IT IS A LONG ACTING, NON SEDATING SECOND GENERATION ANTIHISTAMINE. H2 RECEPTOR ANTAGONIST THAT BINDS PREFERENTIALLY TO PERIPHERAL H-1 RECEPTOR IN VIVO. IT HAS ANTIHISTAMINIC & ANTIALLERGIC ACTIVITY & PROTECTS ASTHMA PTIENTS AGAINST HISTAMINE INDUCED BRONCHOCONSTRICTION.
clinically it is used in alopecia areata & all kinds of allergic conditions including asthma.
Although its etiology is not entirely clear, the infiltration of inflammatory cells is increased around hair follicles in lesions of alopecia areata (AA), and the type of immune cells that are increased are mast cells. Such evidence suggests that mast cells play some role in the pathogenesis of AA. Objective: The aim of this study was to evaluate the efficacy of a second-generation antihistamine in the treatment of AA. Methods: Two studies were performed. In study I, 9 patients with moderate AA were treated with diazepam for 3 months and patients who did not respond to the diazepam therapy were then treated with ebastine, a second-generation antihistamine, instead of diazepam. In study II, 22 patients with moderate AA were initially treated with ebastine for at least 3 months. The efficacy of these medications was checked after 3 months of the therapy. If any benefit effects were noted at that time, the therapy was continued until 5 months and the final efficacy was evaluated. Results: In study I, of the 9 patients, only one (11%) showed an excellent response to diazepam. Of the remaining 8 patients, 5 (62%) showed an excellent response to the subsequent ebastine therapy. In study II, 13 out of the 22 patients (59%) showed an excellent response. Together, 18 out of 30 patients (60%) were excellent responders to ebastine therapy, excluding the patient who responded to diazepam. Ebastine therapy also showed a tendency to be more effective in patients with emotional stress than in those without stress. There were no statistical differences in eosinophil counts, in serum IgE levels, and in serum interleukin 4 levels between excellent or poor responders to ebastine. Serum IgE levels were, however, significantly decreased after ebastine therapy in the excellent responders, while the poor responders had no change in IgE levels. Conclusion: We propose that the administration of a second-generation antihistamine is an efficient therapy for moderate AA however, the results obtained here should be interpreted with caution, as is the case for most open studies
ebastine
Barcelona -- Ebastine, a second-generation antihistamine currently marketed in Europe and Japan, offers many advantages as a treatment for mild to moderate alopecia areata, according to Yusuke Yoshizawa, M.D., assistant professor of dermatology, Nippon Medical School, Tokyo.
Alopecia areata is a T-cell mediated autoimmune disorder targeting the hair follicles. "The pathogenesis of alopecia areata is still unclear," Dr. Yoshizawa said, "but expression of certain cell surface molecules on the hair follicle cells and the presence of peribulbar lymphocytic infiltrates are consistent and reproducible immunological abnormalities seen in alopecia areata."
Key players responsible for hair loss in alopecia areata appear to be interferon-gamma, IL-1, and substance P, among others.
T cells produce interferon-gamma, which induces expression of a variety of cell surface molecules such as MHC receptors, HLA-DR, and ICAM-1 on hair follicular keratinocytes and dermal papilla cells.
"IL-1 is thought to be the crucial inducer of hair loss in alopecia areata," Dr. Yoshizawa said at the 10th European Hair Research Society meeting. "IL-1b mRNA can be detected in skin lesions of alopecia areata. IL-1b has been shown to inhibit hair growth in vitro and stimulate ICAM-1 expression in endothelial cells."
Substance P may be responsible for stimulating expression of the IL-1 family in keratinocytes. The anti-inflammatory effects of second-generation antihistamines such as ebastine include inhibition of T cell activation, inhibition of expression of various cell surface molecules stimulated by interferon-gamma, and inhibition of histamine-induced expression of substance P.
Immunosuppressive and immunomodulatory agents have traditionally been used for treatment of alopecia areata, although often with limited success. Corticosteroid therapy is associated with potentially serious side effects and is no longer widely used. Diphenylcyclopropenone (DCPC) and squaric acid dibutylester (SADBE) solutions are used in Europe and Canada. However, local immunotherapy is more complicated for an inexperienced dermatologist to administer, and application of DCPC or SADBE solution to alopecia lesions causes contact dermatitis, resulting in itching and discomfort for the patient. By contrast, ebastine is an oral medication, and is generally well tolerated, with slight sedation as the most common side effect.
Dr. Yoshizawa described two clinical trials evaluating ebastine for treatment of alopecia areata. The first study looked at ebastine as a second-line treatment for patients who had failed diazepam. Nine patients with alopecia areata were initially treated with diazepam, and one patient responded favorably. The remaining eight patients were treated with ebastine for several months. After four to eight months, six patients showed improvement, with three patients considered cured.
In a second study, 29 patients with alopecia areata were treated initially with ebastine. Patients with mild or moderate alopecia areata had a response rate of 75 percent or 46 percent, respectively. Only one of two patients with severe alopecia areata and only one of six patients with alopecia totalis or alopecia universalis responded to ebastine treatment.
Dosage - 10 MG AS SINGLE DAILY DOSE , PREFERABLY IN MORNING.
CHILDREN - 5 MG DAILY