2009Cambridge University Press eBooksRequires access

Inflammatory bowel disease: ulcerative colitis

Richard E. Lovegrove, Paris Tekkis

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Abstract

Introduction Ulcerative colitis is an inflammatory condition of the large bowel that typically presents with frequent bloody stools. In acute cases presentation may be with signs of sepsis, and perforation of the colon may have occurred or be imminent. Incidence Ten new cases per 100 000 population in developed countries. Less commonin Africa and Asia. Bi-modal age distribution with peak at 20–40 and a lesser peak at 60–80 years of age. Incidence is equal between the sexes. Aetiology The aetiology of ulcerative colitis remains unknown. Possible factors are genetic, as demonstrated by 15-fold increase in incidence in first-degree relatives. Other factors include infective organisms, psychosocial wellbeing, immunological, or defects in colonic mucus production. Smoking appears to have a protective effect. Pathophysiology The disease process usually begins in the rectum (proctitis), and spreads proximally. If the ileocaecal valve is incompetent, the terminal ileum may also be involved (backwash ileitis).Macroscopically there is diffuse inflammation with hyperaemia, pus and bleeding. Ulceration may be evident. In long–standing cases, inflammatory polyps (pseudopolyps) may occur in large numbers. In severe fulminant (toxic) colitis, a segment of the colon, most commonly the transverse, becomes acutely dilated and the wall thins and is at risk of perforation (toxic megacolon). Microscopically, acute and chronic inflammatory cells invade the lamina propria and crypts, and there are crypt abscesses. Goblet cell mucin becomes depleted, and the crypts are present in reduced number and atrophic. With increased duration of the disease the cells undergo dysplastic changes and there is an increase in the risk of colorectal cancer.

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Introduction Ulcerative colitis is an inflammatory condition of the large bowel that typically presents with frequent bloody stools. In acute cases presentation may be with signs of sepsis, and perforation of the colon may have occurred or be imminent. Incidence Ten new cases per 100 000 population in developed countries. Less commonin Africa and Asia. Bi-modal age distribution with peak at 20–40 and a lesser peak at 60–80 years of age. Incidence is equal between the sexes. Aetiology The aetiology of ulcerative colitis remains unknown. Possible factors are genetic, as demonstrated by 15-fold increase in incidence in first-degree relatives. Other factors include infective organisms, psychosocial wellbeing, immunological, or defects in colonic mucus production. Smoking appears to have a protective effect. Pathophysiology The disease process usually begins in the rectum (proctitis), and spreads proximally. If the ileocaecal valve is incompetent, the terminal ileum may also be involved (backwash ileitis).Macroscopically there is diffuse inflammation with hyperaemia, pus and bleeding. Ulceration may be evident. In long–standing cases, inflammatory polyps (pseudopolyps) may occur in large numbers. In severe fulminant (toxic) colitis, a segment of the colon, most commonly the transverse, becomes acutely dilated and the wall thins and is at risk of perforation (toxic megacolon). Microscopically, acute and chronic inflammatory cells invade the lamina propria and crypts, and there are crypt abscesses. Goblet cell mucin becomes depleted, and the crypts are present in reduced number and atrophic. With increased duration of the disease the cells undergo dysplastic changes and there is an increase in the risk of colorectal cancer.

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Available abstract

Introduction Ulcerative colitis is an inflammatory condition of the large bowel that typically presents with frequent bloody stools. In acute cases presentation may be with signs of sepsis, and perforation of the colon may have occurred or be imminent. Incidence Ten new cases per 100 000 population in developed countries. Less commonin Africa and Asia. Bi-modal age distribution with peak at 20–40 and a lesser peak at 60–80 years of age. Incidence is equal between the sexes. Aetiology The aetiology of ulcerative colitis remains unknown. Possible factors are genetic, as demonstrated by 15-fold increase in incidence in first-degree relatives. Other factors include infective organisms, psychosocial wellbeing, immunological, or defects in colonic mucus production. Smoking appears to have a protective effect. Pathophysiology The disease process usually begins in the rectum (proctitis), and spreads proximally. If the ileocaecal valve is incompetent, the terminal ileum may also be involved (backwash ileitis).Macroscopically there is diffuse inflammation with hyperaemia, pus and bleeding. Ulceration may be evident. In long–standing cases, inflammatory polyps (pseudopolyps) may occur in large numbers. In severe fulminant (toxic) colitis, a segment of the colon, most commonly the transverse, becomes acutely dilated and the wall thins and is at risk of perforation (toxic megacolon). Microscopically, acute and chronic inflammatory cells invade the lamina propria and crypts, and there are crypt abscesses. Goblet cell mucin becomes depleted, and the crypts are present in reduced number and atrophic. With increased duration of the disease the cells undergo dysplastic changes and there is an increase in the risk of colorectal cancer.

Key concepts: Ulcerative colitis, Inflammatory bowel disease, Medicine, Gastroenterology, Internal medicine, Disease

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