Open AccessMetabolism of Salbutamol Differs between Asthmatic Patients and Healthy Volunteers
Author(s) -
Sjöswärd Kerstin Naidu,
Josefsson Martin,
Ahlner Johan,
Andersson Rolf G.G.,
Schmekel Birgitta
Publication year - 2003
Publication title -
pharmacology & toxicology
Language(s) - English
Resource type - Journals
eISSN - 1600-0773
pISSN - 0901-9928
DOI - 10.1034/j.1600-0773.2003.920105.x
Subject(s) - salbutamol , asthma , medicine , ingestion , bronchodilator , cmax , cortisone , corticosteroid , pharmacology , endocrinology , pharmacokinetics
Patients with asthma are a target group for medication with β2‐agonists, often in combination with corticosteroids. Salbutamol is commonly marketed as racemate. R‐Salbutamol carries β2‐agonistic property whereas S‐salbutamol does not. The racemate undergoes stereoselective sulphatisation by sulfotransferases mainly in the gut and liver, so that S‐salbutamol rests for a longer time in the body and reaches higher plasma levels than R‐salbutamol. Ten patients with mild stable asthma and at present without cortisone medication were given racemic salbutamol as ventoline 4 mg orally. Plasma and urine levels were estimated until 24 hr after ingestion. For comparison healthy volunteers were treated in the same way.The group of asthma patients was then treated with budesonide inhalations 800 μg daily for one week and the initial programme resumed. Non‐cortisone‐treated asthmatic patients displayed higher levels of both R‐ and S‐salbutamol in plasma than did healthy volunteers after one single ingestion of racemic salbutamol (CMAX both comparisons P<0.05). Plasma levels of salbutamol isomers in cortisone‐treated asthmatic patients resembled the levels in volunteers. The most plausible explanation for the discrepancy in values between asthmatic patients and volunteers is a defective metabolic function by asthmatic patients possibly enzymatic in origin.