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Abstracts

Abstracts

Asians (Ulcerative Colitis)

Asians

Ulcerative colitis is associated with abnormalities of mucin synthesis and secretion, features that may also be associated with malignant change. It has been shown that South Asians in Britain have a high incidence of ulcerative colitis but a low incidence of colorectal carcinoma compared with their European counterparts.

Results suggest that South Asians with ulcerative colitis show a different distribution of terminal N-acetyl neuraminyl residues, either in their alpha-2,6 or alpha-2,3 linkage, compared with their European counterparts. The changes in sialylation observed in European cases compared with normal disease-free control subjects were present in quiescent disease, but were also related to disease activity. Their absence in Asians with ulcerative colitis may imply an inherent, genetically determined variation in this group, which may also play a part in their reduced risk of subsequent malignancy.

McMahon RF et al., South Asians with ulcerative colitis exhibit altered lectin binding compared with matched European cases. Histochem J, 1997 Jun, 29:6, 469-77.

Elemental Diets

Elemental Diets

Do elemental diets improve "nutritional" status?

The mechanisms by which elemental diets induce remission in patients with "Crohn's disease" is unknown, but it has been suggested that improvement in nutritional state may play a part.

The fact that changes in disease activity appear to precede any detectable changes in nutritional state, it suggests that the beneficial action of elemental diet in patients with active Crohn's disease is not due to an improvement in nutritional status.

Teahon-K: Alterations in nutritional status and disease activity during treatment of Crohn's disease with elemental diet. Scand-J-Gastroenterol. 1995 Jan; 30(1): 54-60.

Essential Fatty Acid

Essential Fatty Acid

Patients with chronic intestinal disorders causing malabsorption, nutritional losses through "diarrhea", or catabolic illness would be expected to have essential "fatty acid" (EFA) deficiency (EFAD), but such deficiency has not been demonstrated.

Patients with chronic intestinal disease should be evaluated for likely EFA deficiencies and imbalances, and treated with substantial amounts of supplements rich in EFAs, such as oral vegetable and "fish oils", or IV lipids if necessary.

Siguel-EN & Lerman-RH: Prevalence of essential fatty acid deficiency in patients with chronic "gastrointestinal" disorders. Metabolism. 1996 Jan; 45(1): 12-23.

Fatty Acids (Ulcerative Colitis)

Fatty Acids

Short chain fatty acid (SCFA) deficiency is associated with colitis in animals and humans, and the mucosal metabolism of these compounds is decreased in ulcerative colitis. Trial of rectal SCFA twice daily.

Although SCFA enemas were not of therapeutic value in this controlled trial, the results suggest efficacy in subsets of patients with distal ulcerative colitis including those with short active episodes. Prolonged contact with rectal mucosa seems to be necessary for therapeutic benefit.

Breuer RI et al., Short chain fatty acid rectal irrigation for left-sided ulcerative colitis: a randomised, placebo controlled trial. Gut, 1997 Apr, 40:4, 485-91.

Food Sensitivities

Food Sensitivities

It has been claimed that prolonged remissions of Crohn's disease can be achieved after enteral or "parenteral" "nutrition", by identifying and excluding foods that "exacerbate" a patient's symptoms.

"Food sensitivities" are evident after treatment of Crohn's disease with elemental diet but are variable, often do not persist, and are of insufficient importance to warrant putting all patients through elimination diets.

Pearson-M et al: Food intolerance and Crohn's disease [see comments]. Gut. 1993 Jun; 34(6): 783-7.

Gallstones

Gallstones

"Gallbladder" "bile" stasis during long-term continuous enteral feeding may contribute to the high prevalence of "gallstones" in patients with Crohn's disease. We therefore examined the effects of continuous enteral nutrition on gallbladder motility and cholecystokinin (CCK) release in six patients.

During continuous enteral nutrition the gallbladder is completely contracted, and CCK concentrations remain elevated. It is therefore unlikely that long-term enteral nutrition contributes to the increased prevalence of gallstones in patients with Crohn's disease.

Stolk-MF et al: Gallbladder motility and cholecystokinin release during long-term enteral nutrition in patients with Crohn's disease. Scand-J-Gastroenterol. 1994 Oct; 29(10): 934-9.

