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  Genetic Factors Predicting the Relapse of Autoimmune Pancreatitis
  ID : admin     DATE : 07-12-29 10:52     HIT : 2071    
Substitution of Aspartic Acid at Position 57 of the DQbeta1 Affects Relapse of Autoimmune Pancreatitis.

Park DH, Kim MH, Oh HB et al. Gastroenterology. 134/2 pp. 440-446

Background & Aims
Although autoimmune pancreatitis (AIP) responds well to corticosteroid therapy, relapse during maintenance corticosteroid therapy or after the withdrawal of corticosteroid treatment is not uncommon. To date, the factors related to relapse of AIP have not been fully explored.

Methods
To determine the clinical and genetic predictors relating to the relapse of AIP, we evaluated clinical factors, HLA polymorphisms, and the amino acid sequences in 40 patients with AIP.

Results
At a median follow-up period of 40 months (range, 12-67 months), relapse developed in 13 of 40 patients with AIP (33%), in whom complete remission was achieved with oral corticosteroid therapy. Among demographics, clinical characteristics in the initial diagnosis of AIP, we could not find any clinical predictor for relapse of AIP; however, in amino acid sequence analysis for relapse of AIP, the substitution of aspartic acid to nonaspartic acid at residue 57 of DQβ1 showed a significant association with relapse of AIP (nonrelapse group, 29.6%; relapse group, 100%; P = .00003; odds ratio, 3.38; 95% confidence interval, 1.9-6.0). There was a significant difference in the timing of relapse of AIP, according to density of the nonaspartic acid residue at DQβ1 57 (nonaspartic acid homozygosity: mean ± SD, 6.7 ± 4.2 months; nonaspartic acid heterozygosity: mean ± SD, 33 ± 11 months; P < .001).

Conclusions
Substitution of aspartic acid to nonaspartic acid at DQβ1 57 appears to represent a key genetic factor for relapse of AIP (ClinicalTrials.gov number, NCT00444444).