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Crohn's Disease- Pathophysiology and Conventional and Alternative Treatment Options

Crohn's Disease

Table 1: Subcategories of Crohn's Disease

Table 2: Signs and Symptoms of Crohn's Disease and Ulcerative Colitis

Risk Factors



    The Genetic Component of Crohn's Disease

    Stress in the Etiology of Crohn's Disease

    Microbial Factors

    Inflammation/Immune Response

    Intestinal Permeability

    Other Abnormalities Contributing to the Etiopathogenesis of Crohn's Disease

Conventional Treatment of Crohn's Disease

Table 5: Conventional Medications and their Mechanisms in Crohn's Disease

Nutrient Deficiences in Crohn's Disease

Table 6: nutrient Deficiencies Associated with Crohn's Disease

Dietary Interventions in Crohn's Disease

Table 7: Diet Therapies Compared to Steroid Medications in Crohn's Disease

Probiotics in the Treatment of Crohn's Disease

Fatty Acids for the Treatment of Crohn's Disease

Table 8: A Summary of Omega-3 Fatty Acid Studies in Crohn's Disease


N-acetyl Glucosamine

Remicade Increasing Risk of Cancer

Botanicals in the Treatment of Crohn's Disease

Dehydroepiandrosterone (DHEA)

Potential Sequelae of Crohn's Disease


Other Abnormalities Contributing to the Etiopathogenesis of Crohn's Disease

Platelet Abnormalities Increased platelet count is a common feature of active Crohn’s disease and contributes to the increased incidence of thromboembolism seen in both Crohn's Disease and Ulcerative Colitis.121 In addition to increased platelet count, Crohns Disease is characterized by increased platelet activation in the mesenteric vessels.122 Although platelet function has historically been considered to involve primarily blood clotting, there is considerable evidence for platelet involvement in inflammation. Platelets from inflammatory bowel-diseased tissues have been found to express a number of inflammatory mediators, including CD40L, a substance similar to tumor necrosis factor that directs platelets toward inflammation instead of aggregation.121 A sequence of events has been postulated in which platelets trigger chemokine-mediated adhesion of white blood cells to the endothelium, causing leukocyte migration and subsequent focal inflammatory lesions. 121

Elevated Homocysteine

Higher than normal incidence of hypocoagulation states and subsequent thrombosis led investigators to examine homocysteine levels in IBD patients, since high homocysteine levels are known to contribute to risk for thromboembolism. Total homocysteine, vitamin B12, and folate levels were tested in 64 IBD patients (25 Crohns Disease patients) and 121 controls. Seventeen of 64 patients (26.5%) compared with three of 121 controls had hyperhomocysteinemia (defined as homocysteine 12.8 microM/L). Folate levels were significantly lower in the IBD group, while there was no statistically significant difference in B12 levels between the two groups. There was also no statistical difference between patients with Crohns Disease or Ulcerative Colitis.123

In another study of 65 IBD patients (56 with Crohn's Disease; 9 with Ulcerative Colitis), using 12.0 microM/L as the cutoff point, 10 patients (15.4%) demonstrated hyperhomocysteinemia compared to 3/138 (2.2%) in the control group. In this study, a vitamin B12 deficiency was associated with high homocysteine. 124

Yet another study found elevated levels of homocysteine in Crohns Disease patients correlated with both low folate and vitamin B12 levels, although they were more strongly associated with low folate.125

Vitamin B6 is essential for the catabolism of homocysteine to cysteine, taurine, sulfate, and glutathione. Thus, deficiencies of vitamin B6 can also result in hyperhomocysteinemia. The Journal of Neurological Sciences reports a case of a 39-year-old female Crohn's Disease patient with a history of ischemic stroke associated with a vitamin B6 deficiency and hyperhomocysteinemia along with inflammatory factors associated with hypercoagulation.126

Mitochondrial Dysfunction

Research on mitochondrial dysfunction as a cause of chronic disease is in its infancy. Preliminary investigations point to the possible involvement of mitochondrial dysfunction in the pathogenesis of Crohn’s disease. As early as 1985, in vitro examination of rectal biopsy specimens provide evidence of mitochondrial damage in Crohn's Disease.127 More recently, researchers elucidated a potential mechanism for the possible mitochondrial dysfunction in Crohn's Disease. They determined TNF-alpha could enhance mitochondrial NF-kappaB expression, down-regulating mitochondrial RNA expression.128 A recent case report of a young girl with Crohns Disease demonstrated impaired oxidative phosphorylation, with abnormalities in Complexes III and IV. In this case, the only medication that provided therapeutic benefit was an anti-TNF-alpha antibody, infliximab.129 This child had numerous other health problems besides Crohns Disease. Whether mitochondrial dysfunction plays a central role in the pathogenesis of Crohn's Disease remains to be determined.


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