Inflammatory Bowel Disease (IBD)
| Overview |
|---|
- Inflammatory Bowel Disease (IBD) refers to the inflammatory diseases of Crohn Disease (CD) and Ulcerative Colitis (UC) which are considered distinct pathophysiological entities but are thought to share a roughly overlapping etiopathogenesis which is discussed below.
| Etiology |
|---|
- Essentially, IBD is thought to be the result of an imbalance of the body's normally finely tuned inflammatory response to normal intestinal bacterial flora. Although the intestines possess a large population of immune cells, mechanisms appear to prevent an excessive immune response to antigens shed by the enormous numbers of normal gut flora, thus preventing significant inflammatory damage to the intestinal mucosa. IBD patients appear to display an over-zealous immune response to intestinal bacterial antigens, ultimately resulting in substantial damage to the GI Mucosa, typically of the small and/or large intestine mucosa. Because inflammation in IBD is clearly in response to foreign antigens, IBD is likely not an autoimmune disease although derangements of mucosal immunity clearly play a major role in the pathogenesis of the disease. Patients that develop IBD may be genetically prone to such immune derangements, although hereditary factors appear to play a stronger role in development of Crohn Disease than that of Ulcerative Colitis.
| Pathogenesis |
|---|
- Whatever the ultimate etiology, inflammation of the GI mucosa appears to be the proximate cause of clinical symptomology and pathology in IBD. Although the pattern of inflammation and pathology is different between Ulcerative Colitis and Crohn Disease, both conditions are characterized by significant architectural derangements of the inflamed GI mucosa and its ulceration. These pathological changes ultimately result in the clinical consequences characteristic of each disease.
| Epidemiology |
|---|
- IBD displays a range of incidence across different ethnicities with the highest rates among Ashkenazi Jews followed by whites. Disease can manifest at any age although a biphasic distribution is observed across the population with one population presenting as young adults and another presenting in their elder years. Development of IBD clearly displays a hereditary component although genetic factors appear to play a stronger role in Crohn Disease than Ulcerative Colitis. Additionally, those possessing the HLA-B27 allele appear to be at an increased risk of developing disease.
| Clinical Consequences |
|---|
- The clinical consequences of IBD are diverse and we discuss intestinal symptomology and complications on the individual pages of Crohn Disease and Ulcerative Colitis. However, in accordance with the notion that IBD is a result of deranged immunity, several extra-intestinal complications can occur during episodes of IBD that are common to both CD and UC. For example, a minority of patients develop erythema nodosum. Some patients also develop joint disease characterized Peripheral polyarthritis and/or ankylosing spondylitis.
| Subtopics |
|---|