I thought it was very interesting that Kerry brought up the adverse effects of NSAIDs on asthmatic people, so I did some research to see if a mechanism had been found.
I came across an article from the June 2007 edition of the journal Allergy (vol. 62). Wang, X.S. et al were able to culture mast cells (cells that are like basophil granulocytes and are involved in allergies) from peripheral blood progenitors into mature cells that resembled human lung mast cells. They cultured these cells from 3 groups of patients: normal/healthy patients, patients with aspirin tolerant asthma (ATA) and patients with aspirin exacerbated respiratory disease (AERD)--these are the ones at risk for increased bronchospasms due to NSAIDs.
Basically, the research group found that AERD patient mast cells are different from mast cells of the other 2 groups. AERD mast cells, when activated, can produce much more cysteinyl-leucotrienes (cys-LTs), which are chemical messengers involved in inflammation. cys-LTs help regulate the state of blood vessels and airways.
In addition, PGE2 decreases this overproduction of cys-LTs. So when AERD patients take NSAIDs and inhibit COX as well as PGE2 synthesis, this enables the increase in cys-LTs. More specifically, cys-LTs cause asthma attacks by allowing for bronchoconstriction, increased mucus secretion in the airway and infiltration of leukocytes in the airway. In fact, leucotriene receptor antagonists are used to treat asthma.
So...there you have it. =)
24 April 2008
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