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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

Diagnosis

Etiopathogenesis:

    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

Glutamine

N-acetyl Glucosamine

Remicade Increasing Risk of Cancer

Botanicals in the Treatment of Crohn's Disease

Dehydroepiandrosterone (DHEA

Potential Sequelae of Crohn's Disease

References




Diagnosis

Diagnosis of Crohn’s disease is often challenging due to its strong similarity to Ulcerative Colitis. It is vital, when diagnosing either form of IBD, to obtain an accurate patient history of symptomatology at the time of physical exam. Diagnostic imaging to establish lesion type and extent of involvement include barium enema, small-bowel series, colonoscopy,21 and capsule endoscopy.22 Laboratory tests and pathological examination of biopsied intestinal tissue are also important for accurate diagnosis. Tests performed often include complete blood count (CBC) to check for leukocytosis and anemia, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) as markers of inflammation, stool cultures to rule out intestinal pathogens, and IgG/IgA antibody levels to Saccharomyces cerevisiae (SCA) and Mycobacterium avium subspecies paratuberculosis (MAP). These antibodies have been shown to be positive in 60 percent and 86 percent of Crohn's Disease patients, respectively, but are less frequently positive in UC patients and rarely positive in healthy subjects.23

Perhaps the best tool for establishing and monitoring disease severity and activity is the Crohn’s Disease Activity Index (CDAI). The CDAI was developed in the National Cooperative Crohn’s Disease Study to provide assessable, uniform clinical parameters with a consistent numerical index of disease status (refer to patient handout at the end of this article).24,25 The CDAI is a patient assessment form incorporating both objective and subjective information. Using established criteria the physician calculates the CDAI score. CDAI scores > 150 indicate active disease with a poorer prognosis than scores 150. Since the CDAI is not as accurate for monitoring disease activity in children, a second scale known as the pediatric CDAI (PCDAI) was developed. The PCDAI correlates disease severity and activity to levels of serum albumin. The scoring is easy to perform, reproducible by different observers, and sensitive to changes in clinical status.26

Because there is no cure for Crohn’s disease, conventional treatment has been aimed at suppression of the inflammatory response and relief of symptoms of fever, diarrhea, and abdominal pain. Once disease symptoms are stable, drug therapy is employed to decrease the frequency of disease flares and maintain remission. Current conventional treatment of Crohn's Disease includes aminosalicylates, corticosteroids, immune-modulating agents, and antibiotics. While reasonably effective in stabilizing disease and maintaining remission, many of these treatments are fraught with side effects and complications. Natural treatment options, as alternatives or complements to conventional therapy, are presented below.



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