No significant relation between relapse of autoimmune pancreatitis and substitution of aspartic acid at position 57 of DQβ1

Excerpt

To the Editor: In our previous study, we showed that obstructive jaundice at onset could be a significant risk factor for the relapse in patients who were not treated with steroid [1]. However, no report, including ours, has shown any significant risk factor for relapse in patients treated with steroid. Recently, Park et al. [2] reported that the substitution of aspartic acid to nonaspartic acid at codon 57 of DQβ1 showed a significant association with relapse of autoimmune pancreatitis (AIP) treated with steroid (non-relapse group, 29.6%; relapse group, 100%; P = 0.00003; odds ratio, 3.38; 95% confidence interval, 1.9–6.0). Moreover, there was reportedly a significant difference in the timing of the AIP relapse according to the 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 < 0.001). All patients who experienced a relapse during maintenance steroid therapy (n = 7) had a nonaspartic acid homozygosity at codon 57 of DQβ1. In addition, nonaspartic acid heterozygosity at codon 57 of DQβ1 was identified in all patients who experienced a relapse after steroid treatment was discontinued (n = 6). We tried to examine whether their findings would also be applicable to our patients. In addition, we examined the frequency of HLA DQB1*0302, which may be associated with the relapse of AIP [2], and DQB*0401, which was significantly high (58%) in Japanese AIP patients, according to the report of Kawa et al. [3], but not so high in Korean patients [2]. …