Treatment of asthma with lipid extract of New Zealand green-lipped mussel: a randomised clinical trial.

Asthma is a chronic inflammatory disease of the airways mediated, at least in part, by leukotrienes and other lipid mediators. Experimental studies have shown that lipid extract of New Zealand green-lipped mussel, Perna canaliculus, is effective in inhibiting 5'-lipoxygenase and cyclo-oxygenase pathways responsible for production of eicosanoids, including leukotrienes and prostaglandins. The aim of this study was to assess its effect on symptoms, peak expiratory flow (PEF) and hydrogen peroxide (H2O2) in expired breath condensate as a marker of airway inflammation in patients with steroid-naïve atopic asthma in a double-blind randomised, placebo-controlled clinical trial. Forty six patients with atopic asthma received two capsules of lipid extract (Lyprinol) or placebo b.i.d for 8 weeks. Each capsule of lipid extract contained 50 mg omega-3 polyunsaturated fatty acids and 100 mg olive oil, whereas placebo capsules contained only 150 mg olive oil. There was a significant decrease in daytime wheeze, the concentration of exhaled H2O2 and an increase in morning PEF in the lipid extract group compared to the placebo group. There were no significant side-effects. The authors conclude that lipid extract of New Zealand green-lipped mussel may have some beneficial effect in patients with atopic asthma.

Elevated concentrations of exhaled hydrogen peroxide in asthmatic patients.

BACKGROUND: Airway inflammation is important in the development and progression of asthma. Activation of inflammatory cells induces a respiratory burst resulting in the production of reactive oxygen species, such as H(2)O(2). The aim of this study was to measure the concentration of H(2)O(2) in exhaled breath condensate and its correlation with airway obstruction, airway hyperresponsiveness, and concentration of eosinophil cationic protein (ECP) in serum in 70 steroid-naive, atopic patients with unstable asthma (20 men; age range, 18 to 62 years) and 17 normal subjects (7 men; age range, 19 to 34 years). METHODS: Exhaled H(2)O(2) was measured using a colorimetric assay, and the concentration of ECP in serum was measured using radioimmunoassay. Airway hyperresponsiveness was expressed as the provocative concentration of inhaled histamine causing a 20% fall in FEV(1) (PC(20)). RESULTS: In patients with asthma, the mean H(2)O(2) concentration was significantly elevated compared to values in normal subjects: 0.127 +/- 0.083 mol/L vs 0.024 +/- 0.016 mol/L (p < 0.001). There was a significant correlation among H(2)O(2) concentration, FEV(1), PC(20), and ECP in serum. CONCLUSION: We conclude that exhaled H(2)O(2) is significantly elevated in asthmatic patients. This is correlated with disease severity and indirect markers of airway inflammation. Measurement of exhaled H(2)O(2) may be useful to assess airway inflammation and oxidative stress in asthmatic patients.