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. 2018 Nov 12;13(4):525–535. doi: 10.1093/ecco-jcc/jjy185

Table 2.

Single nucleotide polymorphisms of components of the ECS studied in human IBD.

Genotype
FAAH C385A CC CA AA Associations
Storr 2008 CD [n = 202] 67.3% 31.2% 1.5% No differences in prevalence between groups. Phenotype not assessed in this study
Controls [n = 206] 63.6% 35.0% 1.5%
Storr 2009 CD [n = 435] 65.8% 30.1% 4.1% No differences in prevalence between groups. AA associated with more EIMs and penetrating phenotype in CD; earlier age of onset in UC.
UC [n = 167] 65.3% 32.9% 1.8%
Controls [n = 406] 61.6% 34.5% 3.9%
CNR1 G1359A GG GA AA
Storr 2010 CD [n = 216] 53.3% 39.8% 6.9% Lower prevalence of AA in UC versus controls. AA associated with lower body mass index and later age of onset of CD.
UC [n = 166] 58.4% 38.0% 3.6%
Controls [n = 197] 52.3% 37.0% 10.7%
CNR2 Q63R QQ QR RR
Yonal 2014 CD [n = 101] 10.9% 38.6% 50.5% No differences in prevalence or phenotype in this study.
UC [n = 101] 6.9% 43.6% 49.5%
Controls [n = 101] 11.9% 37.6% 50.5%
Striscuglui 2016 CD [n = 112] 2.7% 48.2% 49.1% Paediatric cohort. RR genotype more prevalent in IBD than controls and associated with more severe disease activity at diagnosis. In UC, associated with higher risk of relapse.
UC [n = 105] 18.1% 38.1% 43.8%
Controls [n = 600] 16.0% 51.7% 32.3%

Prevalence of genotypes are displayed alongside associations with disease phenotype. Data extracted from references 45–49.

IBD, inflammatory bowel disease; CD, Crohn’s disease; UC, ulcerative colitis; ECS, endocannabinoid system; EIM, extra-intestinal manifestations.