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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 online pharmacy

To evaluate the effects and safety of penetrating needling on head acupoints for perennial allergic rhinitis (PAR).

astelin pediatric dose

Our results suggest that antihistamine agents may be effective against alcohol-induced asthma by both blocking H1 receptors and inhibiting histamine release.

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Nonallergic rhinitis is a common disease that probably affects as many as 17 million Americans. Of equal importance is that, based on available data, approximately 22 million people suffer with a combination of nonallergic rhinitis and allergic diseases (mixed rhinitis). Both nonallergic and mixed rhinitis occur more frequently in adults than in children, may be more common in female patients than in male patients, and are more likely to be perennial than seasonal. Agents demonstrating efficacy (based on controlled trials or having approval by the FDA) for the therapy of nonallergic rhinitis are azelastine and topical nasal steroids.

astelin alcohol

Allergic rhinitis (AR) is a common condition that can be treated with a number of different therapies. Treatments such as intranasal antihistamines (INAs) and intranasal steroids (INSs) are widely used by AR patients. For some allergy sufferers, a combination of therapies, specifically an INA and an INS, is required to address their symptoms. A new treatment, the formulation of azelastine hydrochloride and fluticasone pro-pionate used as a single spray (MP-AzeFlu), has become available for AR patients who need both types of treatment. In this regard, the comparison with the alternative concomitant use of INAs and INSs is of interest. The current study examines the health care resource utilization and costs for each cohort.

astelin generic brand

The photoproducts produced by irradiating 8-methoxypsoralen (8-MOP) in the presence of spermine (Spm) were fractionated using gel filtration chromatography (GFC) on a Sephadex G-25 column. As a result, two bands which were characterized by the effects on hyaluronidase activity were obtained. The first band strongly activated the hyaluronidase, but a second band did not exhibit any effect on the enzyme activity. The first and second bands contained photoproducts with molecular weights (MW)>2700 and MW<728, respectively, determined by the GFC method. The photoproducts, 8-MOP-Spm-P(GFC) obtained from the first band, but not the photoproducts with lower MW from the second band, showed enzyme activating action. 8-MOP-Spm-P(GFC) induced paw edema, which was stronger in the first phase than the second one in rats, differing from that induced by carrageenin. This photoproduct was a substance with lower cell toxicity because it did not cause hemolysis on red blood cells or the release of lactic dehydrogenase from mast cells in rats. The effects of various drugs on 8-MOP-Spm-P(GFC)-induced edema were investigated. As a result, edema formation was inhibited by drugs with an anti-histaminic action, such as alimemazine, dl-chlorpheniramine, promethazine, ketotifen and azelastine, and with anti-serotonin action such as cyproheptadine. On the other hand, tranilast did not show significant inhibition and indomethacin showed a tendency to increase its formation. These results suggested that 8-MOP-Spm-P(GFC) is a new inflammatory substance and is very useful as an agent to develop new anti-inflammatory drugs without cyclooxygenase inhibitory action.

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Azelastine hydrochloride (AZE) is an anti-allergic drug that inhibits the release of various chemical mediators from mast cells. We compared the immunosuppressive effects of AZE and FK-506 in vivo and in vitro. Topical application of AZE strongly inhibited the efferent phase of contact hypersensitivity, as did application of FK-506. In in vitro experiments, we found that 1) the suppression by AZE on interleukin (IL)-2 production from splenic T cells was partial and considerably large amounts of IL-2 were still produced, even in the presence of 10(-5) M of AZE, which was in sharp contrast to the observed marked inhibition of [3H]-TdR incorporation; 2) AZE significantly inhibited the phorbol myristate acetate-induced IL-2 responsiveness; 3) AZE did not inhibit the IL-2 receptor alpha expression of activated T cells; and 4) the significant inhibitory action was still observed even when AZE was added at 48 h after the initiation of culture. In regard to FK-506, we found that 1) FK-506 completely blocked the production of IL-2; 2) exogeneous IL-2 consistently restored the FK-506-induced inhibition; 3) FK-506 affected the phorbol myristate acetate-induced IL-2 responsiveness very little, if any; and 4) the significant suppression was observed only when FK-506 was added within 24 h after the initiation of culture. Thus, AZE exerts its in vitro immunosuppressive activity preferentially by interfering with the IL-2 responsiveness, with partial inhibition of IL-2 production. Conversely, FK-506 acts as a strong inhibitor of IL-2 production without a prominent effect on IL-2 responsiveness. The immunosuppressive activity of AZE shown in vitro may also be operative in vivo and may be applicable for topical use.

astelin generic nasal

The AHRQ panel MCID threshold for the rTNSS was twelve times larger than the anchor-based estimates resulting in conflicting recommendations on whether different SAR treatments provide clinically meaningful benefit.

astelin drug class

Oral azelastine, a nonsteroidal antiinflammatory respiratory investigational drug has demonstrated activity in the treatment of allergic rhinitis and asthma with a good safety profile.

astelin generic

To investigate the effects of epinastine on eosinophil chemotaxis and changes in eosinophil adhesion molecules induced by epinastine and three other antiallergic agents, using eosinophils of atopic dermatitis (AD) patients.

astelin tablets

Histamine challenge-induced mucosal exudation of plasma appears to be a useful method for studies of the duration of action of antihistamines. We conclude that topical azelastine is suited for b.i.d. therapy and that neither the exudative process nor watery secretion may impede the efficacy or the duration of action of this nasal drug.

