Obesity/Bariatric Surgery and Crohn’s Disease

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Crohn’s disease (CD) following bariatric surgery has been previously described. It is not clear whether the clinical entity is due to rapid metabolism of fat, change in the bacterial milieu of the bowel, the loss of defense mechanisms of the stomach, or even a coincidence.


To present observations which might serve to sort out these various etiologies.


We present 5 cases of colitis, ileocolitis or enteritis, some with fistula formation, with clinical onset following bariatric surgery and add these to the 7 cases previously identified as CD reported elsewhere. We provide the clinical features of these 12 cases to reconcile with causative mechanisms.


It remains possible that the onset of CD (or other inflammatory bowel disease) precedes the bariatric surgery which then accelerates the clinical manifestations described. Furthermore, without controls the association could remain a coincidence.


We review the evidence for release of proinflammatory cells and cytokines contained in fat following the bariatric surgery, and also consider the roles that the surgical resection of stomach and shortening of the bowel may also bring about this syndrome. The earlier onset is more likely due to surgical loss of defenses of the stomach and the later onset to a metabolic alteration of the presurgical obesity, involving fat metabolism, and/or the microbiome. The role of characteristic creeping fat of CD is also addressed.

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