ArticleJHEP reports : innovation in hepatology2022
Alpha-1 antitrypsin Pi∗Z allele is an independent risk factor for liver transplantation and death in patients with advanced chronic liver disease.
Article in JHEP reports : innovation in hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Genetic testing in liver diseases: Clinical applications.JHEP reports : innovation in hepatology · 2026Review
- Noninvasive Tests for Predicting Decompensation in Compensated Advanced Chronic Liver Disease: A Comprehensive Review.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- The Alpha-1 Pi*MZ Genotype Is an Independent Risk Factor for Hepatocellular Carcinoma Development in Patients With ACLD.Alimentary pharmacology & therapeutics · 2026Article
- Protein Aggregates in Heterozygous Alpha-1 Antitrypsin Phenotype Is a Marker for Progressive Disease.Gastro hep advances · 2026Article
- Rare liver diseases - Etiology, diagnosis and management: A review.Biomolecules & biomedicine · 2025Review
- Diagnosis and Monitoring Pathways Using Non-Invasive Tests in Patients With Alpha-1 Antitrypsin Deficiency-Associated Liver Disease: Results From an Expert Delphi Panel.United European gastroenterology journal · 2025Article
- Underdiagnosis of Alpha-1 Antitrypsin Deficiency in Cirrhotic Liver Transplant Candidates: Findings From a Multicenter Retrospective Study.Alimentary pharmacology & therapeutics · 2025Article
- SERPINA1 is a new frontier in cancer immunotherapy and drug targeting by pan-cancer analysis.Discover oncology · 2025Article
- Severe alpha-1 antitrypsin deficiency is associated with a higher risk of complications after first decompensation than other aetiologies of cirrhosis.JHEP reports : innovation in hepatology · 2025Article
- Alpha-1 antitrypsin deficiency-associated liver disease: From understudied disorder to the poster child of genetic medicine.Hepatology communications · 2025Review
- Diagnostic Uptake of Targeted Sequencing in Adults With Steatotic Liver Disease and a Suspected Genetic Contribution.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Future Perspectives in the Diagnosis and Treatment of Liver Disease Associated with Alpha-1 Antitrypsin Deficiency.GE Portuguese journal of gastroenterology · 2023Review
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17 authors.
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Abstract
Background & Aims: Alpha-1 antitrypsin (AAT) deficiency causes/predisposes individuals to advanced chronic liver disease (ACLD). However, the role of the Methods: A total of 1,118 patients with ACLD who underwent hepatic venous pressure gradient (HVPG) measurement and genotyping for the Pi∗Z/Pi∗S allele at the Vienna Hepatic Hemodynamic Lab were included in this retrospective analysis. The outcome of interest was liver transplantation/liver-related death, while non-liver-related death and removal/suppression of the primary etiological factor were considered as competing risks. Results: Viral hepatitis was the most common etiology (44%), followed by alcohol-related (31%) and non-alcoholic fatty liver disease (11%). Forty-two (4%) and forty-six (4%) patients harboured the Pi∗Z and Pi∗S variants, respectively. Pi∗Z carriers had more severe portal hypertension (HVPG: 19±6 Conclusion: Genotyping for the Pi∗Z allele identifies patients with ACLD at increased risk of adverse liver-related outcomes, thereby improving prognostication. Therapies targeting the accumulation of abnormal AAT should be evaluated as disease-modifying treatments in Pi∗Z allele carriers with ACLD. Lay summary: Alpha-1 antitrypsin deficiency is a genetic disease that affects the lung and the liver. Carrying two dysfunctional copies of the gene causes advanced liver disease. Harbouring one dysfunctional copy increases disease severity in patients with other liver illness. However, the significance of this genetic defect in patients who already suffer from advanced liver disease is unclear. Our study found that harbouring at least one dysfunctional copy of the alpha-1 antitrypsin gene increases the risk of requiring a liver transplantation or dying from a liver disease. This indicates the need for medical therapies aimed at treating the hepatic consequences of this genetic defect.
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