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Homologous passive cutaneous anaphylaxis (PCA) was induced by IgE antibody and, simultaneously, cutaneous reactions were induced by some allergic mediators such as histamine, serotonin and leukotriene (LT) C4 on rat back skin. Disodium cromoglycate and tranilast with inhibitory actions on mediator release inhibited PCA specifically, whereas antihistaminics, including ketotifen, azelastine, mequitazine and diphenhydramine, inhibited histamine- and serotonin-induced cutaneous reactions as well as PCA. Anti-slow-reacting substance of anaphylaxis drugs, KC-404 and FPL-55712, significantly inhibited PCA and histamine- and serotonin-induced reactions, but at the same doses they did not produce significant inhibition of the LTC4-induced reaction. All reactions tested were strongly inhibited dose dependently with the beta stimulants, salbutamol and isoproterenol, and a xanthine derivative, theophylline, which are known to increase the intracellular cyclic AMP level. We think that this method enables the determination of the properties of anti-allergic drugs.

astelin medication

Azelastine hydrochloride is an H1-receptor antagonist with antiinflammatory properties that is available in the US as Astelin Nasal Spray for the treatment of seasonal allergic rhinitis. The symptoms of seasonal allergic rhinitis can initially be treated with monotherapy using either an antihistamine or an intranasal corticosteroid. Patients whose symptoms do not respond adequately are often prescribed a combination of both an antihistamine and an intranasal corticosteroid.

astelin dosage instructions

Azelastine nasal spray can be effectively administered as adjunctive therapy, in an outdoor environment in which subjects are exposed to pollen and other aeroallergens.

astelin dosage form

Azelastine is an oral antiallergic drug. Although oral antiallergic drugs are classified as controllers because of the possession of anti-inflammatory effect, the mechanism of action has remained obscure. Thus the author investigated the effects of azelastine on inflammatory cells infiltrating into the bronchial mucosa and on the expression of cytokines in patients with atopic asthma. Biopsy specimens of the bronchial mucosa were bronchoscopically obtained before and after the administration of azelastine for 3 months. Inflammatory cells in the bronchial mucosa, including eosinophils, mast cells, macrophages, and T lymphocytes, were stained immunocytochemistry; expression of cytokine mRNA [Interleukin (IL)-4 and IL-5] was examined by the in situ hybridization method. The results obtained revealed that the number of eosinophils (p < 0.01), T lymphocytes (p < 0.01), and cells expressing mRNA of IL-4 (p < 0.05) or IL-5 (p < 0.01) significantly decreased after the administration of azelastine. These results suggest that azelastine inhibits the action on local infiltration of inflammatory cells and following proinflammatory cytokine production as one mechanism of bronchial asthma.

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Azelastine hydrochloride is a nasally administered antihistamine that is effective and safe for the treatment of perennial and seasonal allergic rhinitis. In addition to acting as a histamine H1-receptor antagonist, azelastine also inhibits the production or release of many chemical mediators of the allergic response such as leukotrienes, free radicals, and cytokines. After nasal administration, azelastine is systemically absorbed with a bioavailability of about 40%. The side effects of azelastine are drowsiness, headache, and bitter taste. Azelastine has a rapid onset of action with a benefit in about 2 hours and a prolonged duration of activity (12 to 24 hours). Studies have shown azelastine to be more effective than placebo in terms of reduction of the major and total symptom complexes of allergic rhinitis. Comparison studies have demonstrated that azelastine is as effective as ebastine, loratadine, cetirizine hydrochloride, and terfenadine at symptom reduction, with varying results when compared with the corticosteroids budesonide and beclomethasone. Although there are conflicting studies, some have demonstrated that azelastine reduces the nasal congestion of allergic rhinitis. This feature that distinguishes it from oral antihistamines is of great interest because corticosteroids are known to be quite effective for the relief of nasal congestion, whereas the antihistamines are effective for the sneezing, itchy eyes, itchy nose, and watery eyes, but not the congestion. Azelastine nasal spray seems to be an efficacious treatment for allergic rhinitis with a rapid onset and long duration of activity, but without the systemic adverse effects of traditional sedating antihistamines.

astelin patient reviews

Tissue distribution was performed in male guinea pigs that received a single oral dose of 1 mg/kg [14C]azelastine. Determination of 14C concentrations by liquid scintillation counting in 16 tissues and by whole-body autoradiography showed preferential uptake of the radioactivity by the lung. The liver had a higher and all other tissues had lower concentrations of 14C than the lung. The lowest 14C concentrations were in the eyes and brain. Light microscopy autoradiography of lung and trachea sections indicated localization of 14C, possibly in alveolar macrophages. The radioactivity cleared completely from lung tissue, as well as from other tissues within 48 hr.

