Hepatology research : the official journal of the Japan Society of Hepatology · 2026
Anti-Integrin αvβ6 Autoantibodies as Diagnostic and Monitoring Biomarkers for Pediatric-Onset Primary Sclerosing Cholangitis.
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Maeda Yukako, Umetsu Shuichiro, Hiejima Eitaro, Suzuki Mitsuyoshi, Iwama Itaru, Kimura Takeshi, Kondo Sonoko, Inui Ayano, Kondou Hiroki, Okamoto Tatsuya, Ito Takashi, Shirahase Hiroyuki, Izawa Kazushi, Yasumi Takahiro, Kuwada Takeshi, Shiokawa Masahiro, Seno Hiroshi, Takita Junko
Аннотация
AIM: Pediatric primary sclerosing cholangitis (PSC) is a rare progressive cholestatic liver disease that often presents diagnostic challenges owing to overlapping clinical and histological features with autoimmune hepatitis (AIH). We hypothesized that anti-integrin αvβ6 autoantibodies may serve as a noninvasive biomarker to differentiate pediatric PSC from AIH and monitor disease activity.
METHODS: We retrospectively analyzed serum samples from 65 patients with pediatric-onset PSC, 39 with AIH, and 66 controls. Anti-integrin αvβ6 autoantibodies were quantified using enzyme-linked immunosorbent assay. Functional activity of the autoantibodies was assessed using a solid-phase fibronectin-binding inhibition assay.
RESULTS: Anti-integrin αvβ6 autoantibody levels were significantly higher in pediatric-onset PSC than in AIH and controls. The sensitivity and specificity for distinguishing PSC were 63.9% (95% confidence interval [CI]: 51.4-74.8) and 97.1% (95% CI: 91.9-99.2), respectively. Higher levels were observed in PSC with inflammatory bowel disease than without (p = 0.0069) and in PSC-AIH overlap compared with AIH alone (p = 0.0018). In one case, rising autoantibody levels preceded the clinical transition from AIH to PSC-AIH overlap. Levels declined during remission and after liver transplantation; however, increased again upon recurrence. Functional assays demonstrated that autoantibodies from patients with pediatric-onset PSC inhibited binding of integrin αvβ6 to fibronectin.
CONCLUSIONS: Anti-integrin αvβ6 autoantibodies may serve as a noninvasive clinically informative biomarker for distinguishing pediatric-onset PSC from AIH and reflecting longitudinal changes in disease activity, including posttransplant recurrence. These findings support their potential clinical utility in the diagnosis and longitudinal assessment of pediatric-onset PSC.
METHODS: We retrospectively analyzed serum samples from 65 patients with pediatric-onset PSC, 39 with AIH, and 66 controls. Anti-integrin αvβ6 autoantibodies were quantified using enzyme-linked immunosorbent assay. Functional activity of the autoantibodies was assessed using a solid-phase fibronectin-binding inhibition assay.
RESULTS: Anti-integrin αvβ6 autoantibody levels were significantly higher in pediatric-onset PSC than in AIH and controls. The sensitivity and specificity for distinguishing PSC were 63.9% (95% confidence interval [CI]: 51.4-74.8) and 97.1% (95% CI: 91.9-99.2), respectively. Higher levels were observed in PSC with inflammatory bowel disease than without (p = 0.0069) and in PSC-AIH overlap compared with AIH alone (p = 0.0018). In one case, rising autoantibody levels preceded the clinical transition from AIH to PSC-AIH overlap. Levels declined during remission and after liver transplantation; however, increased again upon recurrence. Functional assays demonstrated that autoantibodies from patients with pediatric-onset PSC inhibited binding of integrin αvβ6 to fibronectin.
CONCLUSIONS: Anti-integrin αvβ6 autoantibodies may serve as a noninvasive clinically informative biomarker for distinguishing pediatric-onset PSC from AIH and reflecting longitudinal changes in disease activity, including posttransplant recurrence. These findings support their potential clinical utility in the diagnosis and longitudinal assessment of pediatric-onset PSC.