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Augmentation therapy for alpha1 antitrypsin deficiency: a meta-analysis.
Kenneth R Chapman1, Robert A Stockley, Clara Dawkins
1Asthma & Airway Centre, University Health Network, Toronto Western Hospital, Toronto, Ontario, Canada. kchapman@ca.inter.net
COPD
|October 9, 2009
Summary
Augmentation therapy for alpha1-antitrypsin (alpha1-AT) deficiency slows lung function decline, particularly in patients with moderate obstruction. This finding supports alpha1-AT augmentation as a beneficial treatment for slowing FEV1 decline.
Area of Science:
- Pulmonary Medicine
- Genetics and Inherited Diseases
- Pharmacology and Therapeutics
Background:
- Alpha1-antitrypsin (alpha1-AT) deficiency is a genetic disorder.
- Exogenous alpha1-AT augmentation is the sole specific therapy.
- Its clinical effectiveness in slowing disease progression remains under investigation.
Purpose of the Study:
- To evaluate the efficacy of augmentation therapy in slowing the rate of FEV1 decline.
- To test the hypothesis that augmentation therapy benefits patients with alpha1-AT deficiency.
Main Methods:
- Systematic review and meta-analysis of randomized and nonrandomized clinical studies.
- Inclusion criteria: comparison of augmentation vs. control, longitudinal FEV1 data (>1 year).
- Data synthesis using random-effects meta-analysis.
Main Results:
- Combined data from five trials involving 1509 patients.
- Augmentation therapy showed a 23% slower FEV1 decline (13.4 ml/year) across all patients.
- A significant protective effect was observed in patients with moderate obstruction (FEV1 30-65% predicted), with a 26% slower decline (17.9 ml/year).
Conclusions:
- Meta-analysis provides evidence that augmentation therapy can slow lung function decline in alpha1-AT deficiency.
- Patients with moderate airflow obstruction are identified as the primary beneficiaries of this therapy.
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