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Azelastine, an orally effective antiasthmatic agent, has been reported to inhibit antihistamine-resistant, leukotriene-mediated allergic bronchoconstriction in guinea pigs. This suggests that azelastine might act through inhibition of leukotriene (LT) C4/D4 synthesis. We have examined the effect of azelastine on allergic and nonallergic histamine secretion and LTC4 formation. Azelastine and the known 5-lipoxygenase inhibitors, nordihydroguaiaretic acid and AA-861, exerted concentration-dependent inhibition of allergic LTC4 formation in chopped lung tissue from actively sensitized guinea pigs and calcium ionophore A23187-stimulated LTC4 synthesis in mixed peritoneal cells from rats. Azelastine also produced concentration-dependent inhibition of allergic and nonallergic histamine secretion from rat peritoneal mast cells. The ability of azelastine to inhibit allergic and nonallergic histamine secretion and LTC4 generation may contribute to its mode of action and its therapeutic efficacy.
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The effects of azelastine hydrochloride on cell proliferation and collagen synthesis in cultured human skin fibroblasts were studied. Azelastine inhibited cell proliferation during proliferating cell phases. Azelastine was found to inhibit collagen synthesis without altering cell proliferation during quiescent phases. It did not alter the ratio of type I to III collagen synthesis. Northern blot analysis of collagen chain mRNAs revealed that the levels of alpha1 (I), alpha1 (III) and alpha1 (VI) mRNAs were reduced by azelastine treatment, whereas the level of alpha2 (VI), alpha3 (VI) mRNAs were not significantly changed. These results suggest that azelastine modulates collagen synthesis at a pretranslational level. Azelastine inhibited collagen synthesis in fibroblasts from scleroderma patients to the same extent as in normal skin fibroblasts. This drug may be useful in the treatment of fibrotic diseases.
To our knowledge, there are no published studies that evaluated the efficacy of azelastine hydrochloride nasal spray in combination with an intranasal corticosteroid, although anecdotal reports of the use of these agents in combination are common.
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Ginsenoside Re was orally administered to the mice treated with antibiotics (cefadroxil, oxytetracycline and erythromycin mixture (COE), streptomycin or/and tetracycline) and then investigated the relationship between ginsenoside Re-metabolizing β-glucosidase and α-rhamnosidase activities of intestinal microflora and its antiscratching behavioral effect. The anti-scratching behavioral effects of ginsenosides were investigated in the increments of 1 h and 6 h after their oral administrations. The scratching behavioral frequency was measured for 1 h after treatment with histamine.
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The objective of this study was to evaluate the long-term safety of MP29-02 in subjects with chronic allergic (perennial) or nonallergic (vasomotor) rhinitis.
In a pilot open 'real-life' study treatment targeted towards rhinosinusitis accompanying PND syndrome and chronic cough led to an improvement in cough. A randomised controlled study is now needed to confirm or refute these findings.
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Allergic rhinitis is a frequent presenting problem in primary care in the UK, and has increased in prevalence over the last 30 years. When symptomatic, patients report significant reduction in their quality of life and impairment in school and work performance. Achieving adequate symptom control is pivotal to successful allergic rhinitis management, and relies mostly on pharmacotherapy. While it is recognised that most mild-moderate allergic rhinitis symptoms can be managed successfully in primary care, important gaps in general practitioner training in relation to allergic rhinitis have been identified. With the availability of new effective combination therapies, such as the novel intranasal formulation of azelastine hydrochloride and fluticasone propionate in a single device (Dymista®; Meda), the majority of allergic rhinitis symptoms can be treated in the primary care setting. The primary objective of this consensus statement is to improve diagnosis and treatment of allergic rhinitis in primary care, and offer guidance on appropriate referral of difficult-to-treat patients into secondary care. The guidance provided herein outlines a sequential treatment pathway for allergic rhinitis in primary care that incorporates a considered approach to improve the management of allergic rhinitis symptoms and improve compliance and patient satisfaction with therapy. Adherence with this care pathway has the potential to limit the cost of providing effective allergic rhinitis management in the UK by avoiding unnecessary treatments and investigations, and avoiding the need for costly referrals to secondary care in the majority of allergic rhinitis cases. The fundamentals presented in this consensus article should apply in most health-care settings.
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It is unclear what constitutes a clinically meaningful response for allergic rhinitis (AR) outcomes. The objectives of these post hoc analyses were (1) to define a clinically meaningful response using novel efficacy analyses (including a responder analysis), and (2) to compare the efficacy of MP29-02 [a novel intranasal formulation of azelastine hydrochloride (AZE) and fluticasone propionate (FP)] with commercially available FP, AZE and placebo in seasonal AR (SAR) patients, using these novel analyses.
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We examined the effect of antiallergic drugs, azelastine and epinastine, on the expression of FcepsilonRIalpha, beta, and gamma chains and phosphorylation of the gamma chains in rat basophilic leukemia (RBL-2H3) cells. The cells were cultured for 24 h with IgE treatment in the presence of azelastine or epinastine at the concentration of 10(-5) M. The FcepsilonRIalpha mRNA expression was determined by northern blot analysis. The protein level of FcepsilonRI expressed on the plasma membrane was examined following IgE treatment by immunoprecipitation with anti-IgE light chain, followed by western blot analysis with anti-gamma chain of FcR. Azelastine and epinastine had no effect on the FcepsilonRIalpha, beta and gamma mRNA levels. Although the amount of gamma chain assembled into IgE-bound FcepsilonRI was not changed by treatment with azelastine nor epinastine, phosphorylation levels of gamma chains of IgE-bound FcepsilonRI were inhibited by azelastine. The inhibitory effect of azelastine on the IgE-mediated expression of FcepsilonRIgamma protein is not due to their inhibition of mRNA and protein expression, but due to abrogating phosphorylation of the gamma chains, which is important for initiation of FcepsilonRI signaling cascade elicited by IgE interaction.
