ArticleChronic obstructive pulmonary diseases (Miami, Fla.)2023
Augmentation Therapy Modulates Systemic Inflammation in Individuals with Alpha-1 Antitrypsin Deficiency and Chronic Obstructive Pulmonary Disease.
Article in Chronic obstructive pulmonary diseases (Miami, Fla.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Alpha-1 antitrypsin deficiency and cardiovascular disease: a review.Respiratory research · 2026Review
- Neutrophil-derived extracellular vesicles in the plasma of alpha-1 antitrypsin deficient individuals reveal pro-inflammatory metabolic and transcriptomic signatures.Extracellular vesicle · 2025Article
- Pioglitazone reduces hepatic α-1 antitrypsin accumulation through autophagy and AMPK activation in α-1 antitrypsin-deficient mice.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- αERJ open research · 2025Article
- Liver Characterization of a Cohort of Alpha-1 Antitrypsin Deficiency Patients with and without Lung Disease.Journal of clinical and translational hepatology · 2024Article
- Immunological and homeostatic pathways of alpha -1 antitrypsin: a new therapeutic potential.Frontiers in immunology · 2024Review
- Advancing the understanding and treatment of lung pathologies associated with alpha 1 antitrypsin deficiency.Therapeutic advances in respiratory diseaseReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Background: Alpha-1 antitrypsin (AAT) deficiency is a genetic disorder that leads to chronic obstructive pulmonary disease (COPD) and lower circulating levels of AAT, which is a protease inhibitor with potent anti-inflammatory effects. In order to better understand the presence of systemic inflammation in AAT-deficient individuals with COPD, we investigatedthe plasma levels of C-reactive protein (CRP). Methods: AAT-deficient individuals and a matched cohort with a normal AAT genotype were recruited from the Alpha-1 Foundation DNA and Tissue Bank. AAT genotypes were determined by a combination of a Taqman-based assay. AAT and CRP levels were determined by nephelometry. Comparisons were determined by unpaired Results: Our study included 40 control participants and 742 AAT-deficient participants, of which 498 received augmentation therapy. In the AAT-deficient participants, the plasma AAT was 20.2±11.6µM and 4.5±1.3µM ( Conclusion: Compared to healthy individuals, AAT-deficient individuals with COPD have higher levels of circulating CRP, suggesting increased systemic inflammation. However, AAT-deficient individuals receiving augmentation therapy had lower plasma CRP levels compared to those who are not.
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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 OpenQuestion graph.