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Pathophysiology of Chron’s Disease

Pathophysiology of Chron’s Disease. The incidence of crohn’s disease reaches up to 20 per 100,000 people per year, with a median age of 30 years, and is higher in the developed world. Although the exact cause and pathophysiology is unknown, several environmental and genetic factors have been linked with higher risk or severity of the disease.

CD is a debilitating and incurable chronic inflammatory bowel disease (IBD) affecting more than 2.5 million individuals in the Western world and has an increasing incidence in the developing world [1]. CD is characterized by mucosal ulceration and inflammation, which may occur anywhere along the gastrointestinal tract but most commonly affect the distal small intestine. Distinguishing features include discontinuous, transmural inflammation involving the whole thickness of the bowel wall, and an inflammatory response associated with lymphoid aggregates and granulomas [2]. Current treatments include traditional anti-inflammatory agents (corticosteroids), immunomodulators (thiopurines and methotrexate), biological agents with antibodies directed against tumor necrosis factor (anti-TNF), antibiotics, and surgery.

The exact etiology is still unknown, and the most famous hypothesis suggests that crohn disease is an autoimmune disease that attacks individuals with genetic susceptibility. The onset of the disease was found to be influenced by environmental exposures that affect the natural balance of the gut flora, alter the mucosal protection, and stimulate abnormal immune responses in the GI tract. Gut flora (microbiota), gut immune response, and genetic predisposition, all work together with the environmental factors to develop crohn’s disease [3] .

Pathophysiology of Chron’s Disease

Crohn disease is subdivided into three phenotypic types: fistulizing, stricturing, and inflammatory. In inflammatory crohn disease, there is GIT inflammation without the presence of fistulas or strictures. Inflammatory crohn disease will consequently cause narrowing of the lumen with fibrosis, and the disease will then be classified as stricturing. This fibrotic changes are considered irreversible and the only possible treatment is surgery. The conversion of the disease into a fistulizing crohn disease requires continuous transmural inflammation that will lead to the formation of a fistula or a sinus tract. Fistulae can form between any organs near the guts. Examples include the urinary bladder, vagina, and other near organs. An intra-abdominal abscess may also occur if the sinus fails to complete between the gut and the organ. Perianal complications and manifestation may also occur in any of the previous subtypes, and are not considered a separate subtype, but a long-term sequelae.

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