Table 4.

H. pylori infection and seroprevalence to CagA as risk factor for precancerous lesions, gastric cancer, and duodenal ulcer

Non–atrophic gastritis (controls)
Intestinal metaplasia
Gastric cancer
Duodenal ulcer
nnOR (95% CI)*nOR (95% CI)*nOR (95% CI)*
H. pylori infection, histology
    Negative133341.0371.0111.0
    Positive227761.5 (0.9-2.4)260.5 (0.3-0.9)482.8 (1.4-5.5)
H. pylori infection, serology
    Negative98191.0221.071.0
    Positive270912.0 (1.1-3.5)430.9 (0.5-1.6)522.9 (1.3-6.6)
H. pylori serology, magnitude
    0.15-1.24122221.0251.081.0
    1.25-4.91123472.4 (1.3-4.3)291.4 (0.7-2.6)233.0 (1.3-7.1)
    4.92-18.99123412.2 (1.2-4.0)110.6 (0.3-1.4)283.9 (1.7-9.0)
    TrendP = 0.15P = 0.02P < 0.01
CagA
    Negative132221.0221.0161.0
    Positive236882.4 (1.4-4.1)431.4 (0.8-2.5)431.6 (0.9-3.0)
CagA, magnitude
    0.51-1.34122171.0211.0121.0
    1.35-5.05123402.3 (1.2-4.4)281.4 (0.7-2.8)231.9 (0.9-4.1)
    5.06-27.77123534.0 (2.1-7.5)161.2 (0.6-2.6)242.3 (1.1-4.7)
    TrendP < 0.01P = 0.94P = 0.14
  • * Patients with non–atrophic gastritis were used as the control group; OR adjusted for sex, age, ever smoking, ever drinking alcohol, and level of education.

  • ELISA units.