Kimura's disease associated with bronchial asthma presenting eosinophilia and hyperimmunoglobulinemia E which were attenuated by suplatast tosilate (IPD-1151T)

A 29-year-old man developed atopic bronchial asthma in association with eos inophilia and hyperimmunoglobulinemia E (hyper-IgE). A biopsy specimen from an inguinal lymph node showed changes consistent with Kimura's disease. IP D-1151T (suplatast tosilate), an anti-allergy drug, attenuated eosinophilia and hyper-IgE as well as the serum level of eosinophil cationic protein (E CP). The drug, how ever, did not affect the positivity for specific IgE ant ibodies against common allergens or the bronchial hyperresponsiveness to ac etylcholine, Interleukin (IL)-2, IL-4, IL-5, interferon (IFN)-gamma, and tu mor necrosis factor (TNF)-alpha were measured to be undetectable in serum b efore or during therapy. However, the expressions of mRNAs for IL-2, IL-4, IL-5, IFN-gamma and TNF-alpha in peripheral blood T-lymphocytes and the exp ression of IL-5 mRNA in peripheral blood eosinophils were detected before a nd during therapy, which were unchanged by therapy with IPD-1151T. The pres ent results suggest that different mechanisms other than the predominance o f type 2 helper (T-H2)-like T-lymphocytes may underlie Kimura's disease and atopic bronchial asthma regarding the findings of eosinophilia and hyper-I gE, which could he modulated by IPD-1151T.