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Astelin (Azelastine)

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Astelin is a nasal spray which is used for treating allergy symptoms and symptoms of nasal passage inflammation. Astelin contains azelastine, an antihistamine. It blocks the effects of the chemical histamine in your body. Astelin prevents sneezing, itching, runny nose, and other nasal symptoms of allergies.

Other names for this medication:

Similar Products:
Astepro, Patanase


Also known as:  Azelastine.


Astelin belongs to a group of medicines called antihistamines.

Astelin provides relief from bothersome nasal symptoms such as congestion, itchy/runny nose, sneezing and postnasal drip due to seasonal allergens or environmental irritants.

Astelin is steroid-free, does not contain pseudoephedrine, and relieves your symptoms by blocking the effects of histamine - the primary cause of allergy symptoms.

What makes Astelin unique is that it is a steroid-free antihistamine nasal spray that provides symptom relief whether the trigger is an allergen (grass, trees, pollen, mold, etc.), an irritant (cigarette smoke, perfume, cleaning agents, car exhaust, cold air, etc.), or both.

Astelin is also know as Azelastine, Arzep, Rhinolast, Alerdual, Allergodil, Rinalin.

Generic name of Astelin is Azelastine.


Follow the directions for using this medicine provided by your doctor. Use Astelin exactly as directed.

Astelin can be used by patients as young as 5 years of age, depending on what type of rhinitis they have been diagnosed with.

For those with seasonal allergic rhinitis, patients from 5 to 11 years of age should administer 1 spray in each nostril twice daily.

Patients 12 years of age and older with seasonal allergic rhinitis should administer 2 sprays of Astelin in each nostril twice daily.

For those with nonallergic vasomotor rhinitis, patients 12 years of age and older should administer 2 sprays of Astelin in each nostril twice daily.

Before using Astelin for the first time, remove the child-resistant screw cap and replace with the pump unit. Prime the delivery system (pump unit) with four sprays or until a fine mist appears. If 3 days or more have elapsed since your last use of the nasal spray, reprime the pump with two sprays or until a fine mist appears.


If you overdose Astelin and you don't feel good you should visit your doctor or health care provider immediately.


Store at a room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and sunlight. Keep in a tightly closed container. Throw away the after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Astelin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Astelin if you are allergic to Astelin components.

It is not known whether Astelin will harm an unborn baby. Do not use this medicine without your doctor's advice if you are pregnant or breast-feeding.

The medicine has a antihistamine in it. Before you start any new medicine, check the label to see if it has an antihistamine (e.g., diphenhydramine) in it too. If it does or if you are not sure, check with your doctor or pharmacist.

Astelin may cause harm if it is swallowed. If you may have taken it by mouth, contact your poison control center or emergency room right away.

Astelin should be used with extreme caution in children younger than 5 years old; safety and effectiveness in these children have not been confirmed.

Do not drink alcohol or use medicines that may cause drowsiness (e.g., sleep aids, muscle relaxers) while you are using Astelin; it may add to their effects. Ask your pharmacist if you have questions about which medicines may cause drowsiness.

Astelin may cause drowsiness. These effects may be worse if you take it with alcohol or certain medicines. Use Astelin with caution. Do not drive or perform other possibly unsafe tasks until you know how you react to it.

Do not stop taking Astelin suddenly.

astelin drug class

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.

astelin drug interactions

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.

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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.

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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.

astelin pediatric dose

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.

astelin dosing

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.

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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.

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astelin buy online 2017-07-31

A global assessment of efficacy was used to estimate the number needed to treat for azelastine nasal spray compared with placebo or active comparators. The total symptom score was used to compare the effect size between azelastine and placebo. In five comparisons of azelastine and placebo, azelastine was most efficacious, with a summary number needed to treat of 5.0 (95% confidence interval [CI] 3.3-10.0). In reviewing 11 studies of azelastine versus active comparators, we found no significant difference between azelastine and active comparators (number needed to treat 66.7, 95% CI 14.3 to infinity to 25). Azelastine was more efficacious than placebo in terms of total symptom score (effect size astelin buy of 0.36, 95% CI 0.26-0.46).

