Editor,—Increased release of pro-inflammatory eicosanoids such as prostaglandin E₂ and thromboxane B₂ from mononuclear cells occurs during relapse in patients with inflammatory bowel disease (IBD).1 The key enzyme in eicosanoid synthesis is phospholipase A₂(PLA₂). Raised serum concentrations of the PLA₂group II isoenzyme can be detected by immunoassay during the acute stages of IBD.2 We read with interest the recent article by Peterson et al about the role of a phospholipase A₂ activating protein, PLAP (Gut 1996;39: 698–704). The authors showed clearly that PLAP can be detected in monocytes and granulocytes originating from intestinal mucosa of patients with Crohn’s disease and ulcerative colitis. In addition to this finding, extracellular deposits of PLAP antigen were associated with blood vessels and oedematous fluid from the inflamed tissue. Peterson et al postulated that PLAP may be involved in increasing PLA₂ activity with consecutive eicosanoid generation in IBD. We propose a further possible mechanism of PLA₂ activation during acute IBD in which the pro-inflammatory cytokine interleukin-6 …

Professor Peterson.