Abstract
An increase in asthma mortality in 1960s noted by British authors stirred a debate about the use of beta-adrenergic therapy that has persisted in the medical literature. The cause appears to be isoproterenol and fenoterol overuse. A second debate evolved around the possible deleterious, pro-inflammatory effects, of the albuterol distomer. Most clinical studies showed improved bronchodilatation, but limited benefits from using levalbuterol. Recently, genotyping has uncovered a single nucleotide polymorphism at codon 16 that appears to affect the long term response to both regular and as needed use of albuterol, calling for a new genotype based therapeutic approach in asthma.
Abbreviations | ||
β | = | beta |
FEV1 | = | the mean forced expiratory volume in 1 second |
hBSMC | = | human bronchial smooth muscle cells |
IBMX | = | isobutyl methylxanthine |
Ca2+ | = | Calcium ion |
GM-CSF | = | granulocyte-macrophage colony stimulating factor |
Arg16 | = | arginine16 |
NADPH | = | the reduced form of the nicotinamide adenine dinucleotide phosphate-oxidase |
NFκB | = | nuclear factor kappa B |
PEFR | = | peak expiratory flow rate |
Gly16 | = | glycine16 |
Gln27 | = | glutamine27 |
Glu27 | = | glutamic acid 27 |
Gs | = | stimulatory G protein |
Gi | = | inhibitory G protein |
SNP | = | single nucleotide polymorphism |
Abbreviations | ||
β | = | beta |
FEV1 | = | the mean forced expiratory volume in 1 second |
hBSMC | = | human bronchial smooth muscle cells |
IBMX | = | isobutyl methylxanthine |
Ca2+ | = | Calcium ion |
GM-CSF | = | granulocyte-macrophage colony stimulating factor |
Arg16 | = | arginine16 |
NADPH | = | the reduced form of the nicotinamide adenine dinucleotide phosphate-oxidase |
NFκB | = | nuclear factor kappa B |
PEFR | = | peak expiratory flow rate |
Gly16 | = | glycine16 |
Gln27 | = | glutamine27 |
Glu27 | = | glutamic acid 27 |
Gs | = | stimulatory G protein |
Gi | = | inhibitory G protein |
SNP | = | single nucleotide polymorphism |