Changes in malondialdehyde levels in bronchoalveolar fluid and serum by the treatment of asthma with inhaled steroid and beta2-agonist.
OBJECTIVE
Oxidative stress plays an important role in the pathogenesis of asthma. Recent data suggest that clinical indices of the patients with asthma may not correlate with the underlying inflammatory process. We aimed to measure the level of malondialdehyde (MDA), which is a marker of lipid peroxidation, a free radical-mediated process, before and after a well-accepted treatment of asthma.


METHODS
Nine non-smoking females and five non-smoking males with mild-moderate asthma were included. Twenty-four age- and sex-matched, non-smoking healthy people (17 females and seven males, mean age 32.1 years, range 20-59) were included for control. After initial evaluation, spirometry, bronchoscopy with bronchoalveolar lavage (BAL), and blood sample were maintained. The patients were treated with twice-daily salmeterol inhaler (100 microg/d) and fluticasone propionate inhaler (500 microg/d). One month later the investigations were repeated. Serum MDA levels before treatment were compared with both the levels after treatment and levels of controls. Malondialdehyde levels of BAL were compared before and after treatment.


RESULTS
Serum MDA level of the patient before treatment was 6.7+/-0.8 nmol/mL, significantly higher than that of healthy controls; 3.8+/-0.4, P < 0.001. One month after the treatment, serum MDA level decreased to 5.3+/-0.7 nmol/mL (P < 0.001). However, this level is still significantly higher than healthy controls (P < 0.0001). Forced expiratory volume in 1 s level of the patients increased from 2.43+/-0.79 L to 3.50+/-1.21 L after the treatment (P < 0.001).


CONCLUSIONS
Although treatment with beta2-agonist and corticosteroid inhalers for the duration of 1 month reduced lipid peroxidation significantly, it was still at a level significantly higher than healthy controls. The treatment may need a longer duration to improve lipid peroxidation or an alternative regimen which is more effective in controlling inflammation may be warranted.
Ozaras
R
R
Internal Medicine, Istanbul University, Turkey. rozaras@yahoo.com
Tahan
V
V
Turkmen
S
S
Talay
F
F
Besirli
K
K
Aydin
S
S
Uzun
H
H
Cetinkaya
A
A
D000318:Adrenergic beta-Agonists / Q000627:therapeutic use*; D000328:Adult; D000420:Albuterol / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000730:Androstadienes / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry*; D001993:Bronchodilator Agents / Q000627:therapeutic use*; D005260:Female; D000068298:Fluticasone; D005541:Forced Expiratory Volume; D006801:Humans; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism*; D008875:Middle Aged; D000068299:Salmeterol Xinafoate
D000318:Adrenergic beta-Agonists; D000730:Androstadienes; D000893:Anti-Inflammatory Agents; D001993:Bronchodilator Agents; D008315:Malondialdehyde; D000068299:Salmeterol Xinafoate; D000068298:Fluticasone; D000420:Albuterol