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Crohn's disease

Crohn's disease is a chronic inflammatory disease of the digestive tract and it can involve any part of it, from the mouth to the anus. It typically affects the caecum and/or the terminal ileum as well as demarcated areas of large bowel, with other areas of the bowel being relatively unaffected. It is often associated with auto-immune disorders outside the bowel, such as aphthous stomatitis and rheumatoid arthritis. more...

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Crohn's disease should not be confused with a non-progressive and non-degenerative digestive disorder called irritable bowel syndrome (IBS), which is not an autoimmune disease. Ulcerative colitis is a sibling autoimmune disease to Crohn's but only impacts the colon while Crohn's can impact any part of the digestive tract. Furthermore, Crohn's tends to affect multiple layers of the bowel lining, which can lead to many additional and hard-to-treat complications.

Symptoms

Crohn's patients typically suffer from abdominal pain, chronic diarrhea and disrupted digestion, which may make it difficult for sufferers, particularly in the acute phase of the disease, to eat and/or digest food. The inflammation can be extremely painful and debilitating. Other common complications of Crohn's include fistulas of the colon, hemorrhoids, lipid absorption problems, and anemia. Bleeding is seen in 20% cases, against 98% cases in ulcerative colitis. Rectal bleeding may be serious and persistent, leading to anemia. Bruising of the shins, varying fever symptoms, varying levels of pain, and psychological damage is seen in many cases. Children with Crohn's disease may suffer delayed development and stunted growth.

Epidemiology

The disease typically first appears in young adults in their late teens and twenties, although it is not unknown for symptoms to first appear quite late in life. Additionally, there has been an increase in cases occurring in young children. Recent studies suggest that up to 30% of all newly diagnosed cases are in children and teens under the age of 18. Estimates suggest that up to 60,000 people in the UK (about 1 in 1200) and 1,000,000 Americans have the disease (around 1 in 300). Some ethnic groups (such as Ashkenazi Jews) have a significantly higher rate of prevalence than others. Increased rates of disease have also been noted in some families, leading to speculation of a possible genetic link (see below). Epidemiological research indicates that Crohn's belongs to the group of diseases of affluence. In other words, the incidence of the disease is much higher in industrialized countries than elsewhere. However, this finding may be associated with the fact that Crohn's symptoms are typically diagnosed over a long period of time, in order to establish a pattern; in countries where medical help is less available, it may be difficult to arrive at a diagnosis.

Smoking increases the risk of Crohn's disease. Some women find that their disease is exacerbated by taking oral contraceptives, while others find it can help keep their flare ups at bay.

Causes

Barrier problem and autoimmunity to the luminal flora

The efficacy of immunosuppression, as well as scanty reports of complete disease resolution after bone marrow transplant, is highly suggestive of an autoimmune pathogenesis. A definite epitope to which the autoimmunity is directed is unknown, which also hampers the search for a virus or other pathogen that could induce molecular mimicry.

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Fish oil and antioxidants in Crohn's disease
From Nutrition Research Newsletter, 12/1/04

Crohn disease (CD) is an inflammatory condition of the gastrointestinal tract associated with extraintestinal manifestations that include altered bone turnover and poor nutritional status. The mechanism through which localized inflammation in the CD-affected gastrointestinal tract is associated with systemic manifestations remains unconfirmed but can

involve activated mononuclear cells that migrate by way of the peripheral blood (PBMCs) to bone, muscle, liver, and other tissues. PBMCs release inflammatory mediators, including tumor necrosis factor alpha (TNF-alpha), prostaglandin E2 (PGE2), and interferon a (IFN- a), with independent effects on bone turnover or nutritional status. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are n-3 polyunsaturated fatty acids (PUFAs), whereas arachidonic acid (AA) is an n-6 PUFA. These PUFAs are acquired directly from the diet or by metabolism of dietary essential fatty acids and are substrates for the production of the eicosanoid family of inflammatory mediators (prostaglandins and leukotrienes) by mononuclear cells. Fish oil is a rich source of EPA and DHA and, in healthy subjects, alters the n-3 PUFA composition of PBMCs. The proportions of EPA and DHA in plasma phospholipid and PBMCs are altered in patients with CD compared with healthy subjects but can also be influenced by CD activity. Evidence exists that fish oil inhibits clinical disease relapse in patients with CD with raised laboratory markers of systemic inflammation [that is, erythrocyte sedimentation rate (ESR)]. This response is accompanied by a significant reduction in inflammatory markers, consistent with a systemic anti-inflammatory effect. The present study investigated the effect of fish oil plus antioxidants on cytokine production by PBMCs from patients with CD with raised C-reactive protein concentrations (e"6.9 mg/L) or erythrocyte sedimentation rates (e"18 mm/h).

