Inflammatory bowel disease (IBD) is made up of two related disorders – Crohn’s disease and ulcerative colitis – in which the intestinal tract experiences severe and chronic inflammation. No cure currently exists for the disease; thus, the primary goal of disease management is to minimize complications and unnecessary suffering. As a disease class, IBD is distinct from irritable bowel syndrome (IBS), although the two share some symptoms. IBD causes irreversible damage to the bowel and healthcare utilization. Disease-associated morbidity is significant for those with progressive and difficult-to-manage disease.
Crohn’s disease and ulcerative colitis have distinct pathological and clinical characteristics, and despite decades of research into their origins, disease pathogenesis for both conditions remains poorly understood.
Crohn’s Disease
Crohn’s disease is characterized by transmural inflammation (i.e., inflammation that extends through the entire wall of the digestive tract), as well as by skip lesions (i.e., sections of inflamed tissue separated by noninflamed tissue). The transmural inflammatory nature of Crohn’s disease often leads to fibrosis and to obstructive clinical presentations that are not typically seen in ulcerative colitis.
Transmural inflammation also can result in gut microperforations and the formation of fistulae (i.e., a permanent abnormal passageway between two organs in the body or between an organ and the exterior of the body).
Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory condition characterized by relapsing and remitting episodes of inflammation limited to the mucosal layer of the colon. It almost always involves the rectum and, in some cases, it may extend to involve other portions of the colon in a continuous manner (i.e., inflamed tissue forms a continuous patch of disease tissue).
The peak age of onset for IBD is between 20 and 30, although it may occur at any age. Approximately 10% of cases occur in individuals younger than 18. Ulcerative colitis is slightly more common in males, whereas Crohn’s disease is marginally more frequent in females. IBD occurs more in people of Caucasian and Ashkenazic Jewish origin than in other racial and ethnic subgroups.
Hyperactive inflammation is a hallmark of IBD, and several therapeutic strategies for controlling inflammation are part of its current treatment plan. Aminosalicylates, corticosteroids, immunosuppressants, and biologic therapies all are used to control the inflammation associated with IBD.
The mechanisms through which these compounds suppress inflammation may be different, but the ultimate goal of pharmacotherapy for IBD is to suppress the abnormal activation of the immune system to allow for the body’s natural repair mechanisms to operate and fix the damaged intestinal tract.
The above is an extract from the BCC Research report, Therapies and Biomarkers for Inflammatory Bowel Disease (PHM125A). To download the complimentary first chapter, please click above.
Crohn’s disease and ulcerative colitis have distinct pathological and clinical characteristics, and despite decades of research into their origins, disease pathogenesis for both conditions remains poorly understood.
Crohn’s Disease
Crohn’s disease is characterized by transmural inflammation (i.e., inflammation that extends through the entire wall of the digestive tract), as well as by skip lesions (i.e., sections of inflamed tissue separated by noninflamed tissue). The transmural inflammatory nature of Crohn’s disease often leads to fibrosis and to obstructive clinical presentations that are not typically seen in ulcerative colitis.
Transmural inflammation also can result in gut microperforations and the formation of fistulae (i.e., a permanent abnormal passageway between two organs in the body or between an organ and the exterior of the body).
Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory condition characterized by relapsing and remitting episodes of inflammation limited to the mucosal layer of the colon. It almost always involves the rectum and, in some cases, it may extend to involve other portions of the colon in a continuous manner (i.e., inflamed tissue forms a continuous patch of disease tissue).
The peak age of onset for IBD is between 20 and 30, although it may occur at any age. Approximately 10% of cases occur in individuals younger than 18. Ulcerative colitis is slightly more common in males, whereas Crohn’s disease is marginally more frequent in females. IBD occurs more in people of Caucasian and Ashkenazic Jewish origin than in other racial and ethnic subgroups.
Hyperactive inflammation is a hallmark of IBD, and several therapeutic strategies for controlling inflammation are part of its current treatment plan. Aminosalicylates, corticosteroids, immunosuppressants, and biologic therapies all are used to control the inflammation associated with IBD.
The mechanisms through which these compounds suppress inflammation may be different, but the ultimate goal of pharmacotherapy for IBD is to suppress the abnormal activation of the immune system to allow for the body’s natural repair mechanisms to operate and fix the damaged intestinal tract.
The above is an extract from the BCC Research report, Therapies and Biomarkers for Inflammatory Bowel Disease (PHM125A). To download the complimentary first chapter, please click above.
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