Malnutrition (Ulcerative Colitis)

Malnutrition

"Malnutrition" is common in "inflammatory" "bowel disease"; deficiencies of multiple micronutrients and macronutrients can present a diagnostic and therapeutic challenge to the clinician. Enteral and parenteral nutrition have been used as adjunctive therapy to correct or prevent malnutrition in inflammatory bowel disease. In addition, some authors have advocated enteral and parenteral nutrition as primary therapy of acute inflammatory bowel disease.

Zurita-VF et al: Nutritional support in inflammatory bowel disease. Dig-Dis. 1995 Mar-Apr; 13(2): 92-107

Mesalamine & Nicotine

Mesalamine & Nicotine

Characterized the usefulness of mesalamine and nicotine in the treatment of active ulcerative colitis and inactive Crohn's disease.

In patients with inactive Crohn's disease, mesalamine 2 g/d significantly reduced the risk of relapse in high-relapse-risk patients compared with placebo, reducing the relapse rate from 71% to 55%, but was ineffective in preventing recurrence of inactive Crohn's disease following surgical resection.

Whereas nicotine 15-25 mg/d administered as a transdermal patch produced greater symptomatic improvement in active ulcerative colitis compared with placebo, nicotine 15 mg/16 h produced results no different from those with placebo in maintaining remission in active colitis. Nicotine appears to have an adverse effect on the course of Crohn's disease and is not recommended.

Mesalamine has demonstrated clinical effectiveness as a therapeutic agent in the treatment of active ulcerative colitis and inactive Crohn's disease.

Although its relationship to inflammatory bowel disease has been known for many years, the usefulness of nicotine for the treatment of active ulcerative colitis requires further exploration before it can be recommended as therapeutic agent.

Bonapace CR & Mays DA: The effect of mesalamine and nicotine in the treatment of inflammatory bowel disease. Ann Pharmacother, 1997 Jul-Aug, 31:7-8, 907-13.

Nitric Oxide (Ulcerative Colitis)

Nitric Oxide

It is postulated that an enhanced production of nitric oxide by inflamed intestine plays a role in the pathophysiology of active inflammatory bowel disease.

Determined systemic NOx concentrations and colonic nitric oxide synthase activity in patients with ulcerative colitis or Crohn's disease.

Patients with active ulcerative colitis and Crohn's disease had significantly elevated plasma NOx concentrations; a positive correlation was found between NOx values and inducible nitric oxide synthase activities in the active mucosa of these patients.

In active ulcerative colitis, levels of inducible nitric oxide synthase were significantly elevated in both normal and inflamed mucosa, although inducible nitric oxide synthase activity was higher in the latter. These colonic inducible nitric oxide synthase activities correlated well with the results of endoscopic and histologic grading of inflammation.

There was no increase in constitutive nitric oxide synthase activity in patients with active ulcerative colitis.

However, constitutive nitric oxide synthase activity was significantly increased in the inflamed mucosa in patients with Crohn's disease. In Crohn's disease, elevated inducible nitric oxide synthase activity was found in both normal and inflamed mucosa, with no significant difference between the tissues. Such differences in nitric oxide production in the colonic mucosa possibly reflect the significant differences in the pathophysiology and characteristic clinical features between ulcerative colitis and Crohn's disease.

Kimura H et al., Increased nitric oxide production and inducible nitric oxide synthase activity in colonic mucosa of patients with active ulcerative colitis and Crohn's disease. Dig Dis Sci, 1997 May, 42:5, 1047-54.

Selenium Deficiency

Selenium Deficiency

A patient with Crohn's disease receiving short-term postoperative parenteral nutrition supplemented with trace elements, nevertheless became "selenium" deficient with evidence of a cardiomyopathy. This was fully reversible with oral selenium supplementation. Current parenteral feeding regimes may not contain enough selenium for malnourished patients.

Levy-JB et al: Selenium deficiency, reversible cardiomyopathy and short-term intravenous feeding [see comments]. Postgrad-Med-J. 1994 Mar; 70(821): 235-6.

Vitamin D Deficiency

Vitamin D Deficiency

In search for the reasons of "vitamin D" deficiency in Crohn's disease (CD).

A specific diet with a high vitamin D content, or vitamin D supplementation is recommended in patients with CD to overcome the negative effects of low sun exposure on "bone" mineral density.

Vogelsang-H et al: Dietary vitamin D intake in patients with Crohn's disease. Wien-Klin-Wochenschr. 1995; 107(19): 578-81.

 


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