One explanation of the asthma paradox: inhibition of natural anti-inflammatory mechanism by beta 2-agonists

Lancet. 1991 Mar 23;337(8743):717-20. doi: 10.1016/0140-6736(91)90289-2.

Abstract

Our understanding of the mechanisms contributing to the pathogenesis of bronchial asthma has increased substantially over the past decade. This has been accompanied by the introduction of a range of new drugs for the treatment of this disorder, and the usage of anti-asthma drugs is increasing. Despite these changes and an increased awareness of the disease, asthma remains the only "preventable" disease where the morbidity and mortality are still increasing in most parts of the world. This "asthma paradox" requires explanation, and this article is an attempt to provide a plausible scientific one. The hypothesis expresses concern that a long recognised, but little publicised, pharmacological property of the drug class most widely prescribed for the treatment of asthma, the beta 2-adrenoceptor agonists--namely, the inhibition of mast-cell degranulation--may be contributing to the world wide increase in morbidity and mortality from asthma via the inhibition of a natural anti-inflammatory mechanism.

MeSH terms

  • Adrenergic beta-Agonists / adverse effects*
  • Adrenergic beta-Agonists / pharmacology
  • Anti-Inflammatory Agents / adverse effects*
  • Anti-Inflammatory Agents / pharmacology
  • Asthma / drug therapy*
  • Asthma / pathology
  • Bronchitis / chemically induced*
  • Bronchitis / pathology
  • Cromolyn Sodium / pharmacology
  • Heparin / metabolism
  • Heparin / physiology
  • Histamine Release / physiology
  • Humans
  • Plasma Cells / drug effects
  • Plasma Cells / metabolism

Substances

  • Adrenergic beta-Agonists
  • Anti-Inflammatory Agents
  • Heparin
  • Cromolyn Sodium