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The efficacy of MP29-02 (a novel intranasal formulation of azelastine hydrochloride and fluticasone propionate in an advanced delivery system) has been well established in controlled clinical trials. This study was designed to assess the use of MP29-02 and its effectiveness in routine clinical practice. This was a German multicenter, prospective, noninterventional study, including 1781 allergic rhinitis (AR) patients. Eligible patients (i.e., acute AR symptoms and visual analog scale [VAS] score >50 mm) were included, assigned MP29-02 at baseline, and reassessed after ∼14 days. Patients assessed symptom control using a VAS from 0 (not at all bothersome) to 100 mm (very bothersome) in the morning before MP29-02 use, on days 0, 1, 3, and 7 and after ∼ 14 days. Patients' perceived levels of disease control were assessed on day 3. The Youden index determined patient-reported VAS score cutoffs on day 3 for "well controlled" and "partly controlled." MP29-02 reduced the VAS score from 75.4 mm (SD = 17.2) at baseline to 21.3 mm (SD = 18.3) by the last visit, a shift of 54.1 mm (SD = 24.6). One in every two patients felt their symptoms were well controlled at day 3. This perception of well-controlled symptoms at day 3 corresponded to an optimal VAS cutoff of 36 mm. On average, patients treated with MP29-02 crossed this well-controlled VAS cutoff by last visit. Similar results were found in adolescents, adults, and older adults, in those with perennial AR (PAR), seasonal AR (SAR), or PAR + SAR and in those with more and less severe disease. MP29-02 provides effective and rapid symptom control across all age groups in a real-life setting with responder rates higher than those observed in controlled clinical trials, supporting MP29-02's position as the drug of choice for the treatment for AR.

astelin dosage adults

Antiallergic effects of AL-3264 (N-[4-[4-(diphenylmethyl)-1-piperazinyl]butyl]-3-(6-methyl-3- pyridyl)acrylamide, CAS 118420-47-6) were compared with those of ketotifen, oxatomide, azelastine and tranilast in experimental animals. AL-3264 inhibited passive cutaneous anaphylaxis (PCA) in rats with an ED50 value of 6.1 mg/kg p.o. In inhibiting PCA, AL-3264 was the most potent among the antiallergic drugs examined. The anti-PCA effect of AL-3264 was long-lasting. Tolerance was not produced by repeated administration of AL-3264. AL-3264 inhibited antigen-induced bronchoconstriction in actively sensitized rats and in passively sensitized guinea pigs, with ED50 values of 14.5 and 0.44 mg/kg p.o., respectively. In the in vitro experiments, AL-3264 inhibited 5-lipoxygenase activity of guinea pig leukocytes with an IC50 value of 4.9 mumol/l, being the most potent among antiallergic drugs examined, and suppressed the antigen-induced histamine release from rat peritoneal mast cells with an IC50 value of 12.2 mumol/l. AL-3264 antagonized histamine-induced contractions in isolated guinea pig trachea with an IC50 value of 0.16 mumol/l. These results suggest that AL-3264 is an orally active, potent and long-lasting antiallergic compound which inhibits 5-lipoxygenase activity, histamine release and histamine H1 receptors at the similar concentrations.

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Pruritus is a very common complication in chronic hemodialysis (HD) patients, however the exact mechanism for this affliction is still not known. Anti-histaminics usually failed to alleviate uremic pruritus. In others, an anti-allergic drug, which inhibits the release of chemical mediators, such as leukotrienes or histamine from mast cells, was reported to be effective. We evaluated the values of leukotriene B4 and interleukin 6 in HD patients with pruritus and the effect of an anti-allergic drug on these factors. Leukotriene B4, interleukin-6, C3a, C5a, the number of eosinophil and IgE at 0, 15 and 180 minutes after the start of regular HD in 11 HD patients suffering from pruritus and as well as in 11 HD patients without pruritus were examined. These HD patients in both groups showed significantly higher (p < 0.001) values of leukotriene B4 and C3a compared to healthy non-HD subjects. There was no difference in the leukotriene B4, interleukin-6, IgE, C3a and C5a levels between the patients with and without pruritus. Two mg/day of azelastin hydrochloride, an anti-allergic drug was orally given to the pruritus group for 3 weeks. In 5 of 11 patients, the pruritus symptoms disappeared, while in 4 of 11 they improved. Independent of the effect of the drug on pruritus, leukotriene B4 levels significantly decreased compared with those before the administration of this drug in the pruritus group (p < 0.01). Interleukin 6, C3a, C5a and the number of eosinophils demonstrated no significant change. In conclusion, although azelastin hydrochloride was effective in treating pruritus and also suppressed leukotriene B4 levels in hemodialysis patients, the high leukotriene B4 activity itself did not seem to be related to the development of pruritus in these patients.

astelin pediatric dosage

It seems that all reported topical antihistamines and mast cell stabilisers reduce symptoms and signs of seasonal allergic conjunctivitis when compared with placebo in the short term. However, there is no long-term data on their efficacy. Direct comparisons of different antihistamines and mast cell stabilisers need to be interpreted with caution. Overall, topical antihistamines and mast cell stabilisers appear to be safe and well tolerated. We observed a large variability in outcomes reported. Poor quality of reporting challenged the synthesis of evidence.

astelin usual dosage

Nonallergic rhinitis patients exhibited increased blood flow to several regions of the brain in response to both pleasant and unpleasant odorants, specifically in odor-sensitive regions, while off intranasal azelastine. Treatment with intranasal azelastine significantly attenuated blood flow to regions of the brain relevant to either olfactory sensation or sensory processing in response to these odorants compared with fresh air.

astelin user reviews

Nonetheless, at least one double-blind, placebo-controlled multicenter trial has found that intranasal azelastine relieves symptoms of this disorder better than placebo. The mechanism responsible for its beneficial effect in nonallergic rhinitis is unclear but probably relates to "anti-inflammatory/antiallergic" activities.