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Urticaria is a cutaneous syndrome characterized by dermal edema (wheal) and erythema (flare) that blanches with pressure. The lesions typically last less than 24 hours and are usually pruritic. In 1983, Christensen and Maibach summarized the theory behind the use of histamine H1 receptor antagonists (antihistamines) in clinical dermatology. These agents remain the mainstay of treatment for urticaria. This article reviews the medical literature on the effectiveness of antihistamines in urticarial syndromes, including acute, chronic idiopathic and the physical urticarias. Older antihistamines, such as chlorpheniramine and hydroxyzine, are effective in the treatment of urticarias, but they also have marked sedative and anticholinergic astelin buy effects. Newer nonsedating antihistamines (second-generation antihistamines) have been developed that have reduced adverse effects because they do not cross the blood-brain barrier; these agents (acrivastine, cetirizine, loratadine, mizolastine, fexofenadine, ebastine, azelastine and epinastine) cause significantly less sedation and psychomotor impairment than their older counterparts. A review of the literature reveals that there are few studies which document the efficacy of second-generation antihistamines in the treatment of acute urticaria, a biologic entity that usually resolves within 3 weeks. We did not identify controlled studies that suggested superiority of any antihistamine in the treatment of acute urticaria. Loratadine or cetirizine, and possibly mizolastine, appear to be treatments of choice for chronic idiopathic urticaria. For symptomatic dermatographism, the combination of an antihistamine and an H2 antagonist, e.g. chlorpheniramine and cimetidine, appears to be effective. Very few studies have been conducted on the use of antihistamines in the treatment of cold, cholinergic, and pressure urticaria. Antihistamines are the mainstay of urticarial therapy. This evidence-based review suggests that there are efficacy differences between newer, nonsedating antihistamines and older agents in some forms of the disorder. Clearly, further well-controlled clinical trials in larger numbers of patients are needed to clarify the role of these agents in the treatment of urticaria.

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Over 50% of patients who seek treatment for allergies present with ocular symptoms. Our current ability to control ocular allergic symptoms is greater than ever before. Newer dual-acting topical eyedrops attack multiple facets of the allergic cascade. Azelastine has antihistaminic effects providing immediate relief, mast cell stabilization providing early-phase intervention, and inhibition of expression and activation of anti-inflammatory mediators which characterize the late phase of the immune reaction. The ophthalmic eyedrop formulation is approved for treatment of allergic conjunctivitis in adults and children aged over 3 years. In clinical trials comparing azelastine with Prednisone 4 Mg other dual-acting eyedrops, such as levocabastine and olopatadine, azelastine was reported to be slightly less efficacious and to sting briefly upon administration. Even so, many patients experienced the full benefit of symptom relief, and preferred azelastine. As a broad-spectrum drug, azelastine offers many desirable properties for management of ocular allergies. Because it can often produce maximal effect with just twice-daily dosing, azelastine is a particularly good choice for the allergic population in whom minimizing exposure to topical products and preservatives is a key concern.

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The capacity of sublingual allergen immunotherapy (SLIT) to provide effective symptom relief in pollen-induced seasonal allergic rhinitis is often questioned, despite evidence of clinical efficacy from meta-analyses and well-powered, double-blind, placebo-controlled randomized clinical trials. In the absence of direct, head-to-head, comparative trials of SLIT and symptomatic medication, Casodex Y Alcohol only indirect comparisons are possible.

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Continuous treatment was more effective 2 Diflucan Pills than on-demand use as assessed by both clinical evaluation and antiinflammatory action.

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Overall, across all 4 weeks of treatment, the mean percent improvements in the total and major symptom complex severity scores in both azelastine treatment groups were greater than those for the placebo group. For the azelastine 2 sprays bid group, the overall results were significant at P = .05 for the major symptom complex score and at .05 < P = .10 for the total symptom complex score versus placebo. For both azelastine treatment groups, improvements in all of the individual rhinitis symptoms were superior to those for the placebo group and, in general were clinically and statistically significant. Azelastine nasal spray was well tolerated; adverse experiences were generally application site reactions, mild to Geodon Dosage Range moderate, and not limiting to continued treatment.

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This study supports a once to twice daily dosing regimen for 2 sprays of 0.1% azelastine in the acute Cialis 0 Mg treatment of allergic rhinitis with onset of action within 2 to 3 hours.

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The significant improvement in the TNSS with combination therapy relative to the individual agents alone is in contrast to Tofranil Max Dose previously published studies that found no advantage with an oral antihistamine and an intranasal corticosteroid in combination. Azelastine nasal spray and fluticasone nasal spray in combination may provide a substantial therapeutic benefit for patients with seasonal allergic rhinitis compared with therapy with either agent alone.