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All 3 groups had statistically significant (P < .001) improvements from their baseline TNSS after 2 weeks of treatment. The TNSS improved 27.1% with fluticasone nasal spray, 24.8% with azelastine nasal spray, and 37.9% with the 2 agents in combination (P < .05 vs either agent alone). All 3 treatments were well tolerated.
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Mean percent improvements in the total symptom complex severity scores for azelastine were statistically significant (P < or = .05) or showed a trend toward statistical significance (.05 < or = P < .10) versus placebo from the second through the first ten hours after the initial dose and for each of the last five hours of the second day, demonstrating a rapid onset of action and sustained efficacy over the 2-day study period. Azelastine was well tolerated, and no subject discontinued therapy with azelastine due to an adverse experience.
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The effects of the novel antiasthmatic/antiallergic compound azelastine on IL-1 beta were investigated in vitro and in vivo. In leukocytes both, intra- and extracellular IL-1 generation stimulated by LPS was inhibited dose dependently. In contrast azelastine did not prevent IL-1 beta-induced immigration of PMNs into the mouse ear. These findings suggest that azelastine is not an IL-1 antagonist but inhibits IL-1 synthesis and/or release in leukocytes.
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At 10 Gy with 15 mg PLM and 1,250 mg 5-FU, grade 1 mucositis (redness of the oral mucosa) was induced in 14 patients in the control group and five patients in the Azelastine group. At 20 Gy with 30 mg PLM and 2,500 mg 5-FU, grade 2 (erosion with mild irritation) and grade 3 (extensive erosion with marked irritation) stomatitis were observed in 9 and 3 of the control patients and 5 and 1 in the Azelastine group, respectively. At the completion of treatment, mucositis in 21 patients in the Azelastine group remained at grade 1 or grade 2, whereas grades 3 and 4 (ulceration with severe contact pain) mucositis were observed in 6 and 10 patients, respectively. However, in the control group, grades 1 and 2 were observed in only 2 and 3 cases, whereas grades 3 and 4 stomatitis were induced in 6 and 15, respectively. Azelastine suppressed neutrophil respiratory burst both in vivo and in vitro, and also suppressed cytokine release from lymphocytes. However, neutrophil superoxide dismutase (SOD) activity was negligibly suppressed.
We studied the duration of the protective effect of azelastine against histamine-induced bronchoconstriction in six subjects with asymptomatic asthma. The study was performed in two periods of five consecutive days each. After a histamine inhalation test, we randomly administered either placebo or a single oral dose of 8.8 mg azelastine in a double-blind crossover fashion. Histamine challenges were repeated 5 hours after ingestion and at 1 PM on the following four days. The geometric means of the dose of histamine (in cumulative breath units [cbu]) necessary to increase specific airway resistance by 100% as compared with baseline (PD100SRaw) were 8.7 and 8.5 cbu before placebo and azelastine, respectively. Placebo did not significantly influence PD100SRaw within 99 hours after treatment. Five and 27 hours after azelastine, PD100SRaw increased to 178.2 and 46.7 cbu, respectively (p less than 0.05). Two patients showed a highly significant protection against the airway effect of histamine even 99 hours after ingestion (p less than 0.01). These data demonstrate a variable duration of the antihistaminic property of azelastine. The prolonged therapeutic effect in some patients may be beneficial in the timing of medication intervals.
The calculation of red density of the conjunctiva by digital analysis proved to be a sensitive tool for measuring the conjunctival allergic reaction. It is possible to overcome the insufficient subjective evaluation of the CPT by objective measurements of the vascular reaction.
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In addition, the mediators of AR, including histamine, leukotrienes, cytokines, and prostaglandins, may play a role in sleep regulation and, thus, may be directly involved in this impairment independent of nasal obstruction. Recumbency and/or diurnal variation augments turbinate swelling, causing nasal blockage during nocturnal sleep. Medications directed toward reversal of nasal congestion often concomitantly work through suppression of inflammatory mediators and constitute the primary therapy for sleep disturbance associated with allergic rhinitis. Some pharmaceutical interventions that reduce nasal congestion have adverse effects on sleep. Decongestants effectively reduce nasal congestion but frequently produce stimulatory effects and even insomnia. Antihistamines reduce sneezing and pruritus, but are less effective in relieving congestion. Earlier, "first-generation" antihistamines are associated with significant sedation. They also have anticholinergic properties, which can cause dry mouth and make mouth breathing even more uncomfortable in the allergic individual with nasal obstruction. The absence of anticholinergic properties in second-generation, largely nonsedating antihistamines limits their efficacy in rhinorrhea. Azelastine, a topical antihistamine, significantly reduces rhinorrhea and congestion and improves subjective sleep quality, but is also associated with increased sedation. Intranasal corticosteroids and oral leukotriene receptor antagonists effectively reduce rhinorrhea, congestion, and inflammatory mediators.