We measured serum, blood, or red cell concentrations of various vitamins in 24 patients with Crohn's disease who had been free from any nutritional treatment, and compared them with those in 24 healthy controls. Twelve of the patients were affected in the small bowel only, two in the large bowel only, and the remaining 10 in both the small and large bowel. The fat-soluble vitamins A and E were significantly decreased in patients with Crohn's disease compared to controls. Among the water-soluble vitamins, vitamins B1, B2 and B6 and folic acid were more depleted in patients with Crohn's disease than in the controls, whereas vitamins B12 and C, nicotinic acid, and biotin were not different between the two groups, and pantothenic acid was increased in patients with Crohn's disease. In addition, vitamin B2 and nicotinic acid showed a negative correlation with the Crohn's disease activity index. These findings suggest that there is a variety of vitamin deficiencies in Crohn's disease prior to treatment and also that concentrations of some vitamins, such as vitamin B2 and nicotinic acid, may reflect the severity of the disease.
These findings suggest that in active UC, IL-4 is pivotal, in combination with other Th2-like cytokines. In contrast, Th1-like cytokines and IL-15 bear no definite relation to local inflammation of UC.
Backgroud/Aims: Selenium is an important trace element and its deficiency has been reported to be associated with cardiomyopathy or gastrointestinal cancer. The aim of this study is to clarify the selenium status in Crohn’s disease (CD) on enteral nutrition. Methods: We measured serum selenium concentrations in 53 patients with CD and compared them with those in 21 healthy controls. Twenty-nine patients were under the treatment by enteral nutrition (EN group), and the remaining 24 patients were free from formulated enteral nutrition (non-EN group). Results: While the serum selenium concentration in the non-EN group was not decreased when compared to controls, the value in the EN group was significantly lower than those in the non-EN group and in controls. Clinical manifestations of selenium deficiency were found in a patient on exclusive enteral nutrition. In the EN group, the serum selenium concentration showed an inverse correlation with the duration and the daily dose of enteral nutrition. In the non-EN group, the serum selenium concentrations were inversely correlated with the Crohn’s disease activity index. Conclusion: These findings suggest that patients with CD on enteral nutrition are at risk for selenium deficiency and that even patients without enteral nutrition may develop selenium deficiency at the active phase of the disease.
The mechanism of nonsteroidal antiinflammatory drug-induced intestinal ulcers is not clearly understood. To evaluate whether immunosuppressants have a preventive effect against indomethacin-induced gastrointestinal damage, we investigated the effects of prednisolone, cyclosporin, and the newly developed immunosuppressant FK-506 in intracolonically indomethacin-treated rats: 24 mg/kg of indomethacin, administered intracolonically for two days, caused gastric ulcers and two types of small intestinal ulcers (longitudinal ulcers and scattered small ulcers). Pretreatment with intraperitoneal immunosuppressants reduced the size of gastric ulcers. Both cyclosporin (10 mg/kg) and FK-506 (1 mg/kg, 2 mg/kg) treatments significantly reduced the incidence and the length of the longitudinal ulcers of the small intestine when compared to the vehicle-treated controls, whereas prednisolone (20 mg/kg) did not show any preventive effect. Furthermore, the number of small scattered ulcers of the small intestine was significantly reduced by the high dose of FK-506 (2 mg/kg), but not by cyclosporin or prednisolone. These findings indicate that immunosuppressants have protective and antiinflammatory effects in indomethacin-induced gastroenteropathy, suggesting that cytokines may be important mediators in the pathogenesis of enteropathy induced by nonsteroidal antiinflammatory drugs.
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