Platelet factor 4 and beta-thromboglobulin in inflammatory bowel disease and giant cell arteritis

A.A. Vrij, J. Rijken, J.W.J. van Wersch, R.W. Stockbrügger

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

As platelet factors are important in the inflammatory response, we examined the course of platelet factor 4 and ß-thromboglobulin in relation to disease activity in inflammatory bowel disease and in giant cell arteritis. Patients and methods in a prospective study, the platelet count, platelet factor 4 and ß-thromboglobulin were measured in 20 patients with crohn's disease, 18 with ulcerative colitis and 19 with giant cell arteritis, during active and inactive disease, as well as in 51 controls without inflammation. Results platelet counts were significantly higher in active vs. Inactive crohn's disease, ulcerative colitis and giant cell arteritis. Levels of platelet factor 4 and ß-thromboglobulin were significantly higher in active inflammatory bowel disease and giant cell arteritis, as well as in inactive inflammatory bowel disease and giant cell arteritis, than in the non-inflammatory controls. A positive correlation was found between the crohn's disease activity index and the platelet count, platelet factor 4 and ß-thromboglobulin. Also, a positive correlation was found between the ulcerative colitis activity index and ß-thromboglobulin. However, even after 12 months of follow-up, in crohn's disease and ulcerative colitis the mean levels of platelet factor 4 and ß-thromboglobulin were significantly higher than the levels of the controls. Conclusion platelet factors were correlated with inflammatory bowel disease activity. Levels of platelet factor 4 and ß-thromboglobulin, however, were markedly raised for a long time in clinically inactive inflammatory bowel disease, which might point to a pre-thrombotic state of disease.
Original languageEnglish
Pages (from-to)188-194
Number of pages7
JournalEuropean Journal of Clinical Investigation
Volume30
DOIs
Publication statusPublished - 1 Jan 2000

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