title: Clinical response is associated with elevated plasma interleukin-1 receptor antagonist during selective granulocyte and monocyte apheresis in patients with ulcerative colitis.
abstract: Depletion of granulocytes and monocytes (GM) by selective apheresis (GMA) with an Adacolumn exerts an anti-inflammatory effect in patients with ulcerative colitis (UC) or rheumatoid arthritis. However, the mechanism of the anti-inflammatory effect of GMA is not fully understood yet. We investigated the effect of GMA on the plasma concentration of interleukin-1 receptor antagonist (IL-1ra), a potent anti-inflammatory cytokine. Twenty-six patients with active UC received GMA at one session per week for 5 consecutive weeks. Clinical response was defined as Deltaclinical activity index (DeltaCAI=CAI at entry - CAI at post)>or=4, while clinical remission was defined as CAI<or=4. Twenty-one of twenty-six patients (80.8%) responded to GMA. In the first session, plasma from responder patients showed a significant (P < 0.01) increase in IL-1ra in the Adacolumn outflow. In contrast, there was no change in IL-1ra in nonresponders. In conclusion, release of IL-1ra during GMA might be one mechanism of clinical efficacy associated with this therapy.
authors.affiliation: Department of Internal Medicine, Saitama Red Cross Hospital, Saitama, Japan.
authors.forename: Kyoya
authors.initials: K
authors.lastname: Sakimura
authors.forename: Toshihide
authors.initials: T
authors.lastname: Omori
authors.forename: Etsuro
authors.initials: E
authors.lastname: Iwashita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Tsuzuki
authors.forename: Kenji
authors.initials: K
authors.lastname: Fujimori
authors.forename: Fumio
authors.initials: F
authors.lastname: Konishi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Hiroo
authors.initials: H
authors.lastname: Anzai
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Suzuki
authors.forename: Souichi
authors.initials: S
authors.lastname: Sugawara
authors.forename: Yuji
authors.initials: Y
authors.lastname: Takeda
authors.forename: Katsuya
authors.initials: K
authors.lastname: Hiraishi
authors.forename: Abbi R
authors.initials: AR
authors.lastname: Saniabadi
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Ide
authors.forename: Soichiro
authors.initials: S
authors.lastname: Miura
authors.forename: Shinichi
authors.initials: S
authors.lastname: Ota
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001772:Blood Cell Count; D003093:Colitis, Ulcerative / Q000097:blood* / Q000276:immunology* / Q000628:therapy; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006098:Granulocytes / Q000473:pathology / Q000502:physiology; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007937:Leukapheresis / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000473:pathology / Q000502:physiology; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors / Q000502:physiology; D012074:Remission Induction; D012720:Severity of Illness Index; D012795:Sialoglycoproteins / Q000097:blood* / Q000502:physiology; D016896:Treatment Outcome
chemical_list: C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D017472:Receptors, Interleukin-1; D012795:Sialoglycoproteins