[Eicosanoid metabolism in peripheral blood cells in patients with cystic fibrosis]

The autosomal recessive inherited cystic fibrosis is the most common genetic disorder in white patients. Disturbances in the eicosanoid metabolism seem to play an important role in the pathogenesis of the disease. The present study shows examinations on the release of prostaglandin E2 (PGE2) and peptide leukotrienes (pLT) in peripheral blood cells.

In this respect heparinised blood samples of 10 cc were obtained from 25 patients with cystic fibrosis. The peripheral blood cells were separated from the remaining blood components. PGE2 and pLT were measured by a particularly developed sensitive enzyme immunoassay with specific monoclonal antibodies. Both the basal release of the metabolites and the concentrations after stimulation with arachidonic acid (AA) were explored. The control group consisted of 25 healthy individuals.

A distinct elevation in the basal release of pLT compared to the control group was noticed. Further stimulation with AA could only be achieved to a remarkably smaller extent. In contrast to these findings no elevation of the basal release of PGE2 and no stimulative effect of AA could be detected. In general we observed a distinct shift in the eicosanoid metabolism in favour of pLT and their proinflammatory effects.

The increased synthesis of pLT in patients with cystic fibrosis seems to play an important role in the pathogenesis of the disease. Future studies will have to proof, if we can achieve any improvement in the clinical courses in patients with cystic fibrosis using leukotriene receptor antagonists or 5-lipoxygenase inhibitors.