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1. The effect of 4.4 mg azelastine administered orally on airway responsiveness, skin prick testing, daily peak expiratory flow rates and symptoms of asthma was compared with placebo in a 7 week double-blind, parallel group study of 24 patients with extrinsic asthma. The study was in Aggrenox Drug Coupons two parts: a 2 week assessment period, during which all patients received placebo tablets but recorded daily peak flow rates (PEFRs) and symptoms, preceding the 7 week double-blind comparison. 2. Azelastine, 4.4 mg, significantly decreased airway responsiveness to histamine compared with placebo both after a single dose (P less than 0.001), and following 7 weeks continuous treatment (P less than 0.02). Airway responsiveness to methacholine was not altered by administration of azelastine compared with placebo. 3. Skin prick test weal diameters to both allergen and histamine were significantly reduced after both a single dose and following 7 weeks continuous therapy treatment with azelastine. 4. There was a significant improvement in both the mean of the morning and the evening peak flow rates recorded during the last week compared with the first week of the study in the group receiving 4.4 mg of azelastine twice daily compared with placebo. Scores for wheeze were significantly reduced during the final 3 weeks of the study in patients receiving azelastine compared both with those receiving placebo and with the first week of the study (P less than 0.05, P less than 0.01). Consumption of inhaled bronchodilators fell significantly during the study in the group receiving azelastine therapy (P less than 0.05); no such fall occurred in the placebo treated patients. 5. A bitter metallic taste was reported by 58% of patients who received azelastine therapy.

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Budesonide caused a rapid but reversible Celexa Dosage Ocd ciliostasis and showed no ciliotoxic effect at 10% dilution. Fluticasone propionate induced an irreversible ciliostatic activity and showed a reversible decrease in CBF at 10% dilution. Azelastine hydrochloride and levocabastine hydrochloride both induced a dose-dependent and irreversible decrease in CBF, although the ciliotoxic effect was not evident at 5% dilution. BKC resulted in an irreversible ciliostasis at 0.005 or 0.01% concentrations, whereas PS did not show any change in CBF at 0.12 or 0.24% concentrations.

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We studied the effect of (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate (OKY-046.HCl), a specific thromboxane (TX) A2 synthetase inhibitor, on airway hyperresponsiveness of guinea pigs. OKY-046.HCl (30-100 mg/kg, intraduodenally (i.d.) or orally (p.o.)) suppressed dose dependently the airway hyperresponsiveness to acetylcholine (ACh) induced by formyl-methionyl-leucyl-phenylalanine (FMLP), platelet activating factor (PAF) and repetitive antigen. OKY-046.HCl (100 mg/kg) also inhibited the increase in TXB2 in bronchoalveolar lavage fluid (BALF) induced by FMLP, PAF and antigen. Aspirin 10 or 30 mg/kg i.d. or p.o.) suppressed the airway hyperresponsiveness induced by FMLP and PAF but not by antigen. Azelastine (10 mg/kg i.d.) was ineffective on PAF- and Zofran Toddler Dosage antigen-induced airway hyperresponsiveness. TXA2 mimetic drugs caused airway hyperresponsiveness that was not inhibited by OKY-046.HCl (30 mg/kg i.v.). Furthermore, OKY-046.HCl showed no effect on propranolol- and physostigmine-induced airway hyperresponsiveness which did not accompany TXB2 generation in BALF. The number of eosinophils in BALF increased after FMLP exposure, an effect which was not inhibited by OKY-046.HCl. These results suggest that OKY-046.HCl inhibits airway hyperresponsiveness by suppressing TXA2 generation. We suggest that OKY-046.HCl will be a new antiasthmatic drug.

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Azelastine has the potential to inhibit the proliferation of haSMCs. If a sufficient dose can be applied either systemically or locally Voltaren Generic Name it could be a valuable substance to prevent restenosis.

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Individual severity scores for itching (evaluated by patient) and conjunctival redness (evaluated by physician) for each eye at 3, 5, and 10 minutes after CPT at visits 3 and 4 using a 5-point scale (0 = none to 4+ = very severe).

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Azelastine (azelastine hydrochloride) was orally administered to 43 patients with recurrent aphthous ulcers (RAU), and its clinical effects and in vitro influence on leukocytes were examined. During at least 6 months after drug treatment, no oral ulcers occurred in 7 patients, and an improvement of the oral condition was exhibited in all except 4 of the remaining patients. The frequency of occurrence of RAU was significantly reduced, from 1.7 +/- 0.9 to 0.9 +/- 0.5 times/month, and ulcer duration and oral irritation were also significantly reduced from 12.5 +/- 2.5 and 7.5 +/- 2.4 days to 9.8 +/- 2.6 and 5.3 +/- 2.4 days, respectively. Neutrophils from patients treated with Azelastine generated a suppressed volume of superoxide (O2-). Suppression of O2- generation and chemiluminescence by in vitro Azelastine was also confirmed to occur in a dose-dependent manner. Furthermore, the production of TNF-alpha and GM-CSF in lymphocytes was suppressed in the presence of Azelastine, and the drug protected sheep red blood cells and epithelial tumor cell lines against hydrogen peroxide impairment and hypotonic shock. These clinical and experimental results lead to the conclusion that improvement of RAU by Azelastine depends on the protection of cell membranes and the suppression of leukocyte-function, including reactive oxygen generation.

astelin buy online 2015-08-16

Recently, mast cell stabilizers, so called antiallergic drugs, that also have blocking effects on receptors for chemical mediators (CM) have been developed. The present study investigated the effects of a new antiallergic drug, epinastine (3-amino-9,13b-dihydro-1H-dibenz[c,f]imidazol [1,5-a]azepine hydrochloride, WAL 810 CL; CAS 80012-43-7) on the in vivo bronchoconstriction (BC) induced by several CM as compared with those of other antiallergic drugs such as ketotifen, azelastine and oxatomide. Male Hartley guinea pigs were used. The BC was measured with a modified Konzett-Rössler method and expressed as a change in ventilation overflow (VO) under anesthesia. Antiallergic drugs were given orally 1 h before i.v. administration of CM. I.v. administrations of histamine (His), U-46619 (thromboxane A2 mimetic), leukotriene D4 (LTD4), prostaglandin D2 (PGD2), substance P (SP), neurokinin A (NKA), bradykinin (BK) and endothelin-1 (ET-1) increased VO in a dose dependent manner. The potency was as follows; ET-1 greater than LTD4 greater than NKA much greater than U-46619 greater than SP greater than His greater than BK much greater than PGD2. All the antiallergic drugs used markedly inhibited the His-induced BC. Epinastine, ketotifen and azelastine also significantly inhibited the BK-induced BC; epinastine had the strongest anti-BK effect among them. On the other hand, the four antiallergic drugs did not inhibit the BC induced by the other CM except for His and BK. Based on the above results, it is suggested that epinastine possesses anti-His and BK effects, and therefore could be promising as a new antiallergic drug without sedative effect.

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Based on the percentage of patients not requiring additional antirhinitis medication and the patient assessment of efficacy, azelastine nasal spray monotherapy was as effective as the combination of oral loratadine plus intranasal beclomethasone in treating moderate-to-severe symptoms of seasonal allergic rhinitis.

astelin buy online 2016-02-23

A comparison of the efficacy of azelastine nasal spray (AZENS) versus triamcinolone acetonide nasal spray (TANS) on total nasal symptom scores (TNSS), nasal peak inspiratory flow rate (nPIFR), and nasal cytology was studied in a 2-week randomized parallel-group trial. The Epworth Sleepiness Scale (ESS) and health-related quality of life (HRQoL) were also analyzed.

astelin buy 2016-05-11

To compare the efficacy of intranasally administered azelastine to budesonide, at their respectively recommended dosage, on the symptoms of perennial rhinitis patients.

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Blood was drawn from healthy human volunteers and neutrophils and eosinophils were purified on a Conray-Ficoll and a Percoll gradient, respectively. Rat mast cells were also purified on a Percoll gradient. Superoxide anion (O2-) generation from the cells were measured by 2-methyl-6-[p-methoxy-phenyl]-3,7-dihydroimidazo[1,2-a]pyrazin+ ++-3-one (MCLA)-dependent luminescence. Addition of 0.5 mumol/l MCLA and a stimulatory agent, such as phorbol myristate acetate, N-formyl-methionyl-leucyl-phenylalanine (fMLP) and compound 48/80, to a suspension of each cell caused a marked luminescence which was inhibited by 0.5 mumol/l superoxide dismutase (SOD). Azelastine (A-5610) significantly inhibited the O2- generation from each activated inflammatory cell in a dose-dependent manner. When eosinophils were activated by fMLP in the presence of cytochalasine (CB), azelastine abolished the luminescence stronger than that from the fMLP-stimulated cells in the absence of CB.

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We treated bronchial asthma patients with anti-allergic agents for more than three months, and examined their effects on the airway hyperreactivity in 15 cases; five were short cases (disease duration was less than one year from the onset) and 10 were long cases (disease duration was more than one year). A significant improvement in airway hyperreactivity to histamine inhalation was observed in all five short cases. In 4 out of 5 short cases, the threshold of histamine concentration reached to the normal level of 10,000 micrograms/ml. On the other hand, the significant improvement was observed only in 2 out of 10 cases. We suggested that in "short asthma cases" the airway hyperreactivity could improve with the use of anti-allergic agents in a relatively short period and at a high rate.

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To explore the relevance between nasal symptoms and laryngopharyngeal reflux disease in patients with allergic rhinitis.

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Olopatadine hydrochloride exerts a wide range of pharmacological actions such as histamine H(1) receptor antagonist action, chemical mediator suppressive action, and eosinophil infiltration suppressive action. Olopatadine hydrochloride 0.1% ophthalmic solution (Patanol((R))) was introduced to the market in Japan in October 2006. In a conjunctival allergen challenge (CAC) test, olopatadine hydrochloride 0.1% ophthalmic solution significantly suppressed ocular itching and hyperemia compared with levocabastine hydrochloride 0.05% ophthalmic solution, and the number of patients who complained of ocular discomfort was lower in the olopatadine group than in the levocabastine group. Conjunctival cell membrane disruption was observed in vitro in the ketotifen fumarate group, epinastine hydrochloride group, and azelastine hydrochloride group, but not in the olopatadine hydrochloride 0.1% ophthalmic solution group, which may potentially explain the lower discomfort felt by patients on instillation. Many other studies in humans have revealed the superiority of olopatadine 0.1% hydrochloride eye drops to several other anti-allergic eye drops. Overseas, olopatadine hydrochloride 0.2% ophthalmic solution for a once-daily regimen has been marketed under the brand name of Pataday((R)). It is expected that olopatadine hydrochloride ophthalmic solutions may be used in patients with a more severe spectrum of allergic conjunctival diseases, such as vernal keratoconjunctivitis or atopic keratoconjunctivitis, in the near future.

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We have examined the effect of azelastine hydrochloride, 8.8 mg, on the early and late responses to inhaled allergen in a group of 12 atopic subjects with asthma. On two separate days, 3 weeks apart, patients were administered either oral azelastine, 8.8 mg, or matched placebo. Four hours later they inhaled via nebulizer, a dose of allergen (grass pollen or Dermatophagoides pteronyssinus) that had previously been demonstrated to produce a 25% fall in FEV1. Plasma-histamine concentrations and FEV1 levels were measured at intervals during the subsequent 8 hours. After placebo, allergen inhalation produced rapid bronchoconstriction in all subjects with a maximum mean fall in FEV1 at 30 minutes of 22.8 +/- 3.4% from the postsaline baseline value. Five subjects also developed a late bronchoconstriction response with a fall in FEV1 of greater than 15% from postsaline baseline value between 2 and 8 hours after challenge. Azelastine reduced the bronchoconstrictor response during the first 10 minutes and produced a maximum mean fall at 30 minutes of 21.2 +/- 4.4% from the postsaline baseline value. Azelastine had a marked inhibitory effect, reducing the maximum mean fall from 23.9 +/- 6.3% to 9.6 +/- 3.9% from the postsaline baseline value. Analysis of the area under the FEV1 response time-course curves revealed that azelastine reduced the early response (first 2 hours) by 32.5% (p less than 0.05) (all subjects) and reduced the late response (2 to 8 hours) by 70.2% (p less than 0.05) (n = 5). Azelastine had no significant inhibitory effect on the early increase in plasma histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

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Allergic rhinitis is a very common disease that causes high economic costs. Furthermore inadequate treatment can lead to bronchial asthma. Against this background, drugs for the treatment of allergic rhinitis should be evaluated from a comprehensive medical-economic perspective. The new combination of an antihistamine and a corticosteroid, introduced in the market in 2013, emerges as useful pharmaceutical alternative, both with regard to the medical outcome parameters as well as cost-effectiveness.

