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.