CROHN’S DISEASE: AN UPDATE

Abstract

Crohn’s disease (CD) is a chronic relapsinginflammatory bowel disease (IBD). It is
characterizedby a transmural granulomatous inflammationwhich can affect any part of the
gastrointestinaltract, most commonly the ileum, colon or both [1]Crohn’s disease is
characterizedby relapsing and remitting chronic intestinal inflammationin a genetically
susceptible host. It is closely related to ulcerativecolitis, but is distinguished by key features
including anatomicdisease location and clinical expression. There is significant heterogeneityin
the clinical manifestations of Crohn’s disease,which may involve any part of the digestive tract,
may includenoncontiguous segments of inflammation (i.e., “skip lesions”)with intervening
normal segments of bowel, and can lead tofibrostenosing and perforating complications from
transmuralinflammation. [2,3] The diversity of the clinical manifestations of Crohn’s
diseaselikely has its underpinnings in the disease’s heterogeneous genetic profile . To date, over
150 susceptibilityor protective genes have been associated with Crohn’s disease. Several of these
genes encode distinct proteins critical toepithelial barrier function, immunological pathways
involved incell-surface microbial recognition and antigen processing,intracellular signaling
pathways implicated in immune activation,T-cell signaling, autophagy, and several other
mechanismsof immune regulation [4].Despite biological treatment beingassociated with an
improved health-related qualityof life, patients stillreport significant impediment on lifestyle
anddaily activities during both flares and remissions. The mortality amongst patients with CD
has been persistently higherthan the general population with a meta-analysis showing a pooled
estimate for the standardizedmortality ratio of 1.52 [5,6,7]