Thus, an accurate and reliable evaluation of the extent of CAG is considered to be important for identifying individuals at high risk of cancer. The diagnosis of CAG is based on histopathology of the stomach mucosa. However, gastric endoscopy with biopsy is an invasive test and inappropriate for mass population screening. In addition, since CAG together with intestinal metaplasia is a multifocal process, it is difficult to ac...

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Two patients developed segmental, diffuse intrahepatic recurrence after percutaneous radiofrequency ablation (RFA) to treat a primary, solitary, and small (2.5 cm) hepatocellular carcinoma (HCC). Despite the size of the HCC, levels of the tumor markers (α-fetoprotein, α-fetoprotein-L3%, and des-γ-carboxyprothrombin) were all elevated before RFA, and tumors in both patients were contiguous with a major branch of the portal vein. Tumor biopsies of both patients revealed moderately differentiated HCC but diagnostic imaging showed an area of reduced tumor blood flow, suggesting a poorly differentiated component. Since early detection of post-RFA malignancies by standard ultrasonography and contrast-enhanced computed tomography was difficult, the most sensitive indicator of recurrence in these two patients was the elevated tumor markers. The diffuse intrahepatic recurrence was thought to be caused by increased intratumoral pressure during RFA, resulting in the dissemination of cancer cells through the contiguous portal vein. The clinical course of these tumors indicate that the choice of RFA should be carefully considered when treating specific subtype of HCC that is adjacent to main portal vein branch and involves a possible poorly differentiated component and that surgical resection or combinations of RFA with other treatment modalities such as transcatheter arterial chemoembolization should be considered as alternative treatment strategies.

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