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1. These results confirm increased macrophage activation in inflammatory bowel disease and suggest functional heterogeneity within the intestinal macrophage population.

2. For inflammatory bowel disease the morbid risk varies with age.

3. With inflammatory bowel disease, the loss of protein through the gastrointestinal tract is also a contributory factor.

4. In our previous study, 34 monozygotic pairs with inflammatory bowel disease were found.

5. Recent evidence favours the idea that inflammatory bowel disease may be caused by mesenteric vasculitis.

6. Patients with gall stones or established inflammatory bowel disease were excluded.

7. Furthermore, cultured mononuclear cells isolated from inflammatory bowel disease mucosa spontaneously secrete large amounts of IgG.

8. Also in patients with inflammatory bowel disease antineutrophil cytoplasmic antibodies have been detected.

9. This case supports the theory that functional disturbances of the thymus may have a role in the pathogenesis of inflammatory bowel disease.

10. Pronounced changes have been found in gut neuropeptides in patients with inflammatory bowel disease.

11. The mode of action of 5ASA and 4ASA in inflammatory bowel disease is unknown.

12. One potential source for the increased values of reactive oxygen species in inflammatory bowel disease is the neutrophil.

13. Several different types of autoantibodies have been described in inflammatory bowel disease and primary sclerosing cholangitis.

14. While corticosteroids have an adverse effect on bone mass, this may be partly counterbalanced by improvement in the inflammatory bowel disease.

15. The rate of liver protein synthesis in patients with inflammatory bowel disease was 43% higher than the control group of patients.

16. Endoscopy was performed at entry to confirm the diagnosis of inflammatory bowel disease.

17. The role of platelet activating factor blocker in the treatment of inflammatory bowel disease deserves investigation.

18. Another possibility is that the genetic regulation of the isotype response is different in the two populations of inflammatory bowel disease patients.

19. Nevertheless the absence of recurrence during long term follow up will be required to exclude underlying idiopathic inflammatory bowel disease.

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20. However, Tsuchiya etal have described an association between thymic abnormalities and inflammatory bowel disease.

21. Ulcerative colitis and Crohn's disease are chronic, remitting and relapsing mucosal disorders, collectively known as inflammatory bowel disease.

22. With regard to the diagnosis in approximately 10% of inflammatory bowel disease patients with colonic involvement a definite distinction can not be made.

23. Little information is currently available on the role of interleukin 1 and tumour necrosis factor in inflammatory bowel disease.

24. New corticosteroid compounds with high topical and little systemic activity seem to offer great benefit to inflammatory bowel disease patients.

25. These results also question the rationale of using n3 polyunsaturated fatty acids in the treatment of inflammatory bowel disease.

26. The possible therapeutic effect of a specific receptor antagonist in inflammatory bowel disease remains to be evaluated.

27. This review examines the evidence that abnormal oxidative metabolism is of central importance to active inflammatory bowel disease.

28. A disturbance in immunoregulatory control has long been suspected to play a major role in the pathogenesis of inflammatory bowel disease.

29. Reports of invitro production of cytokines by peripheral or mucosal mononuclear cells in inflammatory bowel disease, however, conflict.

30. Tumour necrosis factor mRNA was detected in four of nine controls compared with 11/15 inflammatory bowel disease patients.