title: Gastric emptying in patients with autoimmune pancreatitis.
abstract: OBJECTIVE
  Autoimmune pancreatitis (AIP) and its extrapancreatic lesions seem to be clinical manifestations of organs involved in IgG4-related systemic disease. To clarify whether the stomach is a target organ, gastric function was evaluated in patients with AIP.
  
  
  METHODS
  In 6 patients with AIP, gastric emptying was assessed by Carbon 13 (¹³C) acetate breath test before and after steroid therapy. Based on 4-hour breath samples, the half ¹³CO₂ excretion time (T(1/2)) and the time of maximal excretion (T(max)) were calculated as gastric emptying parameters. Data of 20 healthy volunteers were used as controls. The number of IgG4-positive plasma cells in gastrofiberscopic biopsy specimens was counted before and after steroid therapy.
  
  
  RESULTS
  Both T(1/2) and T(max) in patients with AIP decreased significantly after steroid therapy (T(1/2): 1.89 ± 0.21 hours vs 1.69 ± 0.15 hours, P = 0.046; and T(max): 1.1 ± 0.2 hours vs 0.96 ± 0.2 hours, P = 0.027), and became similar to those of the controls (T(1/2): 1.69 ± 0.32 hours and T(max): 0.98 ± 0.2 hour). The number of IgG4-positive plasma cells infiltrating the gastric mucosa decreased after steroid therapy.
  
  
  CONCLUSIONS
  Gastric emptying was impaired in patients with AIP and improved to the reference range after steroid therapy. The stomach may be a target organ of IgG4-related systemic disease.
authors.affiliation: Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Tokyo, Japan.
authors.forename: Hajime
authors.initials: H
authors.lastname: Anjiki
authors.forename: Terumi
authors.initials: T
authors.lastname: Kamisawa
authors.forename: Taku
authors.initials: T
authors.lastname: Tabata
authors.forename: Kensuke
authors.initials: K
authors.lastname: Takuma
authors.forename: Naoto
authors.initials: N
authors.lastname: Egawa
authors.forename: Takatsugu
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Kuyama
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Urita
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Tando
authors.forename: Teruo
authors.initials: T
authors.lastname: Nakamura
mesh_terms: D000284:Administration, Oral; D000368:Aged; D001327:Autoimmune Diseases / Q000188:drug therapy* / Q000503:physiopathology; D001944:Breath Tests / Q000379:methods; D002247:Carbon Isotopes; D004334:Drug Administration Schedule; D005260:Female; D005746:Gastric Emptying / Q000187:drug effects*; D005753:Gastric Mucosa / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D005773:Gastroscopy; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use; D016481:Helicobacter Infections / Q000382:microbiology / Q000503:physiopathology; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000188:drug therapy* / Q000503:physiopathology; D010950:Plasma Cells / Q000187:drug effects / Q000276:immunology; D011239:Prednisolone / Q000008:administration & dosage / Q000627:therapeutic use*; D011446:Prospective Studies; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D002247:Carbon Isotopes; D005938:Glucocorticoids; D007074:Immunoglobulin G; D011239:Prednisolone