Histamine--a major role in allergy?
Since its discovery in 1911, histamine has been recognized as a major mediator in allergic reactions and diseases, and today antihistamines remain important agents in the treatment of these conditions. In addition to its known effects on glands, vessels and sensory nerves, recent data have provided further evidence of histamine's proinflammatory actions, which appear to be mediated mainly by H1 receptors. Thus, findings indicate that histamine is a crucial mediator in both the early and late-phase reactions of an allergic response, playing important roles in cytokine release and in the adhesion process. Histamine has been shown to increase the adhesion of leucocytes to the endothelium and to stimulate production of IL-6 and IL-8 by endothelial cells. It also increases TNF alpha-induced IL-6 production and expression of adhesion molecules. These effects can be inhibited by H1 receptor antagonists. First-generation antihistamines, though moderately effective, showed poor selectivity and caused sedation, due to their penetration of the blood-brain barrier, and other troublesome side-effects. Second-generation antihistamines such as ebastine have increased potency due to greater selectivity for histamine receptors, and improved tolerability due to lack of penetration of the blood brain barrier. Recent studies have shown ebastine 10 mg daily to be effective, safe and well tolerated in the treatment of seasonal allergic rhinitis (SAR), with a rapid onset of action, symptom relief comparable to that seen with topical azelastine or oral loratadine 10 mg o.d., cetirizine 10 mg o.d. or terfenadine 60 mg b.i.d., and no significant side-effects. Ebastine therefore offers a new option in the treatment of seasonal allergic rhinitis.
Bachert
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University Hospital, Ghent, Belgium.
D002448:Cell Adhesion / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D006632:Histamine / Q000276:immunology*; D006634:Histamine H1 Antagonists / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D006967:Hypersensitivity / Q000188:drug therapy / Q000276:immunology*; D007378:Interleukins / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D009297:Nasal Mucosa / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology