title: Long-term prognosis of autoimmune pancreatitis in terms of glucose tolerance.
abstract: OBJECTIVE
  Glucose intolerance is often observed in autoimmune pancreatitis (AIP), although its long-term prognosis after steroid treatment (ST) is still unclear.
  
  
  METHODS
  A total of 47 patients with AIP were enrolled. On the basis of the change in hemoglobin A1c (HbA1c) and the use of diabetic medication, prognosis was classified into 3 categories, namely, "improved," "aggravated," and "unchanged." The relation between the result of an initial glucagon tolerance test (ΔCPR) and the later use of insulin during maintenance ST was examined in 20 patients. The transitions of homeostasis model assessment β cell and insulin resistance (HOMA-β and HOMA-R) were analyzed in 16 patients.
  
  
  RESULTS
  Glucose tolerance was improved in 6 patients (13%), aggravated in 9 patients (19%), and unchanged in 32 patients (68%). All patients with ΔCPR less than 0.6 ng/mL were obliged to use insulin even after long-term observation, whereas all patients with ΔCPR more than 1.0 ng/mL were free from insulin therapy. Moreover, HOMA-β showed significant improvement after ST (43.9% → 56.0% in median, P = 0.030), and HOMA-R showed significant aggravation (1.30 → 1.78, P = 0.039).
  
  
  CONCLUSIONS
  Glucose tolerance that is too severely damaged may not recover fully even after ST. Thus, ST should be performed to preserve insulin secretion at the early stage of AIP.
authors.affiliation: Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. khirano-tky@umin.ac.jp
authors.forename: Kenji
authors.initials: K
authors.lastname: Hirano
authors.forename: Akihiro
authors.initials: A
authors.lastname: Isogawa
authors.forename: Minoru
authors.initials: M
authors.lastname: Tada
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Isayama
authors.forename: Naminatsu
authors.initials: N
authors.lastname: Takahara
authors.forename: Koji
authors.initials: K
authors.lastname: Miyabayashi
authors.forename: Suguru
authors.initials: S
authors.lastname: Mizuno
authors.forename: Dai
authors.initials: D
authors.lastname: Mohri
authors.forename: Kazumichi
authors.initials: K
authors.lastname: Kawakubo
authors.forename: Takashi
authors.initials: T
authors.lastname: Sasaki
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Kogure
authors.forename: Natsuyo
authors.initials: N
authors.lastname: Yamamoto
authors.forename: Naoki
authors.initials: N
authors.lastname: Sasahira
authors.forename: Nobuo
authors.initials: N
authors.lastname: Toda
authors.forename: Rie
authors.initials: R
authors.lastname: Nagano
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yagioka
authors.forename: Yoko
authors.initials: Y
authors.lastname: Yashima
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Hamada
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Ito
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Koike
mesh_terms: D000328:Adult; D000368:Aged; D001327:Autoimmune Diseases / Q000097:blood / Q000188:drug therapy*; D001786:Blood Glucose / Q000378:metabolism; D048909:Diabetes Complications / Q000097:blood / Q000188:drug therapy*; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D018149:Glucose Intolerance / Q000097:blood / Q000188:drug therapy*; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism / Q000627:therapeutic use; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D017063:Outcome Assessment, Health Care; D010195:Pancreatitis / Q000097:blood / Q000188:drug therapy*; D011379:Prognosis; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D005938:Glucocorticoids; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin