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MP29-02 (Dymista, Meda, Solna, Sweden) is the first new class of AR medication (WHO ATC R01AD58) since the introduction of intranasal corticosteroids (INS) almost 50 years ago. It is a novel intranasal formulation of azelastine hydrochloride and fluticasone propionate delivered in a single spray. Here we review all the safety information relevant to MP29-02, from the initial phase I bioavailability and disposition data, to the phase III 14-day and 52-week data and finally to phase IV safety data collected during MP29-02 use in routine clinical practice.
The LDH titers increased after all the antiallergic agents were exposed up to 4 h, maintained its level for 12 h, and then decreased until 24 h. There was no statistical significance among the three agents. The greater titer of LDH, the more conjunctival cells became swollen or round. Azelastine and ketotifen showed greater LDH titer, edema, and cytoplasmic and nuclear degenerations of the conjunctival cells than that of olopatadine. The levels of Na(+), Cl(-), and pH were significantly lower with azelastine and ketotifen, compared with olopatadine, and all antiallergic agents contained the same concentration of benzalconium chloride.
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Statistically significant changes from baseline in TNSS were seen in both the LNS group and the ANS group. No significant differences were seen between the two groups in terms of evaluation of therapeutic effect, total effective rate, and onset of action, except for a higher symptom relief rate in the LNS group than in the ANS group within 30 min of administering the first dose. Adverse reactions were mild to moderate, with an incidence of 0.9% for LNS and 2.5% for ANS.
One of the dose-limiting adverse effects of chemoradiotherapy is mucositis, especially oral mucositis. Prophylaxis of severe mucosal reaction would allow application of aggressive chemoradiotherapy to malignancies.
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These results confirm MP29-02's wide therapeutic spectrum and assert its consistent superiority over an intranasal corticosteroid.
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Azelastine, montelukast and their combination protected against both EAR and LAR (p<0.004, each) by 46% and 43%, 76% and 59%, and 89% and 78%, respectively. Azelastine was not as effective during EAR but equally effective to montelukast during LAR. The combination was superior to each drug alone during both EAR and LAR (p<0.05, each).
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MP29-02 represents a breakthrough in AR management for the following reasons: i) MP29-02 has been extensively studied in comparison to first-line therapies in both seasonal AR (SAR) patients and in those with chronic rhinitis (i.e., perennial allergic rhinitis [PAR] and nonallergic (vasomotor) rhinitis) in one of the largest direct head-to-head clinical trial programmes in AR, to date. ii) With MP29-02, the efficacy of an intranasal corticosteroid (INS), the first-line choice for AR has been exceeded for the first time without safety repercussions. AR patients treated with MP29-02 experience significantly greater relief from their overall nasal and ocular symptoms compared to two first-line AR therapies, irrespective of season, symptom type, or disease severity. More patients treated with MP29-02 achieve a substantial reduction (i.e., 50% reduction) in their symptoms and also complete symptom relief and achieve these clinically relevant responses days faster than an INS or antihistamine. iii) Formulation of a topical medication is critical, and MP29-02's novel formulation and/or its device contribute to its clinical efficacy.
Therapy of experimentally induced allergic conjunctivitis with AZE was highly effective, with an onset of action seen within 3 minutes and a duration of effect of at least 8 to 10 hours.
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In this report are stated the results of an investigation on the long-term prognosis of occupational asthma, recently sending out enquêtes to 28 patients with occupational asthma of various kinds who had been treated and observed in our allergy clinic these 22 years. This study is limited to 17 cases, because 4 questionnaires were not returned, 6 were sent back unopened for the reason that present address was unknown and one patient died in an accident. Eight of the patients were able to avoid exposure to allergens by changing their occupation or work place. The prognosis for these cases were quite favourable, except in one patient with double sensitization to house dust. Of the nine patients who were obliged to continue work in which they were exposed to occupational allergens, two of them benefitted from a change of the materials they used in their work to new ones free from antigenicity. However, for the rest, allergic symptoms continued with their severity for ages in inverse proportion to the the degree of effective countermeasures taken against the allergens. Accordingly, the author would assert that effective measures to improve working conditions and protect workers must be taken as soon as possible.
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Currently, much effort is geared towards developing therapies that impact on the inflammation in respiratory diseases such as asthma and COPD, assuming that this will improve disease pathology. R,R-Glycopyrrolate, a quaternary ammonium compound, is a muscarinic receptor antagonist with the potential to be used as a long-acting bronchodilator in patients with asthma and COPD. In this study we evaluated whether the combination of R,R-glycopyrrolate with known anti-inflammatory drugs results in synergistic effects. Human primary monocytes were used as an in vitro model system. M3, M4, M1 and M2 receptors were expressed in these cells in descending order. The combinatory effects of the drugs on the release of TNF-alpha after lipopolysaccharide stimulation were analyzed. R,R-Glycopyrrolate alone did not affect LPS induced TNF-alpha release. The PDE4 inhibitor rolipram dose dependently inhibited the TNF-alpha release. Maximum inhibition was around 70%. The IC(35) for rolipram was 68.9+/-15.2 nM. The simultaneous administration of 10 microM R,R-glycopyrrolate reduced the IC(35) to 1.70+/-1.18 nM. The anti-histamine azelastine inhibited TNF-alpha release dose dependently. The simultaneous administration of R,R-glycopyrrolate did not influence the action of azelastine. The corticosteroid budesonide inhibited the TNF-alpha release dose dependently with an IC(50) of 0.55+/-0.13 nM. The simultaneous administration of 10 microM R,R-glycopyrrolate reduced the IC(50) to 0.13+/-0.03 nM. Finally, R,R-glycopyrrolate was most effective in the triple combination with budesonide and rolipram in the reduction of TNF-alpha release. In conclusion, R,R-glycopyrrolate acts synergistically with the PDE4 inhibitor rolipram and the steroid budesonide in inhibiting inflammatory mediators.
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Evidence of a different inhibitory effect of multiple action compounds on the pro-inflammatory mediators released from the mast cells suggests the possibility to target different phases of the allergic reaction, leading to a potential improvement in the management of allergic patients.
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This was a prospective, randomized, double-masked, contralaterally controlled, multicenter, allergen-challenge study. Itching was chosen as the primary efficacy variable since it is the only FDA-approved indication these 2 agents have in common. Subjects with a history of allergic conjunctivitis who responded to the CAC at screening visits 1 and 2 were randomized to 1 of 3 treatment groups: olopatadine in 1 eye and azelastine in the other eye; olopatadine in 1 eye and placebo in the other eye; or azelastine in 1 eye and placebo in the other eye. At the assessment visit (visit 3), subjects received masked study medication according to the randomization scheme. After 5 minutes, subjects were bilaterally challenged with the allergen concentration that had elicited a positive conjunctival allergic response at visits 1 and 2. Immediately after challenge, subjects gave itching assessments (scale, 0 = no itching to 4 = severe itching) every 30 seconds for a total period of 20 minutes. Mean itching scores for all eyes were compared by treatment. Mean itching scores at each time point were compared between treatments using 2 sample t tests.
Azelastine is a selective antagonist at the human histamine-1 receptor and is used clinically in the treatment of allergic rhinitis. In this study we have investigated its duration of action in vitro in an effort to characterise the receptor and tissue components involved. Chinese hamster ovary cell membrane fragments were used to determine the kinetics of azelastine at the H₁ receptor in a radioligand binding assay. Further duration of action studies were completed in tissue preparations using guinea-pig trachea and human bronchus. In radioligand binding studies, azelastine reached steady state at the H₁ receptor after approximately 41 min and exhibited a significantly slower dissociation rate constant from the receptor than the first generation antihistamine, diphenhydramine. In washout studies completed in guinea-pig and human airway in vitro tissue preparations, azelastine continued to antagonise the effects of histamine at the H₁ receptor for at least 18 h post-washout of the antagonist. This outcome was reversed following removal of the epithelium from guinea-pig isolated tracheal strips. These studies indicate there is a tissue component contributing to azelastine's duration of action, in addition to its direct H₁ receptor binding, with evidence suggesting a role for the epithelial layer.
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Azelastine was suggested as a supplementary choice of glucocorticoid for the control of moderate to severe allergic rhinitis (AR). However, the underlying mechanism has not been completely understood. In this study, primary cultured nasal epithelial cells and bronchial epithelial cells were stimulated with proinflammatory cytokines (IL-1β and IL-17A) and anti-inflammatory agents (azelastine and budesonide) in vitro. The expression of intercellular adhesion molecule 1 (ICAM-1) and mitogen-activated protein kinase phosphatase-1 (MKP-1) was examined using qPCR and ELISA, respectively. Moreover, the additive effects of azelastine and budesonide nasal spray on nasal ICAM-1 level and total nasal symptom scores were evaluated in six uncontrolled severe AR patients by budesonide nasal spray alone. We found azelastine significantly inhibited cytokine-induced ICAM-1 upregulation, which is reversed by MKP-1 silencing. Azelastine and budesonide additively increased MKP-1 expression and inhibited ICAM-1 expression in vitro. After treatment for two consecutive weeks, combined azelastine and budesonide nasal spray significantly decreased nasal ICAM-1 level and TNSS in six uncontrolled AR patients. Our findings suggested that azelastine is able to additively enhance the anti-inflammatory effect of budesonide by modulating MKP-1 expression, which may implicate in the treatment of uncontrolled severe AR.
In total, 60 children who were found to have adenoid hypertrophy were included. A questionnaire on nasal symptoms, nasal endoscopy and skin prick tests was administered to all patients. All patients had complaints of chronic nasal obstruction symptoms and nasal endoscopy showed > 75% choanal obstruction, attributable to adenoid pads. The adenoid/nasopharyngeal areas were calculated. All of the patients underwent azelastine nasal spray therapy (1 spray per nostril, twice daily; 0.28 mg/dose) for 30 days. After 1 month, all children were reassessed. The efficacy of therapy, symptoms, adenoid / nasopharynx ratio, and obstruction ratio, obtained by endoscopy, were compared.