ArticleFrontiers in pediatrics2025
Circulating C-terminal peptides and polymers of alpha-1 antitrypsin as putative markers of pediatric Pi*ZZ liver disease.
Article in Frontiers in pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Circulating alpha-1 antitrypsin and its c-terminal peptides differentiate bacterial from viral community-acquired pneumonia.Journal of translational medicine · 2026Article
- Protein Fragments: From Biomarkers to Therapeutic Targets-A Focus on α1-Antitrypsin-Derived Peptides.Mediators of inflammation · 2026Review
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Authors and funding
10 authors.
Funding
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Abstract
Objective: Severe Pi*ZZ alpha-1 antitrypsin (AAT) deficiency, caused by the Glu342Lys mutation in the Methods: Plasma from 20 Pi*ZZ children was analyzed by liquid chromatography-tandem mass spectrometry for nine C-terminal AAT peptides and by western blot for AAT polymers. Associations with liver enzymes, ursodeoxycholic acid use, age, and clinical severity scores were evaluated. Results: Peptides C36, C37, and C42 were consistently detectable in plasma. C37 and C42 levels negatively correlated with age and positively with alanine aminotransferase; C42 additionally correlated with aspartate aminotransferase. Both C37 and C42 were reduced in children receiving ursodeoxycholic acid, whereas C36 showed no significant associations. Circulating AAT polymers correlated with Conclusion: Peptides C37 and C42 emerge as promising AAT-derived markers of hepatocellular status in stable Pi*ZZ children, while AAT polymers appear to reflect distinct features of cholestatic or hepatocellular stress. Together, these markers may support early risk stratification and therapeutic monitoring in pediatric AATD-related liver disease. Validation in larger, longitudinal cohorts is warranted to confirm their clinical utility.
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