Crohn’s Disease - PATHOGENESIS
Posted by AlexThe absence of an etiologic factor leaves a gap in our understanding of the pathogenesis of IBD. Although a number of potential factors may influence the initiation of the inflammatory response, a popular view is that a defect exists in the “down-regulation”
TABLE 104-1 — EPIDEMIOLOGY OF INFLAMMATORY BOWEL DISEASE
| More common in whites than nonwhites |
| Increased frequency among European stock |
| More common among Jews (especially Ashkenazic) than non-Jews (3 to 6 times) |
| Most frequent age of onset: 15 to 30 years |
| Aggregation in families (25-40%) |
| Concordance for Crohn’s in twins |
| Cigarette smokers–Crohn’s disease |
| Nonsmokers–ulcerative colitis |
of immune events (see Part XIX), allowing persistent amplification of the tissue-damaging process. The inflammatory reaction in IBD closely mimics infectious enterocolitis with the exception of the failure to halt progressive tissue destruction. Subtle differences exist between the immunologic findings of UC and CD, such as the production of immunoglobulin heavy-chain allotypes or neutrophil-cytoplasmic antibodies; however, pathognomonic findings to classify these disorders remain elusive. Nosology is currently based on descriptive clinical, endoscopic, and histologic criteria, and misclassification often is recognized as the clinicopathologic process evolves over time. When the diagnosis changes, it is almost always from UC to CD and virtually never the converse.