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Age and Severity of Mucosal Lesions Influence the Performance of Serologic Markers in Helicobacter pylori–Associated Gastroduodenal Pathologies

¹ Unidad de Investigación en Enfermedades Infecciosas, Hospital de Pediatría, Instituto Mexicano del Seguro Social, ² Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Cuernavaca, Morelos, Mexico; ³ Instituto de Investigación Epidemiológica, San Jose, Costa Rica; ⁴ Servicio de Patología y Gastroenterología Médica, Hospital General de México, Mexico City, Mexico; and ⁵ Instituto Nacional de Cancerología, Bogotá, Colombia

Requests for reprints: Eduardo Lazcano, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Sta. María Ahuacatitlán, C.P. 62508, Cuernavaca, Morelos, México. Phone: 777-329-3003; Fax: 777-311-1148. E-mail: elazcano{at}correo.insp.mx

Objective: The course of Helicobacter pylori infection and antibody response to CagA in patients with preneoplastic lesions and gastric cancer has not been thoroughly studied. We aimed to study H. pylori infection and antibody response to CagA in patients with non–atrophic gastritis, preneoplastic lesions, and gastric cancer.

Methods: We studied patients attending one Oncology Hospital and one General Hospital in Mexico City. Diagnosis was based on endoscopy and histopathology in biopsies from six stomach regions. H. pylori infection was assessed by histology and serology, and antibodies against CagA were measured with immunoassay.

Results: We included 618 patients, 368 with non–atrophic gastritis, 126 with precancerous lesions, and 65 with gastric cancer; in addition, 59 patients with duodenal ulcer were studied. Detection of infection and IgG against CagA had a significant increase from non–atrophic gastritis to mild and up to advanced stages of metaplasia (P < 0.05), followed by decreased infection and IgG to CagA in patients with gastric cancer (P < 0.05). However, infection and CagA antibodies were associated with young gastric cancer cases. Duodenal ulcer showed a significant association with infection detected by histology and serology, particularly among women, and a trend to associate with IgG to CagA.

Conclusions: This study shows that H. pylori infection and CagA are risk markers for intestinal metaplasia. The prevalence of these risk markers decreases in gastric cancer, probably reflecting that infection decreases after advanced atrophy and metaplasia in the gastric mucosa. State of the disease, age, and sex influence the association of H. pylori infection and IgG response to CagA with gastroduodenal diseases. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2498–504)