The quantitation of inflammation in both antral and body gastric mucosa and the degree of bacterial colonization are presently being investigated

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The quantitation of inflammation in both antral and body gastric mucosa and the degree of bacterial colonization are presently being investigated. In examining the potential impact of eradication on symptoms, it is important to distinguish between patients with duodenal ulcer and those with gastritis only. prevalence of 20 to 60% depending on age, geographic location, and socioeconomic conditions (12, 19). The majority of affected individuals are asymptomatic despite evidence of chronic antral gastritis, and the relevance of this pathology to chronic abdominal pain is questionable (18, 29). Experts have reported consistent evidence of an association of illness with duodenal ulcer (23). Although illness is neither necessary nor adequate for ulcer Suplatast tosilate development (13), its eradication however markedly reduces ulcer recurrence (29). A potential virulence determinant of is the gene product, which is found in approximately 60% of isolates from adults (5). The antigen, a hydrophilic surface exposed protein of 128 kDa, is definitely itself devoid of cytotoxic activity but is definitely strongly associated with it, possibly by the transcription, folding, export, or additional function of the toxin. The gene, which encodes this protein, has been cloned and sequenced (5), and the in vivo manifestation of mRNA in gastric mucosal biopsy samples has been mentioned (22). In addition, mucosal immunoglobulin A (IgA) acknowledgement of the protein (7) and the presence of serum antibodies to the CagA protein are strongly associated with the presence of active gastritis and duodenal ulcer (5, 6, 31), and they may present an increased risk for the development of atrophic gastritis (17) and intestinal metaplasia and gastric malignancy (2). Therefore, strains may be divided into at least two subgroups based on the manifestation (type I) or nonexpression (type II) of CagA and the cytotoxin. Type I strains are variable, with about 30% of isolates possessing either CagA Suplatast tosilate or cytotoxin activity (32). Suplatast tosilate The aim of the present study was to determine the relevance of the presence of CagA to the medical picture and end result of illness in children. MATERIALS YWHAS AND METHODS The study population consisted of 104 consecutive children with endoscopically diagnosed illness who presented to our center between June 1989 and June 1995. Indications for endoscopy were recurrent abdominal pain (RAP) (defined as at least three episodes of abdominal pain over a period of at least 3 months of adequate severity to interrupt normal daily activities), ulcer pain (defined as food cravings pain, nocturnal pain and pyrosis), gastroduodenal bleeding, and suspicion or follow-up of gluten-sensitive enteropathy (GSE). The relevant medical information included a family history (first-degree relatives) of peptic disease and recent antibiotic and antacid therapy. Analysis. Endoscopy was carried out under sedation (intravenous Demerol HCl [1 mg/kg], midazolam [0.1 to 0.2 mg/kg]) having a GIF P3 or XQ20 fiberscope (Olympus). Findings were classified as gastric or duodenal ulcer, nodular gastritis, or normal. One duodenal bulb and one gastric body biopsy sample were acquired for histologic study, and three antral biopsy samples were taken, one for histologic study, one for any 24-hour urease test, and one for tradition. For histology, the samples were fixed in Bouin’s remedy and stained with hematoxylin-eosin, Giemsa stain, and Gram staining. Gastritis was classified as explained by Whitehead (30). The analysis of illness was based on the presence of standard bacilli on histology and a positive urease test and culture. Treatment. Individuals were treated before the serology findings were known. Up to September 1994, infection was regularly treated in our division with a combination of amoxicillin (50 mg/kg/day time) for 3 weeks and metronidazole (20 mg/kg/day time) for 2 weeks and, in addition, with bismuth subcitrate (De-Nol) (120 to 240 mg four instances per day) for 6 weeks or H2 blockers (cimetidine) (20 mg/kg/day time) for 6 weeks. Thereafter, the protocol was changed, and individuals received a combination of clarithromycin (15 mg/kg/day time), amoxicillin (50 mg/kg/day time), and omeprazole (20 mg/day time) for 2 weeks. Those with prolonged infection and severe symptoms received more than one restorative trial. Asymptomatic individuals with GSE were not treated. Outcome. End result was defined relating to medical and bacteriological guidelines. Clinically, patients were considered to be either symptomatic or asymptomatic (no symptoms or occasional discomfort of less than one show per month). No attempt was made to define the severity of symptoms. Healing of duodenal ulcers was confirmed by endoscopy. Bacteriologically, individuals were considered cured (eradication of illness) when endoscopical illness. Serology. Serum samples were.