Despite some studies having indicated a possible association between appendicitis and duodenal ulcers, this association was mainly based on regional samples or limited clinician experiences, and as such, did not permit unequivocal conclusions. In this case-control study, we examined the association of acute appendicitis with peptic ulcers using a population-based database. We included 3574 patients with acute appendicitis as cases and 3574 sex- and age-matched controls. A Chi-squared test showed that there was a significant difference in the prevalences of prior peptic ulcers between cases and controls (21.7% vs. 16.8%, p < 0.001). The adjusted odds ratio (OR) of prior peptic ulcers for cases was 1.40 (95% confidence interval [CI]: 1.24~1.54, p < 0.001) compared to controls. The results further revealed that younger groups demonstrated higher ORs for prior peptic ulcers among cases than controls. In particular, the adjusted OR for cases < 30 years old was as high as 1.65 (95% CI = 1.25~2.19; p < 0.001) compared to controls. However, we failed to observe an association of acute appendicitis with peptic ulcers in the ≥ 60-year age group (OR = 1.19, 95% CI = 0.93~1.52). We concluded that there is an association between acute appendicitis and a previous diagnosis of peptic ulcers.

Bacteria have been implicated in the pathogenesis of inflammatory bowel disease. Helicobacter species have been shown to cause colitis in animal models and have been identified in human diarrhoeal illness and Crohn's disease.

To determine whether Helicobacter species are present in human inflammatory bowel disease tissue.

Thirty patients undergoing colonoscopy for clinical reasons were studied. Nine had Crohn's disease, 11 had ulcerative colitis and 10 had histologically normal colons. Tissue was snap-frozen at -70 degrees C. DNA was extracted and examined by five different polymerase chain reaction (PCR) assays that were either genus or species specific for Helicobacter.

Analyses of colonic biopsies by two Helicobacter genus-specific PCR assays, two H. pylori-specific assays and a PCR assay designed to amplify fragments of 'H. heilmannii'-like organisms demonstrated that product was not generated by any test. Internal control PCR demonstrated that PCR results for the five assays were not negative due to the presence of residual substances inhibitory to PCR.

Helicobacter species were not identified in this study, using multiple PCRs to eliminate the problems of non-specific cross-reaction. This suggests that Helicobacter species do not play a role in the pathogenesis of inflammatory bowel disease.

Researchers have speculated that surgical excision of lymphoid tissue, such as appendectomy, early in life might confer an increased risk of cancer. In this study, we determined the risks of cancer for people who had appendectomy performed during childhood.

We studied the risk of cancer in a large Swedish cohort of children who had appendectomy performed during the period of 1965-1993. Standardized incidence ratios (SIRs) were computed using age-, gender-, and period-specific incidence rates derived from the entire Swedish population as comparison. Hospital discharge diagnosis data were used to examine cancer risks by categories of surgery, medical conditions, and type of appendicitis. The average length of follow-up was 11.2 years.

We found no excess overall cancer risk but noted a significant excess for stomach cancer (SIR: 2.45; 95% confidence interval [CI]: 1.1-4.8) and a borderline increase of non-Hodgkin's lymphoma (NHL; SIR: 1.55; 95% CI: 1.0-2.3). The elevated risks for both cancers were only evident 15 or more years after appendectomy (stomach cancer, SIR: 3.82; 95% CI: 1.7-7.5; NHL, SIR: 2.49; 95% CI: 1.4-4.2).

It is reassuring that there was no overall increase of cancer several years after childhood appendectomy. Increased risks for NHL and stomach cancer, occurring 15 or more years after appendectomy, were based on small absolute numbers of excess cancers. As 95% of the subjects were younger than 40 years at exit, this cohort requires continuing follow-up and monitoring.

BACKGROUND: This study was designed to determine whether Helicobacter pylori forms part of the normal microenvironment of the appendix, whether it plays a role in the pathogenesis of acute appendicitis, and whether it is associated with increased expression of inducible nitric oxide synthetase (iNOS) in appendicular macrophages. METHODS: Serology for H. pylori was performed on 51 consecutive patients undergoing emergency appendicectomy. Appendix samples were tested for urease activity, cultured and stained for H. pylori, graded according to the degree of inflammatory infiltrate, and probed immunohistochemically for iNOS expression. RESULTS: The mean age of the patients was 21 (range 7-51) years. Seventeen patients (33 per cent) were seropositive for H. pylori but no evidence of H. pylori was found in any appendix specimen. However, an enhanced inflammatory cell infiltration was observed in seropositive patients (P < 0.04) and the expression of macrophage iNOS in the mucosa of normal and inflamed appendix specimens was increased (P < 0.01). CONCLUSION: H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.