Study of the gastric mucosal reactivity in patients with urticaria induced by nonsteroidal anti-inflammatory drugs.

Skin prick test, intradermal test, specific IgE by ELISA and immunological blood parameters were tested in 9 patients suffering from nonsteroidal anti-inflammatory drug (NSAID)-induced reactions, i.e. Noramydopyrine (NOR), ASA and Diclofenac (DIC). All were challenged by NSAIDs in gastric antrumthrough endoscope, where biopsies were taken before and after challenge. Lysine acetylsalicylate (LA) was employed instead of the undissolvable ASA. No skin reactions nor specific IgE to NSAIDs were found. Before challenge, a hypereosinophilia (1018+/-280/ml) and an elevated serum eosinophilic cationic protein (ECP) (29,75+/-13 mg/l) was detected in all patients. After challenge, in NOR and DIC sensitive patients a non significant blood eosinophil decrease was observed, whereas, a significant increase in ECP was detected (p<0,03). On the other hand, no changes in ECP was found in the ASA sensitive patients. Histological study showed no changes in the amount of mast cells in biopsies performed after challenge, versus those performed before. Instead, after challenge impressive edema and vasodilation were observed in all biopsies; there was also evidence of early eosinophilic infiltration in the 7 noramydopyrine and diclofenac sensitive patients. The absence of eosinophilic infiltration and changes in serum ECP in the ASA sensitive patients is likely due to the use of LA instead of ASA for the challenge. No changes, except for a minimal edema, were observed in biopsies performed after challenge in the non-NSAID sensitive subjects. The study emphasizes the role of eosinophils in the pathogenesis of NSAID induced reactions and shows ECP as a sensitive marker of eosinophilic activation.