Presence of PAF-acether in stool of patients with pouch ileoanal anastomosis and pouchitis

Platelet-activating factor is an endogenous phospholipid produced by a wide variety of inflammatory cells. Platelet-activating factor induces severe pathological changes in various organs and, among numerous potent effects, causes bowel necrosis. Pouchitis is a poorly understood complication of ileoanal pouch anastomosis which occurs in patients who undergo surgery for ulcerative colitis. The aim of this study was to measure ileal or fecal platelet-activating factor and lyso platelet-activating factor contents in normal volunteers (n = 12), in patients with terminal ileostomy (n = 7), and in patients with ileoanal anastomosis (n = 15) (8 patients have pouchitis defined by the presence of ulcerations on the reservoir). Fecal samples were processed and assessed for platelet-activating factor by platelet aggregation assay. The aggregating material was further characterized as platelet-activating factor by the following: inhibition of the platelet aggregation it induced by specific platelet-activating factor receptor antagonist (BN 52021; IHB, Le Plessis Robinson, France); abolition of platelet aggregation after incubation with phospholipase A2 but not with lipase A1; and retention time on high-performance liquid chromatography. Stool platelet-activating factor content (in nanograms per gram of stool, mean ± 1SD) was significantly increased in patients with pouchitis (22.2 ± 16 ng/g) compared with patients with normal reservoir (1.59 ± 0.63 ng/g, P < 0.01), terminal ileostomy (0.59 ± 0.43 ng/g, P < 0.01), and healthy controls (0 ± 0 ng/g of stool, P < 0.001). Lyso platelet-activating factor (nanograms per gram of stool) was increased in patients with pouchitis (10,704 ± 5499 ng/g) compared with patients with normal reservoir (4721 ± 4549 ng/g of stool, P < 0.05), terminal ileostomy (3042 ± 4019 ng/g, P < 0.02), and healthy volunteers (128 ± 107 ng/g, P < 0.001). In patients with ileoanal anastomosis and pouchitis, increased platelet-activating factor production could be implicated in the inflammation and ulcerations observed in the reservoir.