Interleukin-1β and -10 polymorphisms influence erosive reflux esophagitis and gastritis in Taiwanese patients

Background and Aims: Helicobacter pylori (H. pylori) infection induces cytokine production and is associated with gastrointestinal diseases. This study examined the relationship of gene polymorphisms, including interleukin (IL)-1β, -10, -8, and tumor necrosis factor-α (TNF-α), H. pylori infection, and susceptibility to gastrointestinal disorders in Taiwanese patients. Methods: IL-1β−511/−31/+3953, -10−1082/−819/−592, -8−251, and TNF-α−308 polymorphisms were assessed in 628 gastrointestinal disease patients, and 176 healthy controls were analyzed using the polymerase chain reaction−restriction fragment length polymorphism method. Results: IL-1β−511 T/T and −31 C/C genotypes, and IL-1β−511 T and −31 C alleles were associated with an increased risk of reflux esophagitis (P = 0.034, odds ratio [OR] = 1.384, 95% confidence interval [CI]: 1.023–1.871; P = 0.031, OR = 1.388, 95% CI: 1.028–1.873; P = 0.044, OR = 1.342, 95% CI: 1.008–1.786; and P = 0.040, OR = 1.349, 95% CI: 1.014–1.796, respectively). No relationship was found between H. pylori infection and the risk of reflux esophagitis. IL-10−819 C/T and -10−592 A/C genotypes and IL-10−1082/−819/−592 ATA/ACC and ATA/GCC haplotypes were associated with an increased risk of gastritis (P = 0.021, OR = 1.721, 95% CI: 1.084–2.733; P = 0.016, OR = 1.766, 95% CI: 1.112–2.805; P = 0.039, OR = 1.662, 95% CI: 1.024–2.697; and P = 0.035, OR = 1.600, 95% CI: 1.024–2.499, respectively). Conclusion:  Among Taiwanese patients, IL-1β and -10 polymorphisms were associated with an increased risk of erosive reflux esophagitis and gastritis, respectively.