The clinicopathological features of 748 solitary early gastric cancers were examined with regard to lymph node metastasis. Among several factors, only depth of invasion and tumour size correlated significantly with node involvement. Tumours which satisfy the following criteria may not metastasize to lymph nodes: (1) confined to the mucosa; (2) less than 1.5 cm in diameter; (3) macroscopically elevated; (4) macroscopically depressed, without intramural ulcers or ulcer scars (endoscopically, no fold convergence); and (5) histologically differentiated. With a recently developed endoscopic technique small gastric tumours can safely be resected. The cut margin and depth of tumour invasion can be verified histologically in the specimen. If an endoscopically removed tumour satisfies the above criteria, further surgical intervention may be optional as the outcome of endoscopic resection is comparable to that of radical surgery in the absence of node involvement.

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Helicobacter pylori is thought to be involved in the pathogenesis of gastric cancer, but the time point at which it produces its effects (critical time) is unknown. We measured the serum level of H. pylori antibody in 787 gastric cancer patients and 1007 controls aged 20 to 69. Odds ratios for different gastric cancer types and stages were determined for each 10-year age class. The overall odds ratio for gastric cancer decreased with age, being 7.0 for those aged 20-29, 14.5 for those aged 30-39, 9.1 for those aged 40-49, 3.5 for those aged 50-59, and 1.5 for those aged 60-69 (trend in odds ratios: P < < < <0.01). However, there was no such age-dependent trend for early diffuse-type cancer; the odds ratios were 12.6, 4.0, 7.2, 6.5, and 18.5 respectively (P = = = =0.29). Early cancer tended to show higher seroprevalence than advanced cancer, especially in older subjects. No significant difference in seroprevalence was observed between diffuse and intestinal cancers within each age-class. Seroreversion must have occurred in the time interval between the critical time and the diagnosis of the cancer, especially in older patients. The age-dependent relationship between H. pylori and gastric cancer may be due to seroreversion, which itself may be independent of age. This age-independence indicates that prolonged exposure to H. pylori does not increase the magnitude of its influence on gastric carcinogenesis. Possible mechanisms through which H. pylori exerts pathogenic effects are continuous inflammation in adulthood and/or irreversible damage to gastric mucosa in childhood or the teenage years. Key words: Gastric cancer -Helicobacter pylori -Age -Early diffuse-type cancerMany studies have shown that Helicobacter pylori is related to gastric cancer.1-3) While cancer prevention trials focusing on the eradication of H. pylori have already been started, the critical timeframe (critical time), during which it produces its carcinogenic effect, has not been identified yet. Identification of this critical time is important because eradication of H. pylori after this time would have no preventive effect on the incidence of gastric cancer.To begin to determine the critical time, we investigated the relationship between gastric cancer and H. pylori with respect to age. Previous studies on the relationship between smoking and lung cancer have shown that the longer the exposure to smoking, the greater the magnitude of its effect on the incidence of lung cancer. 4,5) In a previous study on H. pylori and gastric cancer, we found a high odds ratio of 13.3 for those under 40 years of age, 6) and a meta-analysis showed that the relationship is stronger in the younger population.7) However, other variables, such as geographic region and ethnicity, certainly affect the incidence of gastric cancer by age-class. 8,9) We sought to more clearly separate the influence of age from these other variables by taking a large sample from within a relatively well defined geographic and ethnic region, which is something that previous studies have la...

Postoperative pulmonary complications are often fatal in patients with oesophageal cancer. The influence of various preoperative and perioperative risk factors in the prediction of such complications was analysed. Some 170 oesophageal resections performed through a thoracotomy between January 1977 and December 1991 were reviewed. Twenty-two parameters generated from various medical risk categories were studied. Six variables were significant (P < 0.05) on univariate analysis: vital capacity, serum albumin level, partial pressure of carbon dioxide in arterial blood, presence of liver cirrhosis, presence of chronic obstructive airway disease and clinical stage of the tumour. Multivariate discriminant analysis of these six factors identified three as significant, namely vital capacity (P < 0.0001), liver cirrhosis (P = 0.01) and tumour stage (P = 0.01), yielding an equation for assessment of the risk of postoperative pulmonary complications. Calculation of the risk score showed that 42 of 53 patients with pulmonary complications had scores of 0 or more and that 74 of 102 without had scores below 0. The mean risk score was 0.34 for patients with complications and -0.26 for those without. The equation predicted pulmonary complications after transthoracic oesophagectomy with 74.8 per cent accuracy, 79.2 per cent sensitivity and 72.5 per cent specificity. It is concluded that the risk of postoperative pulmonary complications can be accurately assessed in individual patients by calculation of a risk score based on vital capacity, liver cirrhosis and tumour stage.

It is now accepted that the incidence of esophageal carcinoma is highest in the middle thoracic region. Esophageal carcinoma after gastrectomy, however, has a tendency to develop in the lower thoracic region. These studies suggest a possible correlation between the development of esophageal carcinoma and gastrectomy, i.e., alkaline reflux into the esophagus. To elucidate this correlation, the role of alkaline reflux of duodenal contents in the development of esophageal squamous-cell carcinoma induced by N-amyl-N-methylnitrosamine (AMN) was investigated in Wistar rats. The animals were divided into 3 groups; gastrectomized rats with or without regurgitation of duodenal contents into the esophagus, and control rats without gastrectomy. All received low doses of AMN for 8 weeks and were subsequently killed for pathological examination. Esophageal squamous-cell carcinomas were found only in gastrectomized rats with regurgitation. The carcinomas were found exclusively in areas of reflux esophagitis and were accompanied by severe dysplasia. Our results indicate that alkaline reflux of duodenal contents strongly contributes to the development of esophageal squamous-cell carcinoma.