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Rhinitis is a common condition that affects a significant proportion of the general population, as well as a high proportion of athletes. Nasal congestion is a predominate symptom of the late-phase reaction in allergic rhinitis and can have far-reaching effects that extend through the airway and beyond the nose. Rhinitis is often found in conjunction with asthma and is a risk factor for asthma. Nasal obstruction, which does not permit conditioning of inspired air by the nasal turbinates, may contribute to asthma symptoms and the development of asthma. These adverse conditions may be especially troublesome for the high-performance athlete who has increased nasal airflow turbulence and who competes under extreme conditions that may worsen rhinitis and asthma. Under the theory of the unified airway, an immune response induced in the nose may extend into the lungs via cytokines and other inflammatory mediators. Nasal congestion can significantly contribute to sleep dysfunction, leading to daytime fatigue and decreased performance. Treatment of allergic rhinitis can improve sleep and foster productivity. Control of rhinitis and nasal congestion, which is obtained by various therapies, may reverse lower airway tendency to bronchoconstriction.

astelin buy 2016-09-17

This study examined the passive cutaneous anaphylaxis-inhibitory activity of the flavanones isolated from the pericarp of Citrus unshiu (Family Rutaceae) and the fruit of Poncirus trifoliata (Family Rutaceae). Naringenin, hesperetin and ponciretin potently inhibited IgE-induced beta-hexosaminidase release from RBL-2H3 cells and the PCA reaction. Among the flavanones examined, naringenin was the most potent with an IC50 value for beta-hexosaminidase release from RBL-2H3 cells of 0.029 mM. Intraperitoneally administered naringenin (5 mg/kg) inhibited PCA by 70 +/- 1.7 %, compared with the control group. The inhibitory activity of naringenin was found to be comparable to that of azelastine, which is a commercially available antiallergic drug. However, their glycosides, hesperidin, naringin and poncirin, did not inhibit the in vitro release of beta-hexosaminidase from the RBL-2H3 cells. On the other hand, these flavanones did not improve the oxazolone-induced dermatitis in the mouse ears. When the flavanone glycosides were administered to rats, the aglycones, but not the flavanone glycosides, were excreted in urine. This suggests that the flavanone glycosides can be activated by intestinal bacteria, and may be effective toward IgE-induced atopic allergies.

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This manuscript addresses the pathogenesis of allergic rhinitis, use of nasal provocation as a method to assess inflammatory mediators and the role of cytokines, and topical glucocorticosteroids. Immunologic changes of allergen immunotherapy, pharmacotherapy with a focus on non-sedating, and topical antihistamines are discussed. The antiinflammatory potential of fexofenadine, azelastine, and newer therapeutic modalities with anti-IgE are addressed.

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Antigen challenge by patch ovalbumin emulsion induced an eczema-like skin lesion in epicutaneously sensitized guinea pigs. Diseased skin sites were macroscopically characterized by manifestations of dermatitis, such as erythema, edema, and papules, and microscopically characterized by acanthosis, spongiosis, and dermal infiltration by eosinophils. Using such lesions as a model of eczema, we evaluated the potential value of TAK-427 [2-[6-[[3-[4-(diphenylmethoxy)piperidino]propyl]amino] imidazo[1,2-b]pyridazin-2-yl]-2-methylpropionic acid dihydrate] as a therapeutic agent for atopic dermatitis by comparing it with dexamethasone and antihistamines. TAK-427 (0.3-30 mg/kg, p.o.) and dexamethasone (3 and 10 mg/kg, p.o.) inhibited eosinophil infiltration into the skin and ameliorated the dermatitis manifestations and epidermal damage. By contrast, none of the antihistamines tested (azelastine, ketotifen, terfenadine, and cetirizine) suppressed the eosinophil infiltration or dermatitis manifestations. To elucidate the mechanism by which TAK-427 inhibited the development of eczema, we investigated cytokine expression in the affected skin. Both TAK-427 and dexamethasone suppressed the increased mRNA expression of interleukin (IL)-13, granulocyte-macrophage colony-stimulating factor, IL-1alpha, tumor necrosis factor-alpha, interferon-gamma, and IL-8, but not IL-10, suggesting that TAK-427 inhibits allergic inflammation of the skin leading to the development of eczema by inhibiting the expression of proinflammatory cytokines after antigen challenge.