Comparison of biopsy and serological methods of diagnosis of Helicobacter pylori infection and the potential role of antibiotics.

OBJECTIVE: Endoscopic biopsy and serological methods were compared for their ability to detect Helicobacter pylori infection in patients undergoing upper gastrointestinal endoscopy at a state university hospital. METHODS: Subjects were characterized on the basis of gastrointestinal symptoms, endoscopic findings, socioeconomic and demographic features, and the use of certain medications, tobacco, and alcohol. Current infection was detected in gastric antral specimens by rapid urease testing, histopathology, and bacterial culture. Serum levels of IgG to H. pylori were measured by ELISA. RESULTS: Of 240 subjects, 115 (47.9%) were currently infected as determined by rapid urease testing, histopathology, and/or culture results, whereas 63.3% had elevated anti-H. pylori IgG levels (p < 0.001). This difference in the prevalence of current infection and seropositivity was preserved when the study population was analyzed according to age, race, gender, and other characteristics. Prior use of antibiotics was associated with a significant reduction in the frequency of H. pylori infection. CONCLUSIONS: Serological evidence of H. pylori infection was consistently greater than the prevalence of infection documented by biopsy methods in this study, suggesting suppression or recent clearance of infection. Further studies are needed to examine the factors that may affect the detection of H. pylori infection.

Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype.

BACKGROUND & AIMS: Studies have shown that gastric T cells are increased during Helicobacter pylori infection. The purpose of this study was to characterize the human gastric T-cell responses in the presence or absence of H. pylori. METHODS: T-cell surface antigens were examined by immunohistochemistry or after isolation for evaluation of surface antigens and cytoplasmic cytokines using flow cytometry. RESULTS: CD4+ and CD8+ T cells were increased in situ during infection with H. pylori. Freshly isolated gastric T cells expressed cytoplasmic interferon gamma (IFN-gamma) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8+ and CD4+ T cells expressed IFN-gamma. Because stimulation through CD30 favors the induction of IL-5 and Th2 cells, gastric and colonic T cells were examined for CD30 expression. Consistent with the notion that Th2 cells are found in the intestine, CD30 was evident throughout the lamina propria of the colon but was virtually absent in the stomach. Furthermore, freshly isolated gastric T cells produced little IL-4 and virtually no IL-5 or tumor necrosis factor beta. CONCLUSIONS: These observations show that gastric T cells resemble the Th1 type, which may explain their failure to induce immunity to H. pylori and their ability to contribute to the pathogenesis of gastric disease.

Mast cell mediated ion transport in intestine from patients with and without inflammatory bowel disease.

BACKGROUND: Mast cells have been shown to regulate intestinal ion transport in animal models and normal human colon but their physiological role in human intestinal inflammatory disorders is unknown. AIMS: To examine mast cell regulation of ion transport in inflammatory bowel disease (IBD). SUBJECTS AND METHODS: Small and large intestine was obtained from patients with and without IBD undergoing surgical resection. Short circuit current (Isc) responses to rabbit antihuman IgE, histamine, and electrical stimulation were measured in Ussing chambers. Specimens were also examined for mast cell numbers and degree of inflammation. RESULTS: Isc responses to anti-IgE and histamine were smaller in magnitude in IBD compared with non-IBD tissues. In all tissues, anti-IgE Isc responses were reduced by about 80% in chloride free buffer. The histamine H1 receptor antagonist, pyrilamine, decreased anti-IgE responses in non-IBD tissues. Greater inhibition with pyrilamine was seen in IBD small intestine but its effect was less in IBD colon. Histamine pretreatment of non-IBD control tissues reduced anti-IgE responses to levels seen in IBD colon but had no effect in small intestine. Mast cell numbers were greater in IBD compared with non-IBD small intestine while no differences were observed between the colonic groups. Isc responses to anti-IgE were not correlated with the degree of mucosal inflammation. CONCLUSIONS: This study provides further evidence that mast cells are capable of mediating alterations of ion transport in human gut but that this regulatory role may be altered in IBD. The data suggest that prior activation of mast cells with release of histamine may account for the reduced secretory response to anti-IgE observed in IBD colonic tissues.