SynthesisEuropean respiratory review : an official journal of the European Respiratory Society2025
Alpha-1 antitrypsin deficiency and granulomatosis with polyangiitis: a systematic review and meta-analysis.
Synthesis in European respiratory review : an official journal of the European Respiratory Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Case Report: Serum Protein Electrophoresis Incidentally Reveals Alpha-1 Antitrypsin Deficiency in p-ANCA-Positive Crescentic Glomerulonephritis.International journal of rheumatic diseases · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAlpha-1 antitrypsin deficiency (AATD) is a genetic disorder characterised by low circulating levels of alpha-1 antitrypsin (AAT) protein, a key inhibitor of neutrophil elastase and proteinase 3 (PR3) which is also the main autoantigen in granulomatosis with polyangiitis (GPA). This systematic review examines the association between AATD and GPA.
methodsA systematic search of PubMed, Embase, Cochrane, EBSCO Medline and Scopus (December 2024) identified studies on AATD and GPA. Data extraction and quality assessment followed PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A random-effects meta-analysis was conducted to calculate pooled odds ratios and assess heterogeneity.
results23 studies (9634 individuals) met inclusion criteria. The Z-allele prevalence was 11.65% in GPA compared to 3.29% in controls and the S-allele prevalence was 10.8% in GPA compared to 5.26% in controls. Among 1755 individuals with GPA across 10 studies that provided specific genotype data, 22 (1.25%) were homozygous for the Z-allele. Meta-analysis showed that Z-allele carriers had 3.11 times higher odds of developing GPA (eight studies; 95% CI 2.43-3.9; I
conclusionThis meta-analysis reinforces the link between AATD and GPA, particularly in carriers of the Z-allele, supporting the role of PR3 dysregulation in GPA pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.