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Novel pharmacotherapy of acute hereditary angioedema with bradykinin B2‐receptor antagonist icatibant

healthy men. Decreased DHEA-S concentration has been recognized in different chronic diseases (2). In particular, it has been suggested that DHEA-S deficiency is a permanent feature of some autoimmune diseases and may contribute to their aetiology and/or pathophysiolgy (4, 5). However, no direct evidence is available to indicate whether reduced circulating concentration of the hormone contributes to the diseases (2, 5). We do not know whether lower serum concentration of DHEA-S observed in CIU patients is the cause or rather the effect of urticarial processes. It has been suggested that, during inflammatory response, the adrenal steroid production is changed in the direction of cortisol, relative to DHEA and DHEA-S, such hormonal changes being probably necessary to achieve adequate cortisol levels at the expense of adrenal androgens (6). It is interesting to speculate that similar abnormalities in steroidogenesis might occur during chronic urticarial inflammation. How does lower circulating DHEA-S actually contribute to CIU pathophysiolgy? The question proves both, difficult and complex as the specific molecular mechanism of action for DHEA-S, including mechanisms of DHEA-S effect upon the immunological function and inflammation, is unclear (2). In conclusion, on the basis of the present study as well as our earlier investigations, it appears probable that circulating DHEA-S concentration may be lower in CIU patients, regardless of their gender. It seems that declining circulating concentration of DHEA-S is a phenomenon accompanying CIU, yet its significance and underlying mechanisms remain unknown. As adrenal androgens have been reported to exert immunoregulatory effects, it is interesting to speculate on DHEA-S deficiency role in urticarial inflammation irrespective of its primary or just secondary character.