Genetic commonality between inflammatory bowel disease and sarcoidosis: the beginning of the end or the end of the beginning?

Crohn’s disease (CD) and ulcerative colitis, collectively known as inflammatory bowel disease (IBD), and sarcoidosis are multifactorial disorders thought to result from complex interactions between environmental stimuli (e.g. infectious agents), susceptibility genes (which may predispose to the development of granulomatous inflammation) and modifier genes (which may affect disease phenotype in people already susceptible). Neither IBD nor sarcoidosis is the result of defects in a single major gene or chemical pathway; instead, multiple genes, each contributing a relatively minor effect, are likely to be involved. In addition to the granulomatous histopathology, both diseases share a number of similarities in terms of ocular, dermatological and joint manifestations, although sarcoidosis rarely involves the gastrointestinal tract and IBD rarely involves the lung. Immunological, bacteriological and genetic data support a link between CD and sarcoidosis. Both disorders share a similar, yet distinct, immune response, histologically defined by non-caseating granulomas. Up to 50% of patients with CD have been reported to test positive for Kveim antigens, although these data are not replicated in all studies.