The first phase of aspirin hypersensitivity is usually a chronic rhinitis. The study attempted to detect aspirin hypersensitivity in patients with allergic rhinitis (AR) or non-allergic rhinitis with eosinophilia syndrome (NARES), without hypersensitive symptoms following an aspirin intake as based upon patient's history. Respective clinical and biochemical features of different types of rhinitis such as aspirin-induced, allergic or NARES were compared. The same evaluations were performed in AIAR patients showing different reactions to the oral aspirin challenge. One hundred patients took part in the study: thirty with AJAR, thirty with AR and thirty with NARES and ten healthy volunteers. Placebo-controlled aspirin oral challenges were conducted. Urinary leukotriene (LT) E4, serum and urinary 9α,11β-prostaglandin (PG) F2 (a PGD2 stable metabolite) and plasma tryptase levels were determined at the baseline and following placebo or aspirin. All patients with AIAR had positive oral aspirin challenge. In nineteen patients the aspirin challenge induced both bronchial and nasal response, whereas in eleven patients it provoked the nasal response only. The significant increase of mean urinary LTE4 level was observed only in the first group of patients. These patients were distinguished by more severe manifestations of bronchial asthma and sinusitis and more elevated mean urinary LTE4 l ; evels. In five out of thirty patients with AR alternations of eicosanoid metabolism following aspirin challenge were observed coexisting with clinical responses in two patients. All these patients suffered from persistent, severe rhinitis. In all patients with NARES and in healthy subjects aspirin challenges were negative. The patients with NARES differed from AR (-) patients in respect to more severe clinical course of their rhinitis and higher mean 9α,11β-PGF2 levels in plasma at the baseline.