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[Alpha 1-antiproteinase deficiency].

D Ritscher1, E W Russi

  • 1Abteilung Pneumologie, Universitätsspital Zürich.

Therapeutische Umschau. Revue Therapeutique
|April 28, 1999
PubMed
Summary
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Pulmonary emphysema may stem from an imbalance between neutrophil elastase and its inhibitor. Low alpha 1-antitrypsin levels in smokers with early emphysema support this elastase-antielastase hypothesis.

Area of Science:

  • Pulmonology
  • Biochemistry
  • Genetics

Context:

  • Pulmonary emphysema is a chronic lung disease.
  • The elastase-antielastase hypothesis proposes a key pathogenetic mechanism.
  • Smokers with premature emphysema exhibit low serum alpha 1-antitrypsin levels.

Purpose:

  • To provide an overview of pulmonary emphysema.
  • To discuss the elastase-antielastase hypothesis.
  • To explore the role of alpha 1-proteinase inhibitor.

Summary:

  • An imbalance between neutrophil elastase and its inhibitor is implicated in pulmonary emphysema.
  • Alpha 1-proteinase inhibitor, synthesized by the liver, circulates to the lungs to inactivate excess neutrophil elastase.
  • This overview covers the epidemiology, clinical aspects, genetics, and molecular biology of emphysema.

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Impact:

  • Understanding the elastase-antielastase mechanism is crucial for emphysema research.
  • Highlights the significance of alpha 1-proteinase inhibitor in preventing lung tissue destruction.
  • Provides a foundational understanding of emphysema's multifaceted origins.