ULCER RECURRENCE - CYTOKINES AND INFLAMMATORY RESPONSE-DEPENDENT PROCESS

H. pylori and nonsteroidal antiinflammatory drugs (NSAIDs) are importa nt factors in the recurrence of peptic ulcer diseases. However, H. pyl ori-negative recurring ulcers can also be found in nonusers of NSAIDs. The aim of this paper is to review recent data pertaining to mechanis ms of ulcer recurrence. Prostaglandin E-2 generation is impaired in th e tissues of the ulcer scar site and prostaglandin depletion induced b y administration of indomethacin during the healing of experimental ga stric ulcer predisposes to future ulcer recurrence. Therefore, the pro staglandin deficiency may impair the quality of ulcer healing and thus increase the likelihood of future ulcer recurrence. Persistent infilt ration of polymorphonuclear cells is the most prominent finding in the gastric ulcer scar in rats treated with indomethacin. Concomitant adm inistration of prostaglandin E-1-analog with indomethacin attenuates i nflammatory infiltration and reduces future ulcer recurrence. Therefor e, the inflammatory responses at the ulcer scar site may be a key to t he quality of ulcer healing. Recent clinical findings suggest a close relationship between the quality of ulcer healing, infiltration of neu trophils and mononuclear cells, and future ulcer recurrence. Gastropro tective drugs such as prostaglandin analogs and prostaglandin inducers improve the quality of ulcer healing and reduce future recurrence. Pr oduction of inflammatory cytokines is stimulated by ulcerogenic factor s such as NSAIDs, stress, and H, pylori infection. Inflammatory cytoki nes such as interleukin-1 beta and tumor necrosis factor-alpha cause r ecurrence of healed ulcer. Synthetic prostaglandin E-2 inhibits recurr ence as well as the production of the cytokines.