Key result
Alpha-1 antitrypsin-deficient individuals receiving augmentation therapy had significantly lower plasma C-reactive protein levels (0.32 mg/dL) compared to those not receiving therapy (0.69 mg/dL).
Why the study?
Does augmentation therapy reduce plasma levels of C-reactive protein in individuals with Alpha-1 antitrypsin deficiency and COPD?
Observational (n=782)
Yes
Does augmentation therapy reduce plasma levels of C-reactive protein in individuals with Alpha-1 antitrypsin deficiency and COPD?
Augmentation therapy is associated with lower systemic inflammation, as measured by CRP levels, in individuals with Alpha-1 antitrypsin deficiency and COPD.
Answers are grounded in this paper and cite their sources.
May indicate systemic inflammation in AAT-deficient COPD; leaves open prognostic value and need for prospective validation.
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). 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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Lascano et al. (2023) conducted an observational in Alpha-1 Antitrypsin Deficiency and Chronic Obstructive Pulmonary Disease (n=782). Alpha-1 antitrypsin augmentation therapy vs. No augmentation therapy was evaluated on Plasma C-reactive protein (CRP) levels (p=0.0169). Alpha-1 antitrypsin-deficient individuals receiving augmentation therapy had significantly lower plasma C-reactive protein levels (0.32 mg/dL) compared to those not receiving therapy (0.69 mg/dL).
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