Source: Gastroenterology  |  Posted 9 years ago

Variations in the NOD2 gene seem to contribute to fibrostenotic Crohn's disease in the small bowel.

Researchers from Cedars-Sinai Medical Center in Los Angeles, California, United States, genotyped 201 patients suffering from inflammatory bowel disease for three single nucleotide polymorphisms of NOD2 (NOD2-R675W, G881R and 3020insC). The authors hypothesised that certain NOD2 mutations, which might influence immune responses, may manifest as distinct Crohn's disease phenotypes.

On univariate analysis, the NOD2 variants showed a significant association with fibrostenosing disease. Indeed, 46 percent of patients suffering from fibrostenosing disease expressed at least one of these alleles, compared to only 23.5 percent of patients without fibrostenosing disease. This is equivalent to an odds ratio of 2.8 that Crohn's disease patients expressing at least one of these NOD2 variants will develop fibrostenosing disease.

Further analysis demonstrated that the association was apparent in both Jews and non-Jews. Moreover, analysis identified "a primary association" between the variations in NOD2 alleles and fibrostenosing disease. No such association emerged with small bowel disease.

The authors concluded that variations in these NOD2 genes might contribute to fibrostenotic Crohn's disease in the small bowel.