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Azelastine nasal spray is a topical antihistamine with a distinctive taste that may be objectionable to some patients. The primary objectives of this clinical trial were (1) to determine if a reformulated azelastine nasal spray (Astepro) with sucralose as a taste-masking agent provides comparable efficacy to the original formulation (Astelin) and (2) to evaluate dose-response relationships between groups.

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Azelastine, a phthalazinone compound, is a second generation histamine H1 receptor antagonist which has shown clinical efficacy in relieving the symptoms of allergic rhinitis when administered as either an oral or intranasal formulation. It is thought to improve both the early and late phase symptoms of rhinitis through a combination of antihistaminic, antiallergic and anti-inflammatory mechanisms. Symptom improvements are evident as early as 30 minutes, after intranasal administration of azelastine [2 puffs per nostril (0.56mg)] and are apparent for up to 12 hours in patients with seasonal allergic rhinitis (SAR). The effect on nasal blockage is variable: in some studies objective and/or subjective assessment showed a reduction in blockage, whereas in other studies there was no improvement. Intranasal azelastine 1 puff per nostril twice daily is generally as effective as standard doses of other antihistamine agents including intranasal levocabastine and oral cetirizine, ebastine, loratadine and terfenadine at reducing the overall symptoms of rhinitis. The relative efficacies of azelastine and intranasal corticosteroids (beclomethasone and budesonide) remain unclear. However, overall, the corticosteroids tended to improve rhinitis symptoms to a greater extent than the antihistamine. Azelastine was well tolerated in clinical trials and postmarketing surveys. The most frequently reported adverse events were bitter taste, application site irritation and rhinitis. The incidence of sedation did not differ significantly between azelastine and placebo recipients and preliminary report showed cardiovascular parameters were not significantly altered in patients with perennial allergic rhinitis (PAR).

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astelin pediatric dosage 2015-12-30

A specific HPLC separation method was used to generate 14C metabolite profiles in lung, muscle, and liver tissue and in bile, urine, and feces obtained from male guinea pigs that received a single oral dose of 1 mg/kg [14C]azelastine. Profiles were also generated in urine and feces of animals that received a single iv dose of labeled drug. In lung and muscle tissue, azelastine (AZ) and desmethylazelastine (DAZ) were the major components buy astelin online of 14C radioactivity. The amount of the amino acid metabolites (2- and 7-ACID), formed by oxidation and azepinyl ring opening, was relatively small. In the liver significant amounts of the 7-ACID were observed in addition to AZ and DAZ. The major metabolite in bile, urine, and feces was the 7-ACID, with much less AZ and DAZ present. The balance of 14C in the form of AZ and three metabolites in excreta (percentage of dose) was: AZ, 9.7-10.5%; DAZ, 8.7-9.6%; 2-ACID, 2.9-3.0%; and 7-ACID, 43.0-54.6%. No large differences in the quantitative profile between the two dosing routes were observed.

astelin generic price 2017-02-23

Results indicated that oxatomide and ketotifen inhibit the production of leukotriene C4 and leukotriene B4 buy astelin online by inhibiting phospholipase A2 activity, whereas, azelastine inhibits the leukotriene C4 production by inhibiting phospholipase A2 and leukotriene C4 synthase.

astelin dosage information 2017-12-22

This was a 1-year, randomized, open-label, active-controlled, parallel-group study in subjects with chronic allergic or nonallergic rhinitis. A total of 612 subjects were randomized in a 2:1 ratio to (1) MP29-02, one spray buy astelin online per nostril twice daily (total daily doses of azelastine hydrochloride and FP were 548 mcg and 200 mcg, respectively); or (2) FP, 2 sprays per nostril once daily (total daily dose 200 mcg). Safety and tolerability assessments were made at months 1, 3, 6, 9, and 12.

astelin medication 2017-05-13

The use of various medications in chronic rhinitis in children is discussed. Evastin has been shown to eliminate histamine papules in 93% of cases and those caused by D. pteronyssinus in 68% of cases. After 10 days of treatment, conjunctival response decreased or disappeared in 80% of cases and buy astelin online nasal response decreased in 69%. Clinically, evastin was effective in 14 of 22 children and produced moderate effects in 2 and no effect in 6. There were no dropouts because of problems of tolerance. In a preliminary study of intranasal azelastin in 21 children with chronic allergic rhinitis, clinical improvement was significant. Various multicenter trials are reported, focusing on those using fluid budesonide. Both medications were effective in reducing symptoms and the antihistamine effect usually was earlier. There were no differences between medications as evaluated by nasal challenge or tolerance. Finally, budesonide was used in 13 patients for 4 months. Nasal obstruction and secretion improved, and rhinomanometry results improved significantly.

astelin usual dosage 2015-03-01

In this study we observed buy astelin online that both Azelastine HCl and cinnamaldehyde reduced allergic symptoms in an AR rat model. Cinnamaldehyde decreased vascular congestion as well as plasma cell, eosinophil, and inflammatory cell infiltration into the lamina propria.

