Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication.
BACKGROUND
Whether Helicobacter pylori infection is a protective or predisposing factor for the development of gastroesophageal reflux disease remains controversial. The most virulent strains, such as those expressing the cytotoxin-associated gene A (CagA), and the site of gastric colonization have been correlated with the prevention or development of esophagitis.


OBJECTIVE
To determine the incidence of erosive esophagitis following eradication of H. pylori in patients with peptic ulcer disease and to evaluate the association of erosive esophagitis with virulent strains of H. pylori and the site of gastric colonization.


METHODS
Triple therapy with lansoprazole, amoxicillin and clarithromycin was administered to 159 patients with peptic ulcer disease. Endoscopy, histopathology, urease and carbon-14 urea breath tests were performed prior to treatment, at 3 months and 1 year following treatment. Genotyping of H. pylori strains using polymerase chain reaction was performed separately on samples from the corpus and antrum.


RESULTS
One year after treatment, 148 successfully treated patients were reevaluated. Twenty-eight patients (19%) had erosive esophagitis, classified as Los Angeles grade A in 24 and B in 4. The samples taken from the corpus were CagA-positive in 18 patients (64%), while the samples taken from the antrum were CagA-positive in 21 patients (75%).


CONCLUSIONS
The incidence of erosive esophagitis in peptic ulcer patients who had their H. pylori eradicated was 19%. No correlation was found between the gastric site colonized by H. pylori or strains expressing CagA and the prevention or development of erosive esophagitis in patients with peptic ulcer disease, 1 year after infection eradication.
Batista
Carlos Alexandre Gonçalves
CA
Departmento de Gastroenterologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
Silva
Fernando Marcuz
FM
Barbuti
Ricardo Correa
RC
Eisig
Jaime Natan
JN
Mattar
Rejane
R
Navarro-Rodriguez
Tomás
T
D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000627:therapeutic use; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D017291:Clarithromycin / Q000627:therapeutic use; D004941:Esophagitis / Q000175:diagnosis / Q000382:microbiology*; D005260:Female; D005773:Gastroscopy; D005838:Genotype; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D064747:Lansoprazole; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000188:drug therapy / Q000382:microbiology*; D012720:Severity of Illness Index; D014774:Virulence; D055815:Young Adult
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000900:Anti-Bacterial Agents; D064747:Lansoprazole; D000658:Amoxicillin; D017291:Clarithromycin