Japanese journal of ophthalmology · 2015
Association between the major histocompatibility complex and clinical response to infliximab therapy in patients with Behçet uveitis.
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Kuroyanagi Kana, Sakai Tsutomu, Kohno Hideo, Okano Kiichiro, Akiyama Goichi, Aoyagi Ranko, Inaba Mayumi, Tsuneoka Hiroshi
Аннотация
PURPOSE: Our aim was to investigate whether major histocompatibility complex (MHC) polymorphisms are associated with response to infliximab therapy in Japanese patients with Behçet uveitis (BU).
METHODS: We retrospectively reviewed 24 patients (17 men and seven women) treated with infliximab for BU. Of them, ten patients were genotyped as HLA A*2601, and nine as HLA B*5101. Therapeutic response levels in the two groups were compared based on ocular attacks and the Behçet disease ocular attack score 24 (BOS24) over 24 months of treatment.
RESULTS: Mean frequencies of ocular attacks at 13-18 and 19-24 months after the start of treatment were significantly higher in the HLA A*2601 group (P = 0.0392 and 0.0177, respectively). Mean BOS24-6 M values for months 1-6, 7-12, 13-18, and 19-24 were also significantly higher in the HLA A*2601 group (P = 0.0459, 0.0150, 0.0394, and 0.0178, respectively). Shortening of the infusion interval was required in eight patients in the HLA A*2601 group but in one only in the HLA B*5101 group. Behçet-disease-related adverse events occurred in eight patients in the HLA A*2601 group and two in the HLA B*5101 group. Nonocular adverse events occurred in four patients in the HLA A*2601 group and none in the HLA B*5101 group.
CONCLUSIONS: Although mean change from baseline in the number of ocular attack scores in the HLA A26 and HLA B51 groups seemed to be similar, the HLA-A26 group had a more severe disease course under infliximab therapy for ocular/extraocular involvement. These data suggest that response to infliximab therapy in Japanese patients with BU is partly due to genetic determinants in the HLA complex.
METHODS: We retrospectively reviewed 24 patients (17 men and seven women) treated with infliximab for BU. Of them, ten patients were genotyped as HLA A*2601, and nine as HLA B*5101. Therapeutic response levels in the two groups were compared based on ocular attacks and the Behçet disease ocular attack score 24 (BOS24) over 24 months of treatment.
RESULTS: Mean frequencies of ocular attacks at 13-18 and 19-24 months after the start of treatment were significantly higher in the HLA A*2601 group (P = 0.0392 and 0.0177, respectively). Mean BOS24-6 M values for months 1-6, 7-12, 13-18, and 19-24 were also significantly higher in the HLA A*2601 group (P = 0.0459, 0.0150, 0.0394, and 0.0178, respectively). Shortening of the infusion interval was required in eight patients in the HLA A*2601 group but in one only in the HLA B*5101 group. Behçet-disease-related adverse events occurred in eight patients in the HLA A*2601 group and two in the HLA B*5101 group. Nonocular adverse events occurred in four patients in the HLA A*2601 group and none in the HLA B*5101 group.
CONCLUSIONS: Although mean change from baseline in the number of ocular attack scores in the HLA A26 and HLA B51 groups seemed to be similar, the HLA-A26 group had a more severe disease course under infliximab therapy for ocular/extraocular involvement. These data suggest that response to infliximab therapy in Japanese patients with BU is partly due to genetic determinants in the HLA complex.