astelin user reviews 2015-07-12

The antiallergic effects of Reitakutuukitokasin'i (RKS) on the increase in blood histamine level by antigen challenge were investigated in actively sensitized rats in comparison with those of azelastine and disodium cromoglycate (DSCG). The increase in blood histamine level after a systemic anaphylactic reaction elicited by intravenously injected antigen (egg albumin) was significantly inhibited by oral and intravenous administrations of RKS and azelastine or DSCG. Namely, RKS at 50 and 100 mg/kg (p.o.) caused 17% and 28% inhibition, respectively, and azelastine at 5 and 10 mg/kg (p.o.) caused 28% and 29% inhibition, respectively. RKS at 0.1 and 0.5 mg/kg (i.v.) caused 33% and 29% inhibition, respectively, and DSCG at 10 mg/kg (i.v.) caused 53% inhibition. However, large doses of RKS (500 mg/kg, p.o., 2.5 and 10 mg/kg, i.v.) caused no significant inhibition. The histamine release from rat peritoneal mast cells (RPMC) by antigen-antibody reaction was also investigated, and proved to be inhibited significantly by buy astelin online RKS. Namely, RKS at 5 x 10(-4), 10(-3) and 2 x 10(-3) g/ml caused 42, 71 and 79% inhibition, respectively. These results suggest that RKS is an antiallergic drug similar to azelastine and DSCG with a common inhibitory action on the release of histamine.

astelin patient reviews 2016-08-04

Sensory nerve endings within the airway epithelial cells and the solitary chemoreceptor cells, synapsing with sensory nerves, respond to airborne irritants. Transient receptor potential (TRP) channels (A1 and V1 subtypes, specifically) on these nerve endings initiate local antidromic reflexes resulting in the release of neuropeptides such as substance P and calcitonin G-related peptides. These neuropeptides dilate epithelial submucosal blood vessels and may therefore increase transudation across these vessels resulting in submucosal edema, congestion, and rhinitis. Altered expression or activity of these TRP channels can therefore influence responsiveness to irritants. Besides these pathogenic mechanisms, additional mechanisms such as dysautonomia resulting in diminished sympathetic activity and comparative parasympathetic overactivity have also been suggested as a probable mechanism. Therapeutic effectiveness for this condition has been demonstrated through desensitization of TRPV1 channels with typical agonists such as capsaicin. Other agents effective in treating nonallergic rhinitis (NAR) such as azelastine have been demonstrated to exhibit TRPV1 channel activity through the modulation of Ca(2+) signaling on sensory neurons and in nasal epithelial cells. Roles of antimuscarinic agents such as tiotropium in NAR have been suggested by associations of muscarinic cholinergic receptors with TRPV1. The associations between these channels have also been suggested as mechanisms of airway hyperreactivity in asthma. The concept of the united airway disease hypothesis suggests a significant association between rhinitis and asthma. This concept is supported by the development of late-onset asthma in about 10-40 % of NAR patients who also exhibit a greater severity in their asthma. The factors and mechanisms associating NAR with nonallergic asthma are currently unknown. Nonetheless, free immunoglobulin light chains buy astelin online and microRNA alteration as mediators of these inflammatory conditions may play key roles in this association.

astelin dosage adults 2016-07-06

Each of the 80 randomized patients completed the trial. Mean itching and conjunctival redness scores at visit 3 (onset) were significantly lower buy astelin online (P: < 0.001) in the AZE-treated eyes than in the placebo-treated eyes. At visit 4 (duration), mean itching and conjunctival redness scores (P:

astelin brand 2015-10-31

The study demonstrated that both azelastine and intranasal phototherapy are able to significantly improve TNSS, including individual nasal symptoms. Nevertheless, phototherapy reduced nasal obstruction better than azelastine (p= buy astelin online 0.038). Both treatments were highly effective in improving RQLQ scores overall and in seven separate domains.

astelin online pharmacy 2017-10-28

To determine whether anti-allergic drugs can inhibit autonomic neurotransmission of airway smooth muscle, we studied the effect of sodium cromoglycate (SCG, Intal) and related anti-allergic drugs on electrically induced neurogenic contractions of isolated guinea pig bronchial muscle. Electrical field stimulation (8 Hz, 0.5 msec, 30 V) evoked a biphasic contraction of bronchial muscle, consisting of an initial phasic component followed by a sustained one which was mediated by cholinergic and non-cholinergic nerve stimulations, respectively. Sodium cromoglycate, tranilast, ketotifen, and azelastine at concentrations higher than 10(-6) M caused a concentration-dependent inhibition in the height of the non-cholinergically mediated contractions. The cholinergically mediated contractions were also inhibited by tranilast, ketotifen, and azelastine but not by SCG. Submaximal contractions of bronchial muscle evoked by exogenous substance P (2 X 10(-7) M) were less potently buy astelin online inhibited by these drugs than those by exogenous acetylcholine (2 X 10(-6) M). These results indicate that in isolated guinea pig bronchial muscle, anti-allergic drugs may inhibit non-cholinergic neurotransmission mainly by prejunctional reduction of the transmitter release and partly by postjunctional depression of the response.

astelin review 2015-05-15

Azelastine intranasal spray reduces buy astelin online SP release into nasal lavage fluid of NAR patients immediately after hypertonic nasal saline challenge. Reduction of neuropeptide release may be an important aspect of the clinical efficacy of topical azelastine in perennial NAR patients.

astelin brand name 2016-10-13

In this study, it was presented that PAF and LTB4 exert a priming effect on PMNs to promote their superoxide anion production. PMNs preincubated with PAF of normal controls or PMNs from asthmatic patients are activated and buy astelin online their responsiveness to inhibitory stimuli such as antiallergic drugs and corticosteroid are attenuated. In conclusions, inflammatory cells of asthmatics may be activated by various mediators and play an important role in the progress of airway damage.

