Does local intestinal ascorbate deficiency predispose to fistula formation in Crohn's disease

Pettit, S H; Irving, M. H.

doi:10.1007/bf02554789

Cited by 12 publications

(2 citation statements)

References 7 publications

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“…Those patients with fistulae have either lower plasma and intestinal ascorbate levels than patients without fistulae (Gerson and Fabry, 1974) or are unable to concentrate ascorbate in inflamed intestine to the same degree as patients without fistulae (Pettit and Irving, 1987). It has been suggested that a relative deficiency of ascorbate in the diseased bowel is partly responsible for the development of these fistulae (Gerson and Fabry, 1974;Pettit and Irving, 1987). The data from the current studies would suggest that such a deficiency of ascorbate may impair the capacity of intestinal smooth muscle to heal by markedly inhibiting the secretion of procollagen by these cells.…”

Section: Discussionmentioning

confidence: 99%

Role of ascorbic acid in procollagen expression and secretion by human intestinal smooth muscle cells

Graham

Willey

Adams

et al. 1995

Journal Cellular Physiology

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The role of ascorbate in the production and secretion of procollagen by human intestinal smooth muscle cells and the conditions in culture for optimal ascorbate bioefficacy were studied. Procollagen synthesis and secretion were determined by the incubation of cells with L-[5-3H]proline, and the quantitation of radiolabelled procollagen bands in the cell layer and the culture medium by polyacrylamide slab gel electrophoresis and densitometry. When cells were cultured without ascorbate in the culture medium, procollagen secretion into the medium was 75% less than in cells receiving fresh ascorbate daily. In the cell layer, in contrast, procollagen accumulation was fourfold greater in the scorbutic cells than in the ascorbate-replete cells. These findings contrasted with those in a control line of scorbutic human dermal fibroblasts in which a 95% decrease in procollagen secretion was not associated with any procollagen accumulation in the cells. In the intestinal smooth muscle cells, the absence of ascorbate resulted in a 25 and 50% decrease in steady-state levels of procollagen I and III mRNA, respectively, compared to a 40 and 75% decrease in fibroblasts. Heat inactivation of the serum in the culture medium augmented the promotion of procollagen secretion by ascorbate two- to fourfold. L-ascorbate phosphate did not increase the activity of L-ascorbate when replaced in medium either daily or every 4 days, and its efficacy was not augmented by serum heat inactivation. The changing of culture medium induced collagen secretion in the absence of ascorbate, but this process was markedly enhanced by ascorbate and induced a transient decrease in the steady-state levels of both procollagen and nonprocollagen mRNAs. The predominant action of L-ascorbate on HISM cells in vitro is to promote procollagen secretion and not procollagen synthesis. L-ascorbate-phosphate is not an adequate substitute for L-ascorbate in this cell line.

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Section: Discussionmentioning

confidence: 99%

Role of ascorbic acid in procollagen expression and secretion by human intestinal smooth muscle cells

Graham

Willey

Adams

et al. 1995

Journal Cellular Physiology

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“…Deficient dietary intake of thiamine (vitamin B\), riboflavin (vitamin B 2 ) , and pantothenic acid is also common (20). Vitamin C deficiency in Crohn's disease has been described (21), and controversy exists as to whether abnormal tissue vitamin C levels contribute to fistula formation in Crohn's disease (22,23). Niacin (24) and biotin (25) deficiencies have also been reported in Crohn's disease.…”

Section: Water-soluble Vitaminsmentioning

confidence: 99%

Nutritional Issues in Pediatric Inflammatory Bowel Disease

Seidman,

LeLeiko,

Ament

et al. 1991

J. pediatr. gastroenterol. nutr.

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SummaryMalnutrition, characterized by weight loss, growth failure and micronutrient depletion, are prominent features of inflammatory bowel disease (IBD) in the pediatric age group. Accurate evaluation of the patient's nutritional status and appropriate nutritional support, whether enteral or parenteral, constitute integral parts of the management of the growing child with IBD. Over the past two decades, a number of studies have supported the potential use of nutritional therapy to induce remission and to control disease activity in symptomatic Crohn's disease. More recently, preliminary studies on the use of dietary supplements of marine‐oil‐derived omega‐3 fatty acids have also indicated a beneficial effect in IBD patients. In parallel with these clinical trials, scientific research has recently focused on the concept that specific dietary alterations can modulate the immune response. Components of the diet that may have particular relevance to mucosal immunity and the pathogenesis of IBD include polyunsaturated fatty acids, nucleotides, and amino acids such as glutamine and arginine. Future research in the interactions between specific nutrients and the immune system will likely increase our understanding of the causes of IBD, as well as enhance the development of novel nutritional therapies for IBD patients.

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Pathogenesis of intestinal strictures in Crohn's disease—an update

Graham

1995

Inflamm Bowel Dis

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: Stricture formation in Crohn's disease is a complication of an important wound healing process in the intestine. The smooth muscle cells of the intestinal musculares bear a responsibility for the repair of injured intestine, and effect this wound healing process by proliferating and laying down collagen at the site of injury. Injury in the submucosa, and chronicity of injury, are important factors in the development of stricture. The resultant accumulation of collagenous scar, thickening of the muscle layers, and contracture, all play a role in producing the critical architectural changes in the intestinal wall that impede the aboral movement of chyme. Important putative facets of intestinal smooth muscle cell biology that are involved in stricture formation include: the synthesis and secretion of procollagen; the peculiar response of these cells to cytokines, ascorbate, and corticosteroids; and changes in cell phenotype that result from chronic inflammation. Therapeutic modalities designed to ameliorate the stricturing process will need to modulate these biological activities in resident intestinal smooth muscle cells.

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Does local intestinal ascorbate deficiency predispose to fistula formation in Crohn's disease

Cited by 12 publications

References 7 publications

Role of ascorbic acid in procollagen expression and secretion by human intestinal smooth muscle cells

Role of ascorbic acid in procollagen expression and secretion by human intestinal smooth muscle cells

Nutritional Issues in Pediatric Inflammatory Bowel Disease

Pathogenesis of intestinal strictures in Crohn's disease—an update

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