This was a randomized, double-blind, placebo-controlled trial of the effect offish oil plus antioxidants compared With placebo on the composition and function of PBMCs. Patients consumed nine capsules of fish oil/d or placebo oil in addition to their habitual diet. The placebo was olive oil containing the monounsaturated fatty acid (MUFA), oleic acid (OA). The fish-oil intervention was equivalent to an additional intake of 2.7 g EPA and DHA/d. Patients in the fish-oil group additionally received a compound antioxidant dietary supplement containing 200 [micro]g selenium, 3 [micro]g manganese, 30 mg vitamin E as d-alpha-tocopheryl succinate, 450 [micro]g vitamin A (300 [micro]g RE as retinol and 150 pg RE as [beta]-carotene), and 90 mg vitamin C as ascorbic acid. The placebo group received an identical capsule containing maltose and lactose. Patients were assessed at baseline and at 8, 16, and 24 wk for treatment compliance and side effects, laboratory markers of disease activity, plasma and mononuclear cell fatty acid composition, and PBMC function and for issuing of fresh capsules. Compliance to the study was assessed by direct questioning and confirmed by analysis of plasma phospholipid composition.

A total of 77 patients were recruited and randomly assigned to fish oil plus antioxidants or placebo. Fifteen patients were excluded from the outcome analysis. Six patients withdrew from the study (two in the fish-oil plus antioxidant group and four in the placebo group). Nine patients were retrospectively identified with laboratory markers of inflammation (ESR or CRP) that were within the locally accepted normal ranges for the healthy population and, therefore, below the threshold for recruitment. There were no reported serious side effects of treatment with either fish oil plus antioxidants or placebo. Values for CDAI, CRP, and ESR were comparable between the two groups and consistent with mild-to-moderate disease activity, but there was evidence of a higher body mass index in the fish-oil plus antioxidants group. No significant differences were observed between fish-oil plus antioxidants and placebo groups in dietary fat or antioxidant intake, quantitatively or qualitatively, or baseline plasma vitamin E, vitamin A, selenium, zinc, or copper. No significant differences were observed in the response to fish oil plus antioxidants compared with placebo of CDAI, CRP, or ESR. Six patients in the fish-oil plus antioxidants group (19.4%) and 7 patients in the placebo group (22.6%) required corticosteroid medication during the intervention period. No significant differences were observed in the response to fish oil plus antioxidants compared with placebo of plasma vitamin A, vitamin E, or copper at 24 wk. However, plasma selenium was higher in the fish-oil plus antioxidants group than in the placebo group. Fish oil plus antioxidants was associated with significantly greater incorporation of EPA, docosapentaenoic acid, and DHA within PBMCs than with placebo and a significantly lower incorporation of AA.

Fish-oil plus antioxidant dietary supplementation was associated with greater incorporation of the long chain n-3 PUFAs, EPA, DPA, and DHA, and lower incorporation in the n-6 PUFA, AA, in PBMCs (and plasma phospholipid). Dietary supplementation with fish oil plus antioxidants results in altered fatty acid composition of PBMCs and plasma phospholipid in CD and in lower production of IF2q-alpha and PGE2 by stimulated PBMCs, activated T cells, and monocytes, respectively. The clinical effects of decreasing IFN- alpha or PGE2 production by PBMCs in CD are uncertain but could be relevant to the management of extraintestinal manifestations and, in particular, bone turnover. This response should be investigated further within an intervention study.

T Trebble, N Arden, S Wootton, P Calder, M Mullee, D Fine, M Stroud. Fish oil and antioxidants alter the composition and fimction of circulating mononuclear cells in Crohn disease. Am J Clin Nutr 80(5):1137-1144 (November 2004) [Correspondence: TM Trebble, Institute of Human Nutrition, School of Medicine, University of Southampton, Tremona Road, Southampton S016 6YD, United Kingdom. E-mail: tt2@soton.ac.uk.]

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