TABLE 5.1 GEOGRAPHIC VARIATION, AGE-STANDARDIZED GASTRIC CANCER INCIDENCE AND PREVALENCE OF HELICOBACTER PYLORI
The year-round availability of fresh produce eliminates the need to use salt to preserve vegetables. Smoking and salting of meat is no longer a necessity with the advent of universal household refrigeration. These two factors have contributed to the dramatic decrease in stomach cancer rates in Western countries after World War II.
the infecting organism with different IL-B phenotypes, with an odds ratio (OR) of 87 (CI = 11 to 697) when the vacAs1 strain associates with IL-B-511*T (43). In contrast, when H. pylori strain vacAm1 associates with this phenotype, the OR is substantial but falls to 7.4 (CI = 3.2 to 17). Importantly, this relationship between high IL-B expression and gastric cancer requires the presence of H. pylori emphasizing the importance of host-environment interactions in the progression to gastric carcinoma (42).
between the degree and extent of these precursor lesions and increased risk of gastric cancer (11,12,76). This holds true even in low-risk, Western populations as observed by a Swedish registry biopsy cohort study, which assessed the incidence of gastric cancer based on the patient’s stage on Correa cascade at initial diagnosis (77). This study predicted that about 1 in 256 people with normal mucosa, 1 in 85 with gastritis, 1 in 50 with atrophic gastritis, 1 in 39 with IM, and 1 in 19 with dysplasia will develop gastric cancer within 20 years after gastroscopy.
TABLE 5.2 AGE-, SEX-, AND ETHNICITY-ADJUSTED ODDS RATIOS FOR SERUM PEPSINOGEN GROUP I (PGI) LEVELS AND HELICOBACTER PYLORI (HP) ANTIBODY STATUS, ACCORDING TO HISTOLOGIC TYPES OF GASTRIC CANCER
TABLE 5.3 THE PADOVA CLASSIFICATION OF GASTRIC DYSPLASIA AND RELATED LESIONS
resection, may be a reasonable treatment option for patients with small intramucosal carcinomas (97).
FIG. 5.8 Gastric dysplasia. A: Low-grade dysplasia as illustrated here is characterized by cellular elongation, generally basally located nuclei, few mitoses, little cellular stratification, mucin depletion, and hyperchromasia. Compare to background intestinal metaplasia. B: In high-grade dysplasia, the cells are hyperchromatic, pleomorphic, and disorganized. The chromatin pattern is distinct from that of reactive/regenerative hyperplasia (Fig. 5.7).