astelin medicine 2015-04-15

Twenty studies met the inclusion criteria: 4 pediatric, 16 adult/adolescent. There were 4 perennial AR studies (381 children, 1607 adults) and 16 seasonal AR trials (3081 children, 6548 adults). In these studies, 2451 subjects (481 children, 1970 adults) received an INCS, 3001 (1116 children, 1885 adults) received an INAH, and 346 adult subjects received MP-AzeFlu. All active treatments were well tolerated and effective as measured by the reduction in nasal symptoms. Head-to buy astelin online -head comparisons were only available for MP-AzeFlu versus the individual active agent components. MP-AzeFlu provided significantly greater symptom relief than either azelastine or fluticasone propionate alone and with an onset starting at 30 minutes after the dose.

astelin reviews 2016-03-29

Familial Mediterranean fever (FMF) is an inherited inflammatory disease occurring mainly in Mediterranean and Middle Eastern populations. FMF is caused by mutations in the MEFV gene that encodes pyrin/marenostrin. Here, we report a Japanese female FMF patient with heterozygosity for the compound pyrin E148Q/M694I showing recurrent fever, serositis or delay in skin wound healing. Her father and elder sister were heterozygous for pyrin variant M694I alone and sometimes suffered from mild fever or delay in wound healing, but her mother was heterozygous for pyrin variant E148Q alone and had no symptoms. This suggested that the inheritance of FMF occurred not only in an autosomal recessive manner but also in an autosomal dominant manner in this Japanese family, and the severity of the disease differed among the family members in relation to the mutation. In the treatment of FMF, colchicine, reserpine or prazosin hydrochloride have been reported to prevent the attacks, but, in our patient such drugs were buy astelin online ineffective or caused side effects, and only the anti-allergic drug azelastine was of benefit in relieving the attacks.

astelin generic brand 2017-04-12

The urticarias are a complex group of disorders characterised by transient whealing or swelling of the skin. Understanding the many possible causes is the first step in assessing urticaria. Allergic and drug-induced urticaria respond to removal of the cause. The physical urticarias, particularly delayed pressure urticaria and also urticarial vasculitis, require separate consideration. For the majority of patients with chronic idiopathic urticaria, nonsedating antihistamines are the mainstay of treatment. There are several to choose from, including cetirizine, astemizole, loratadine, terfenadine and acrivastine, each with its own pharmacokinetics and antiallergic properties. When these fail, histamine H2-antagonists may help either alone or in combination with H1-antagonists. Older sedative antihistamines are still useful. Ketotifen, oxatomide and azelastine have mast cell stabilising effects that are considered an advantage in treating these disorders. Second-line therapies include a wide range of drugs such as doxepin, dapsone, attenuated androgens, calcium antagonists, antimalarials, gold and methotrexate. The most effective and regularly used second-line agents are corticosteroids Lasix 20mg Tab . These are best limited to short term crisis management, except in severe recalcitrant cases, and in patients with pressure urticaria or urticarial vasculitis. Recent work on circulating histamine releasing autoantibodies suggests that there is scope for more aggressive immunosuppression in selected patients. However, effective treatment with immunosuppression often requires plasma exchange and more toxic agents such as cyclosporin. Such treatments are only likely to be entertained in exceptional cases.

astelin tablet 2015-11-26

This study has confirmed azelastine's histamine-blocking activity. In addition, the late-phase results suggest that azelastine has anti-inflammatory activity. The reproducibility and Paracetamol Lethal Dose sensitivity of the thermographic results confirm the usefulness of this technique in immunopharmacology.

astelin buy online 2016-08-17

We studied the effects of OKY-046 on type I allergic reactions. OKY-046 (100 mg/kg) given orally suppressed antigen-induced bronchoconstriction and TXB2 generation in broncho alveolar lavage fluid in rats passively sensitized with anti-DNP-As monoclonal IgE. At the dose of 30 mg/kg given intraduodenally, it also inhibited antigen-induced bronchoconstriction in guinea pigs passively sensitized with anti DNP-As serum and actively sensitized with ovalbumin. However, aspirin (30 mg/kg) didn't suppressed them significantly. Azelastine (10 mg/kg) inhibited bronchoconstriction in passively sensitized rats and actively sensitized guinea pigs. In 48 hour homologous PCA reactions of rats and mice, oral administration of Propecia I Mg OKY-046 (300 mg/kg) and tranilast (100 mg/kg) suppressed the extravasated dye in the skin. OKY-046 decreased histamine release from passively sensitized rat peritoneal exudate cells. There was no effect of OKY-046 on SRS-A and leukotriene release from actively sensitized guinea pig lungs and passively sensitized rats. In conclusion, we think that OKY-046 should be an useful asthmatic drug or anti-allergic drug by oral administration.

astelin spray dosage 2016-09-14

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 Buspar 600 Mg 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.

