Cystic fibrosis, breath pentane, and lipid peroxidation.

SIR,-Dr Weitz and colleagues (April 20, p 933) report the value of breath pentane analysis as an index of increased lipid peroxidation in vivo. However, Weitz et al fail to indicate the potential shortcomings of the method, as we are beginning to see in the context of cystic fibrosis. We have found that techniques involving hydrocarboncontaminated inspired air, as used by Weitz et al, produce unreliably high results for breath pentane analysis. Increased quantities of breath pentane do not provide a specific marker of increased lipid peroxidation since they may accompany infection of the small intestine by colonic bacteria. Reassessment after one week of neomycin helps to assess the contribution of this possible artefact in our patients.1 In addition, isolated measurement of breath pentane does not give a global view of free-radical oxidation of lipids in vivo because pentane is only one of several end-products in the lipid peroxidation pathway, and this method takes no account of the alternative lipid isomerisation pathway.2 For these reasons some suggest that a panel of free-radical markers should be adopted, including those that reflect free-radical damage to non-lipid constituents of blood and tissues. With this approach we have found evidence for oxidative stress in patients with cystic fibrosis: increased quantities of the lipid isomerisation marker 9-ds, 11-trans linoleic acid (9,11 LA) are present in relation to concentrations of the natural fatty acid (9,12 LA) in both nasal epithelia and sera and there is a reduced ratio of bioactive ascorbic acid to total vitamin C in