Interleukin-1A and interleukin-1B gene polymorphisms in gastroesophageal reflux disease.

Inflammation may play contradictory roles in the pathogenesis of gastroesophageal reflux disease (GERD): gastritis decreases gastric output and reduces the risk of esophagitis, while interleukins may favor mucosal inflammation. The inflammation may cause esogastric motility changes and thus increase the risk of esophagitis. Considering the genetic influence of inflammatory response, we looked for the genetic polymorphisms of IL-1 in GERD manifested as reflux esophagitis. This is a prospective study carried out in GERD and healthy controls. We assessed in these groups the following single nucleotide polymorphisms (SNPs): IL-1A (rs1800587), IL-1B (rs16944), IL-1B (rs1143634) and the VNTR for IL-1RN. Both groups were similar according to biographical data. Reflux esophagitis was confirmed by endoscopy and where necessary by pH-impedance monitoring. Reflux esophagitis was associated only with the polymorphism rs16944. No other correlations with the other three genetic polymorphisms were detected. These data suggest that the diverging effects of proinflammatory factors on the upper digestive tract may have deleterious effect on GERD. The IL-1B (rs16944) SNP correlates with reflux esophagitis.