Airway hypersecretion is mediated by increased release of inflammatory mediators and can be improved by inhibition of mediator production. We have recently reported that 1.8-cineol (
eucalyptol) which is known as the major
monoterpene of
eucalyptus oil suppressed
arachidonic acid metabolism and
cytokine production in human monocytes. Therefore, the aim of this study was to evaluate the anti-inflammatory efficacy of 1.8-cineol by determining its
prednisolone equivalent potency in patients with severe
asthma. Thirty-two patients with
steroid-dependent
bronchial asthma were enrolled in a double-blind, placebo-controlled trial. After determining the effective oral
steroid dosage during a 2 month run-in phase, subjects were randomly allocated to receive either 200 mg 1.8-cineol t. i.d. or placebo in small gut soluble capsules for 12 weeks. Oral glucocorticosteroids were reduced by 2.5 mg increments every 3 weeks. The primary end point of this investigation was to establish the oral glucocorticosteroid-sparing capacity of 1.8-cineol in severe
asthma. Reductions in daily
prednisolone dosage of 36% with active treatment (range 2.5-10 mg, mean: 3.75 mg) vs. a decrease of only 7% (2.5-5 mg, mean: 0.91 mg) in the placebo group (P = 0.006) were tolerated. Twelve of 16 cineol vs. four out of 16 placebo patients achieved a reduction of oral
steroids (P = 0.012). Long-term systemic
therapy with 1.8-cineol has asignificant
steroid-saving effect in
steroid-depending
asthma. This is the first evidence suggesting an anti-inflammatory activity of the
monoterpene 1.8-cineol in
asthma and a new rational for its use as
mucolytic agent in upper and lower airway diseases.