Platelet-activating factor--a possible mediator in the pathogenesis of ulcerative colitis

Scand J Gastroenterol Suppl. 1990:172:19-21. doi: 10.3109/00365529009091904.

Abstract

Release of platelet-activating factor (PAF) by cultured colonic mucosa of patients with ulcerative colitis and healthy controls was determined. Before stimulation with calcium ionophore or antihuman IgE, no PAF release by control mucosa and minimal PAF release by mucosa of the colitis patients were detected. After stimulation with calcium ionophore, PAF release was four to five times higher by colonic mucosa of the colitis patients than of the controls. After stimulation with antihuman IgE, PAF release was twice as high by colonic mucosa of colitis patients as by control mucosa. Prednisolone, sulphasalazine, and mesalazine inhibited PAF activity stimulated by calcium ionophore in a dose-dependent manner. The results suggest that the use of PAF antagonists in the treatment of ulcerative colitis should be investigated.

MeSH terms

  • Aminosalicylic Acids / pharmacokinetics
  • Cells, Cultured
  • Colitis, Ulcerative / drug therapy
  • Colitis, Ulcerative / etiology*
  • Colitis, Ulcerative / metabolism
  • Dose-Response Relationship, Drug
  • Humans
  • Ionophores / pharmacology
  • Mesalamine
  • Platelet Activating Factor / physiology*
  • Prednisolone / pharmacokinetics
  • Sulfasalazine / pharmacokinetics

Substances

  • Aminosalicylic Acids
  • Ionophores
  • Platelet Activating Factor
  • Sulfasalazine
  • Mesalamine
  • Prednisolone