Hepatology international · 2026
Clinical and pathological significance of serum anti-PD-1 autoantibodies in acute-onset and chronic autoimmune hepatitis.
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Oda Takashi, Takaki Akinobu, Harada Kenichi, Arinaga-Hino Teruko, Abe Masanori, Matsui Takeshi, Takahashi Atsushi, Ohira Hiromasa, Suzuki Yoshiyuki, Nakamoto Nobuhiro, Tanaka Atsushi, Matsumoto Kazuyuki, Li Jinpeng, Miyake Nozomi, Sue Masahiko, Adachi Takuya, Takeuchi Yasuto, Onishi Hideki, Kawanaka Miwa, Otsuka Motoyuki
Аннотация
BACKGROUND: Acute-onset autoimmune hepatitis (A-AIH) poses diagnostic challenges because autoantibodies are frequently absent or serum IgG levels may only be mildly elevated. Autoantibodies against the immune checkpoint molecule PD-1 have been detected in patients with chronic AIH (C-AIH). To clarify the clinical and pathological significance of anti-PD-1 autoantibodies, we examined their association with the clinical features of patients with liver diseases, including A-AIH, C-AIH, primary biliary cholangitis (PBC), and drug-induced liver injury (DILI).
METHODS: We compared the clinical characteristics and serum anti-PD-1 autoantibody titers of patients with A-AIH, C-AIH, PBC, and DILI (n = 72, 45, 41, and 19, respectively). Correlations between autoantibody titers and biochemical parameters were assessed to identify the factors that discriminate between the diseases. To reduce non-specific IgG response, anti-PD-1 autoantibody titers were normalized to the serum IgG levels. The liver histology was evaluated in a subset of patients with AIH.
RESULTS: A-AIH caused severe liver parenchymal and portal inflammation. The anti-PD-1/IgG ratio showed positive correlations with AST and ALT, but only weak correlations with ALP and γ-GTP. Anti-PD-1/IgG ratio was the highest in A-AIH, followed by DILI, C-AIH and PBC. Histological findings showed that anti-PD-1/IgG ratio was associated with severe inflammation, but not with centrilobular necrosis.
CONCLUSIONS: The serum anti-PD-1 autoantibody/IgG ratio was significantly elevated in A-AIH compared with that in C-AIH and PBC, and A-AIH was independently distinguished from C-AIH. These markers may assist with the assessment of acute-onset liver inflammation and clinical phenotyping of AIH.
METHODS: We compared the clinical characteristics and serum anti-PD-1 autoantibody titers of patients with A-AIH, C-AIH, PBC, and DILI (n = 72, 45, 41, and 19, respectively). Correlations between autoantibody titers and biochemical parameters were assessed to identify the factors that discriminate between the diseases. To reduce non-specific IgG response, anti-PD-1 autoantibody titers were normalized to the serum IgG levels. The liver histology was evaluated in a subset of patients with AIH.
RESULTS: A-AIH caused severe liver parenchymal and portal inflammation. The anti-PD-1/IgG ratio showed positive correlations with AST and ALT, but only weak correlations with ALP and γ-GTP. Anti-PD-1/IgG ratio was the highest in A-AIH, followed by DILI, C-AIH and PBC. Histological findings showed that anti-PD-1/IgG ratio was associated with severe inflammation, but not with centrilobular necrosis.
CONCLUSIONS: The serum anti-PD-1 autoantibody/IgG ratio was significantly elevated in A-AIH compared with that in C-AIH and PBC, and A-AIH was independently distinguished from C-AIH. These markers may assist with the assessment of acute-onset liver inflammation and clinical phenotyping of AIH.