Treatment of severe esophageal Crohn's disease with infliximab.

Esophageal ulceration with fistula is an uncommon manifestation of Crohn's disease. Typical presentation of symptomatic esophageal Crohn's disease may include dysphagia, odynophagia, weight loss, and chest discomfort. We present a patient with severe esophageal and skin involvement of Crohn's disease that was progressive despite conventional therapy including prednisone and 6-mercaptopurine. The diagnosis of Crohn's was based on the presence of typical clinical, endoscopic, and pathologic findings, including granulomas in the skin ulcer and the absence of infectious etiologies. The patient had a nearly complete resolution of her esophageal disease with a single infusion of infliximab.

Mixed infection with cagA-positive and cagA-negative strains of Helicobacter pylori.

BACKGROUND: Helicobacter pylori infection has been implicated strongly in the pathogenesis of gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric lymphoma, but the reasons for these widely different clinical outcomes are unknown. The aim of this study was to determine whether these differences could be due in part to mixed infection in the same individual, with bacteria having differences in pathogenic factors associated with ulcers. MATERIALS AND METHODS: The cagA gene of H. pylori was used to test for mixed infection because it is present in only some strains, and its presence has been associated with ulcers. Polymerase chain reaction (PCR) assays for the cagA gene were applied to H. pylori culture isolates and endoscopic gastric aspirates. Individual bacterial clones were tested for genetic similarity by random primer amplification and restriction endonuclease digestion of urease gene PCR products. RESULTS: The majority of H. pylori-positive patients had strongly cagA-positive culture isolates and endoscopic samples (62.5% and 69.6%, respectively). However, many of these patients had evidence of mixed infection with cagA negative and cagA positive strains in cultures isolates and endoscopic samples (25% and 17.4%, respectively). Mixed infection was found to be due to genetically unrelated strains in two patients in whom genetic analysis was performed. CONCLUSION: Mixed infection with differences in substrain pathogenic factors might occur in H. pylori infection and might contribute to differences in clinical outcome.

Immune evasion by Helicobacter pylori: gastric spiral bacteria lack surface immunoglobulin deposition and reactivity with homologous antibodies.

BACKGROUND: Helicobacter pylori infection persists in the presence of potent serum and gastric mucosal antibody responses against bacterial antigens. The aim of this article is to report on a study determine whether there is antibody deposition on H. pylori in vivo in the stomach of infected patients and whether gastric and cultured forms of H. pylori differ in their antibody reactivity. MATERIALS AND METHODS: Serum, gastric biopsies, and antral brushings were obtained from 10 patients having endoscopy. H. pylori was cultured from gastric biopsies. Bacterial samples were stained directly for immunoglobulin deposition and indirectly using rabbit antiurease serum or patient serum. Samples were examined by immunofluorescence microscopy and flow cytometry. RESULTS: Although spiral bacteria could be identified easily by acridine orange staining and antiurease staining of gastric brushings from H. pylori infected patients, gastric bacteria did not have detectable IgG or IgA present, and only one of five samples could be stained for IgG and IgA indirectly using patient serum. In contrast, cultured bacteria could be stained readily with homologous serum for IgG and IgA in the majority of cases. Low pH inhibited immunoglobulin reactivity with cultured H. pylori. CONCLUSIONS: Gastric H. pylori may evade humoral defense owing to poor deposition of immunoglobulin in the gastric environment or failure to express surface antigens that are present on cultured forms of H. pylori.