title: CagA status and Helicobacter pylori eradication among dyspeptic patients.
abstract: OBJECTIVE
  Triple therapy seems more effective in curing Helicobacter pylori infection in patients with peptic ulcer than in those with non-ulcer dyspepsia. It has been suggested that this difference depends on the expression of CagA protein that is more frequent in the former. The objective of this study was to investigate a potential association between serum CagA positivity, severity of gastric mucosal inflammation and eradication success among peptic ulcer and non-ulcer dyspepsia patients.
  
  
  METHODS
  Patients undergoing upper gastrointestinal endoscopy for investigation of dyspepsia at the Department of Gastroenterology, Hospital Vera Cruz, between March, 2000 and March 2001 were screened. H. pylori positive patients, as diagnosed by rapid urease test and histology were included. Severity of gastric mucosal inflammation was determined and serum CagA positivity was assessed using a commercially available ELISA assay prior to H. pylori 7-day eradication therapy with lansoprazole, clarithromycin and amoxicillin (30 mg, 500 mg and 1 g b.i.d., respectively). Eradication success was determined 8-24 weeks following completion of therapy.
  
  
  RESULTS
  Seventy-four patients were included in the study (mean age 40.8, range 18-67, female = 28). CagA positivity was observed in 48% of patients. Gastroduodenal peptic ulceration was found in 54% of patients. Serum CagA positivity was significantly higher among peptic ulcer patients (62.5%), while CagA negativity was significantly higher among non-ulcer dyspepsia patients (67.7%). Lymphocyte and eosinophil infiltration was significantly higher among CagA + patients, despite being comparable when distributed among peptic ulcer and non-ulcer dyspepsia patients. Eradication was successful in 93.2% of patients, regardless of CagA status on a per protocol analysis. Based on a per protocol analysis, eradication success was comparable among peptic ulcer and non-ulcer dyspepsia patients, regardless of CagA status.
  
  
  CONCLUSIONS
  Our results support the concept that CagA positivity is associated to peptic ulcer disease and to a higher severity of lymphocyte and eosinophil infiltration. Efficacy of treatment eradication of H. pylori may not be affected by serum CagA status.
authors.affiliation: Department of Internal Medicine, Faculty of Medical Sciences, University of Campinas, Campinas, Brazil. fredericomagalhaes@terra.com.br
authors.forename: A F Novaes de
authors.initials: AF
authors.lastname: Magalhães
authors.forename: A
authors.initials: A
authors.lastname: Carvalhaes
authors.forename: J
authors.initials: J
authors.lastname: Natan-Eisig
authors.forename: J G
authors.initials: JG
authors.lastname: Paraíso-Ferraz
authors.forename: M
authors.initials: M
authors.lastname: Trevisan
authors.forename: S
authors.initials: S
authors.lastname: Zaterkaad
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000293:Adolescent; D000328:Adult; D000368:Aged; D000658:Amoxicillin / Q000008:administration & dosage / Q000627:therapeutic use*; D000900:Anti-Bacterial Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D000897:Anti-Ulcer Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D000942:Antigens, Bacterial / Q000097:blood* / Q000235:genetics; D001426:Bacterial Proteins / Q000097:blood* / Q000235:genetics; D015415:Biomarkers; D017291:Clarithromycin / Q000008:administration & dosage / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D004415:Dyspepsia / Q000209:etiology* / Q000382:microbiology; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000097:blood / Q000209:etiology / Q000473:pathology; D004804:Eosinophils / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics / Q000302:isolation & purification*; D006801:Humans; D064747:Lansoprazole; D008214:Lymphocytes / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D010437:Peptic Ulcer / Q000097:blood / Q000209:etiology* / Q000382:microbiology / Q000473:pathology
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; C080866:cagA protein, Helicobacter pylori; D064747:Lansoprazole; D000658:Amoxicillin; D017291:Clarithromycin; D009853:Omeprazole