Quantitative disease progression model of α-1 proteinase inhibitor therapy on computed tomography lung density in patients with α-1 antitrypsin deficiency

Br J Clin Pharmacol. 2017 Nov;83(11):2386-2397. doi: 10.1111/bcp.13358. Epub 2017 Aug 11.

Abstract

Aims: Early-onset emphysema attributed to α-1 antitrypsin deficiency (AATD) is frequently overlooked and undertreated. RAPID-RCT/RAPID-OLE, the largest clinical trials of purified human α-1 proteinase inhibitor (A1 -PI; 60 mg kg-1 week-1 ) therapy completed to date, demonstrated for the first time that A1 -PI is clinically effective in slowing lung tissue loss in AATD. A posthoc pharmacometric analysis was undertaken to further explore dose, exposure and response.

Methods: A disease progression model was constructed, utilizing observed A1 -PI exposure and lung density decline rates (measured by computed tomography) from RAPID-RCT/RAPID-OLE, to predict effects of population variability and higher doses on A1 -PI exposure and clinical response. Dose-exposure and exposure-response relationships were characterized using nonlinear and linear mixed effects models, respectively. The dose-exposure model predicts summary exposures and not individual concentration kinetics; covariates included baseline serum A1 -PI, forced expiratory volume in 1 s and body weight. The exposure-response model relates A1 -PI exposure to lung density decline rate at varying exposure levels.

Results: A dose of 60 mg kg-1 week-1 achieved trough serum levels >11 μmol l-1 (putative 'protective threshold') in ≥98% patients. Dose-exposure-response simulations revealed increasing separation between A1 -PI and placebo in the proportions of patients achieving higher reductions in lung density decline rate; improvements in decline rates ≥0.5 g l-1 year-1 occurred more often in patients receiving A1 -PI: 63 vs. 12%.

Conclusion: Weight-based A1 -PI dosing reliably raises serum levels above the 11 μmol l-1 threshold. However, our exposure-response simulations question whether this is the maximal, clinically effective threshold for A1 -PI therapy in AATD. The model suggested higher doses of A1 -PI would yield greater clinical effects.

Keywords: chronic obstructive pulmonary disease; imaging; modelling and simulation.

MeSH terms

  • Disease Progression
  • Dose-Response Relationship, Drug
  • Female
  • Forced Expiratory Volume / drug effects
  • Humans
  • Lung / diagnostic imaging
  • Lung / drug effects*
  • Male
  • Middle Aged
  • Models, Biological*
  • Pulmonary Emphysema / diagnostic imaging
  • Pulmonary Emphysema / drug therapy*
  • Pulmonary Emphysema / etiology
  • Randomized Controlled Trials as Topic
  • Rare Diseases / complications
  • Rare Diseases / diagnostic imaging
  • Rare Diseases / drug therapy
  • Tomography, X-Ray Computed
  • Treatment Outcome
  • Trypsin Inhibitors / pharmacology*
  • Trypsin Inhibitors / therapeutic use
  • alpha 1-Antitrypsin / pharmacology
  • alpha 1-Antitrypsin / therapeutic use
  • alpha 1-Antitrypsin Deficiency / complications
  • alpha 1-Antitrypsin Deficiency / diagnostic imaging
  • alpha 1-Antitrypsin Deficiency / drug therapy*

Substances

  • Trypsin Inhibitors
  • alpha 1-Antitrypsin

Supplementary concepts

  • alpha-1-Antitrypsin Deficiency, Autosomal Recessive