astelin generic 2017-03-02

Azelastine is a new oral antiasthma agent with bronchodilating and antiallergic properties. This 12-wk study compared azelastine (2, 4, 6, and 8 mg) and placebo given twice a day in asthmatics 12 to 60 yr of age requiring daily bronchodilator therapy. Patients were allowed albuterol aerosol, short-acting theophylline, and pseudoephedrine only as needed. The study was completed by 221 asthmatic subjects. No significant differences in symptoms, medication, or pulmonary function existed between groups at baseline. Analysis of the zero hour FEV1 before azelastine administration on eight occasions during the 12 wk of therapy indicated an increasing slope for azelastine 6 mg that was statistically different from that of placebo; similarly, the slope for azelastine 4 mg showed the same trend, but it did not reach statistical significance. All azelastine groups had significant reductions of as-needed medication after 1 wk; only in the 4-mg and 6-mg groups was this reduction sustained for 12 wk. Asthma symptom scores and peak expiratory flow measurements remained Augmentin 975 Mg stable in the azelastine groups despite significant reductions in concomitant medication administration. Side effects were minor and included: altered taste (30.1 to 51.9%), drowsiness (6.0 to 16.9%), and dry mouth (3.8 to 6.1%). The occurrence of these adverse events decreased with time throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

astelin tablets 2017-11-11

Effects of 4-(p-chlorobenzyl)-2-(hexahydro-1-methyl-1H-azepin-4-yl)-(2H)-phthalazinone hydrochloride (azelastine hydrochloride), a new antiallergic drug, on the gastrointestinal tract were experimentally studied in comparison with diphenhydramine and clemastine. In the isolated guinea pig ileum, the dose-response curve for histamine was shifted to the right by 10(-8) mol/l of diphenhydramine, clemastine or azelastine to the same degree. Clemastine and azelastine reduced the maximum response in the dose-response curve, while diphenhydramine caused a parallel shift. In addition to the potent antihistamine action, azelastine at higher dose antagonized serotonin action and clemastine markedly inhibited the contractile responses of isolated intestinal preparations to acetylcholine and bradykinin. Azelastine and clemastine (50 mg/kg intraduodenally) reduced gastric secretion in pylorus ligated rats. Azelastine (5 mg/kg i.v.), clemastine (1 mg/kg i.v.) and diphenhydramine (1 mg/lg i.v.) depressed gastrointestinal motility in conscious Lexapro Medication Reviews rats. Biliary and pancreatic secretions of anesthetized rats were not affected by 1 mg/kg i.v. of azelastine or clemastine.

astelin drug interactions 2017-06-27

The dissolution of infarcted myocardium occurs after Coumadin 20 Mg the infiltration of leukocytes. In the search for a mechanism of the leukocyte infiltration, we measured the production of lipoxygenase metabolites of arachidonic acid in the canine myocardium after ligation of the circumflex branch of the left coronary artery. At least 2 lipoxygenase products, namely 5- and 12-hydroxyeicosatetraenoic acids (HETEs), were augmented in myocardium subjected to ischemia lasting more than 6 hours, with levels of the latter being raised much more than the former. Augmentation of the HETEs in ischemic myocardium appeared to occur prior to any significant infiltration of leukocytes. More than 12 hours after coronary ligation, the infiltration of leukocytes became prominent and an increase in 12-HETE was observed. Calcium content in the infarcted myocardium appeared to be increased several hours before the increase in 12-HETE. These data suggest that the initial increment in 12-HETE may result from it being a product of infarcted myocardium, where Ca2+ is accumulated in the cell, and that the increased HETEs work as a leukocyte chemoattractant in infarcted myocardium. This hypothesis is supported by the independent experiment which showed that cultured cardiomyocytes produced lipoxygenase metabolites of arachidonic acid, including 12-HETEs etc, which exhibited neutrophil-chemoattractant activity when they were challenged by calcium ionophore and/or arachidonic acid. Azelastine-HCl, a lipoxygenase inhibitor, attenuated not only the above production of HETEs from the cardiomyocytes, but also production of HETEs and infiltration of neutrophils in ischemic myocardium, resulting in attenuation of the fibrous scar of infarcted myocardium.

astelin maximum dosage 2016-10-30

To investigate the mechanism by which azelastine may be effective therapeutically in asthma, we studied its ability to inhibit anti-IgE- and calcium ionophore A23187-stimulated histamine release from human lung and to alter lung cyclic nucleotide levels. Significant inhibition of histamine release from both anti-IgE- and A23187-stimulated human tissue was apparent after 30 minutes preincubation of the lung tissue in azelastine. Significant Cialis 120 Mg inhibition of anti-IgE-stimulated histamine release was consistently seen in azelastine concentrations greater than or equal to 5 microM, and was dose dependent (r = 0.71, p less than 0.05) with maximal mean inhibition of 53 +/- 11%. For A23187-stimulated lung tissue, consistent inhibition of histamine release was not found until we used 30 microM azelastine, mean 35 +/- 11%. Inhibition in azelastine concentrations below 30 microM was variable and not significant. Lung cyclic AMP and cyclic GMP content was not significantly altered by incubation of lung tissue in 100 microM azelastine. We conclude that azelastine inhibits stimulated histamine release from human lung tissue in vitro but does not alter cyclic nucleotide content.

astelin generic equivalent 2017-11-06

From cultures of thermophilic soil fungus Humicola grisea var thermoidea, a δ-lactam derivative (3-(2-(4-hydroxyphenyl)-2-oxoethyl)-5,6-dihydropyridin-2(1H)-one) that displayed anti-allergic activity was isolated, which was predicted by in silico computational chemistry approaches. The in vitro anti-allergic activity was investigated by β-hexosaminidase release assay in rat basophilic leukaemia RBL-2H3 cells. The δ-lactam derivative exhibited similar anti-allergic activity (IC Lanoxin Normal Dose (50) = 18.7 ± 6.7 µM) in comparison with ketotifen fumarate (IC(50) = 15.0 ± 1.3 µM) and stronger anti-allergic activity than azelastine (IC(50) = 32.0 µM). Also, the MTT cytotoxicity assay with RBL-2H3 cells showed that δ-lactam does not display cytotoxicity at concentrations lower than 50 µM. This study suggests that the δ-lactam derivative has the potential to be used as a lead compound in the development of anti-allergic drugs for clinical use in humans.

