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An Introduction to Inflammatory Bowel Disease (IBD)
November 14th, 2008 by Stephen DooganBackground
Inflammatory bowel disease (IBD) commonly refers to ulcerative colitis (UC) and Crohn disease (CD), which are chronic inflammatory diseases of the GI tract of unknown etiology. Crohn disease is also referred to as regional enteritis, terminal ileitis, or granulomatous ileocolitis.
Pathophysiology
Increasing evidence suggests that, at least in CD, there is a defect in the function of the intestinal immune system. As a consequence, there is a breakdown of the defense barrier of the gut, which, in turn, results in exposure of the mucosa to microorganisms or their products. The result is a chronic inflammatory process mediated by T cells. Hence, therapy should be directed at improving the intestinal immune system. It has been postulated that genetic factors may predispose certain individuals to developing a "leaky gut."
In UC, inflammation always begins in the rectum, extends proximally a certain distance, and then abruptly stops. A clear demarcation exists between involved and uninvolved mucosa. The rectum is always involved in UC, and no "skip areas" are present. UC primarily involves the mucosa and the submucosa, with formation of crypt abscesses and mucosal ulceration. The mucosa typically appears granular and friable. In more severe cases, pseudopolyps form, consisting of areas of hyperplastic growth with swollen mucosa surrounded by inflamed mucosa with shallow ulcers. In severe UC, inflammation and necrosis can extend below the lamina propria to involve the submucosa and the circular and longitudinal muscles, although this is unusual.
UC remains confined to the rectum in approximately 25% of cases. In the remainder of cases, UC spreads proximally and contiguously. Pancolitis occurs in 10% of patients. The small intestine is never involved, except when the distal terminal ileum is inflamed in a superficial manner, referred to as backwash ileitis. Even with less than total colonic involvement, the disease is strikingly and uniformly continuous. As the disease becomes chronic, the colon becomes a rigid foreshortened tube that lacks its usual haustral markings, leading to the lead pipe appearance observed on barium enema. The skip areas (ie, normal areas of the bowel interspersed with diseased areas) observed in CD of the colon do not occur in UC.
CD, on the other hand, consists of segmental involvement by a nonspecific granulomatous inflammatory process. The most important pathologic feature is involvement of all layers of the bowel, not just the mucosa and the submucosa, as is characteristic of UC.
Furthermore, CD is discontinuous, with skip areas interspersed between one or more involved areas. Late in the disease, the mucosa develops a cobblestone appearance, which results from deep longitudinal ulcerations interlaced with intervening normal mucosa. The 3 major patterns of involvement in CD are (1) disease in the ileum and cecum, occurring in 40% of patients; (2) disease confined to the small intestine, occurring in 30% of patients; and (3) disease confined to the colon, occurring in 25% of patients. Rectal sparing is a typical but not constant feature of CD. However, anorectal complications (eg, fistulas, abscesses) are common. Much less commonly, CD involves the more proximal parts of the GI tract, including the mouth, tongue, esophagus, stomach, and duodenum. CD causes 3 patterns of involvement: (1) inflammatory disease, (2) strictures, and (3) fistulas.
UC and CD are generally diagnosed using clinical, endoscopic, and histologic criteria. However, no single finding is absolutely diagnostic for one disease or the other. Furthermore, approximately 20% of patients have a clinical picture that falls between CD and UC; they are said to have indeterminate colitis.
The incidence of gallstones and kidney stones is increased in CD because of malabsorption of fat and bile salts. Gallstones are formed because of increased cholesterol concentration in the bile, caused by a reduced bile salt pool. Patients who have CD with ileal disease or resection also are likely to form calcium oxalate kidney stones. With the fat malabsorption, unabsorbed long-chain fatty acids bind calcium in the lumen. Oxalate in the lumen normally is bound to calcium. Calcium oxalate is poorly soluble and poorly absorbed; however, if calcium is bound to malabsorbed fatty acids, oxalate combines with sodium to form sodium oxalate, which is soluble and is absorbed in the colon (enteric hyperoxaluria). The development of calcium oxalate stones in CD requires an intact colon to absorb oxalate. Patients with ileostomies do not develop calcium oxalate stones.
Extraintestinal manifestations of IBD include iritis, episcleritis, arthritis, and skin involvement, as well as pericholangitis and sclerosing cholangitis.
Frequency
United States
The incidence is 70-150 cases per 100,000 individuals.
Mortality/Morbidity
The quality of life generally is lower with CD than with UC, in part because of recurrences after surgery performed for CD.
* The most common causes of death in IBD are peritonitis with sepsis, malignancy, thromboembolic disease, and complications of surgery.
* Toxic megacolon, one of the most dreaded complications of UC, can lead to perforation, sepsis, and death.
* Malnutrition and chronic anemia are observed in long-standing CD.
* Children with CD or UC can exhibit growth retardation.
Race
* Incidence among whites is approximately 4 times that of other races.
* IBD is observed most commonly in Northern Europe and North America. It is a disease of industrialized nations.
* Incidence is higher in Ashkenazi Jews (ie, those who have immigrated from Northern Europe) than in other groups.
Sex
Incidence is slightly greater in females than in males.
Age
* Incidence peaks in the second and third decades of life.
* A second smaller peak occurs in patients aged 55-65 years.
* CD and UC can occur in childhood, although the incidence is much lower in children younger than 15 years.
Original Article: http://www.emedicine.com/emerg/TOPIC106.HTM
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