Raised serum activity of phospholipase A2 immunochemically related to group II enzyme in inflammatory bowel disease: Its correlation with disease activity of Crohn's disease and ulcerative colitis

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Abstract

Calcium dependent phospholipase A2 activity in the mixed micelies of 1-palmitoyl-2-oleoylphosphatidylglycerol and cholate was measured in sera of 39 patients with Crohn's disease, 40 patients with ulcerative colitis, and 40 healthy controls. The phospholipase A2 activity was significantly raised in those sera of the patients with active Crohn's disease and those with moderate and severe ulcerative colitis. The major phospholipase A2 activity derived from the sera was separated into two peaks by reverse phase high performance liquid chromatography. The phospholipase A 2 active fractions were immunochemically characterised using specific antibody directed against human group II phospholipase A2 purified from rheumatoid synovial fluid. The results suggest that raised serum phospholipase A2 activity in patients with Crohn's disease and ulcerative colitis was mainly attributed to the two forms of phospholipase A2 immunochemicaily related to group II enzyme. In patients with Crohn's disease, serum phospholipase A2 activity decreased in paraliel with clinical improvement, and correlated with serum C-reactive protein and erythrocyte sedimentation rate. The results suggest that serum phospholipase A2 activity may serve as an additional indicator of disease activity. Serum phospholipase A2 activity in patients with ulcerative colitis tends to increase in relation with endoscopic severity, and may be a more sensitive laboratory index than serum C-reactive protein and erythrocyte sedimentation rate to evaluate disease activity.

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APA

Minami, T., Tojo, H., Shinomura, Y., Tarui, S., & Okamoto, M. (1992). Raised serum activity of phospholipase A2 immunochemically related to group II enzyme in inflammatory bowel disease: Its correlation with disease activity of Crohn’s disease and ulcerative colitis. Gut, 33(7), 914–921. https://doi.org/10.1136/gut.33.7.914

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