astelin cost 2015-01-29

Azelastine (1-300 microM) inhibited contractions of isolated porcine trachea induced by high K+, carbachol and endothelin-1 (ET-1) with a decrease in [Ca2+]cyt (as measured by fura-2-fluorescence). Verapamil (0.1-10 microM) also inhibited the high K(+)-induced increases in [Ca2+]cyt and contraction, although it only partially inhibited the responses evoked by carbachol or ET-1. In the absence of extracellular Ca2+ (with 0.5 mM EGTA), carbachol induced a transient increase in [Ca2+]cyt and force by releasing Ca2+ from cellular stores. Azelastine (100 microns) completely inhibited these contransient changes. In the absence of extracellular Ca2+, carbachol and 12-deoxyphorbol 13-isobutyrate (DPB) induced small sustained contractions without increasing [Ca2+]cyt. Azelastine inhibited these contractions. In muscle permeabilized with alpha-toxin, Ca2+ (0.3-3 microM) induced contraction in a concentration-dependent manner. DPB (without GTP) and carbachol or ET-1 (with GTP) enhanced the Ca(2+)-induced contraction. Azelastine partially inhibited the contraction induced by 0.3 microM Ca2+ but not the contraction induced by 3 microM Ca2+, and strongly inhibited the potentiating Protonix 100 Mg effects of DPB, carbachol and ET-1. Azelastine had no effect on the content of cyclic AMP or cyclic GMP. These results suggest that azelastine inhibits smooth muscle contraction by (i) decreasing [Ca2+]cyt, by inhibition of Ca2+ channels, (ii) decreasing agonist-induced Ca2+ release, and (iii) direct inhibition of contractile elements.

astelin alcohol 2015-07-11

Three hundred seven patients were randomized to treatment, and 299 completed 2 weeks of study treatment. The age of the population ranged from 12 to 74 years (mean, 35 years), 62.9% were female, and 69.6% were white. Over 2 weeks of treatment, both groups had significant improvements in the TNSS compared with baseline (P < 0.001). The overall change in TNSS was significantly greater with azelastine nasal spray compared with cetirizine (29.3% vs 23.0% improvement, respectively; P = 0.015). In terms of onset of action, azelastine nasal spray significantly improved the instantaneous TNSS compared with cetirizine at 60 and 240 minutes after the initial dose (both, P = 0.040). Scores on each domain of the RQLQ were significantly Astelin Brand Name improved in both groups compared with baseline (P < 0.001); the overall RQLQ score was significantly improved with azelastine nasal spray compared with cetirizine (P = 0.049). Both treatments were well tolerated.

astelin pediatric dose 2016-08-22

The authors have studied the effect of azelastine nasal spray in the treatment of seasonal allergic rhinitis. The trial was a double-blind, placebo controlled study, with 33 allergic subjects (17 female, 16 male), 15-40 years old. The patients were randomized into two parallel groups, to receive daily 0.56 mg of azelastine intranasally or placebo during two weeks. Before and after treatment severity of nasal symptoms such as: sneezing, itching, nasal blockage, nasal discharge and general feeling were evaluated by patients according to VAS (visual analogue scale). At the same time the physician's evaluation of nasal oedema, nasal discharge and general patient's condition were performed (VAS). Additionally during the treatment patients noted possible adverse events. Patient's and physician's evaluations showed clinical efficacy in the azelastine group and no evident efficacy in the placebo group--between those two groups statistical significances were noted for all evaluated parameters (p < 0.001). The bitter taste in the mouth was the only serious side effect in some patients in azelastine group, although this was quite well accepted. Generally the treatment was well-tolerated. Azelastine nasal spray is an effective and well-tolerated drug in the treatment of seasonal allergic rhinitis.

astelin generic otc 2017-07-16

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.

astelin dosage 2016-09-23

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.

astelin dosing 2017-05-19

The antipruritic and vascular permeability-inhibitory effects of ginsenoside Rb1, a main component of ginseng frequently used as a traditional medicine in Asian countries, and its metabolite compound K by intestinal microflora were investigated in scratching behavior animal models induced by compound 48/80, substance P, and histamine. Ginsenoside Rb1 and compound K orally administered 1 and 6 h before the treatment of compound 48/80 showed antipruritic effect. These ginsenosides administered at a dose of 50 mg/kg 6 h before the treatment of compound 48/80 inhibited scratching behaviors by 51% and 64%, respectively, compared with that of the control. These ginsenosides also inhibited the vascular permeability of skin. Compound K intraperitoneally administered 1 h before the treatment of compound 48/80 potently inhibited the scratching behaviors induced by compound 48/80. However, intraperitoneally administered ginsenoside Rb1 did not inhibit scratching behaviors. Compound K inhibited compound 48/80-, substance P-, and histamine-induced scratching behaviors, with 50% inhibitory doses of 4.2, 5.9, and 3.8 mg/kg, respectively, and vascular permeability, with 50% inhibitory doses of 5.8, 6.8, and 4.1 mg/kg, respectively. These results suggest that ginsenoside Rb1 and its metabolite compound K by intestinal microflora can improve scratching behaviors.