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Macrophage migration inhibitory factor (MIF), an immunoregulatory cytokine that has pro-inflammatory, hormonal and enzymatic activities, has been found to be markedly increased in the serum of patients with inflammatory bowel disease (IBD).1,2 MIF-deficient mice failed to develop disease1 and blockage with anti-MIF antibody reduced disease activity.1,2 Finally, functional polymorphisms of the human MIF gene have been associated with increased susceptibility to inflammatory and autoimmune diseases.3 These findings prompted us to investigate the potential association of the functional MIF −173G/C and −794 (CATT)n gene variants with the susceptibility and clinical expression of IBD.
We studied a case–control cohort (cohort 1) comprising 336 patients with Crohn’s disease and 287 patients with ulcerative colitis from south Spain and 361 controls from the same area. An additional cohort (cohort 2) was analysed, comprising 325 patients with Crohn’s disease, 347 patients with ulcerative colitis and 526 controls from Madrid. Table 1 shows the clinical characteristics …
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