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Singulair (Montelukast)

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Singulair is a high-quality medication which is used to treat symptoms of asthma. It can also be used to treat symptoms of perennial and seasonal allergic rhinitis. Sometimes Singulair is taken to prevent exercise-induced bronchoconstriction in patients who take this medicine only for this condition.

Other names for this medication:
Aeron, Airlukast, Airon, Asmalair, Asmenol, Astecon, Astmirex, Brolukat, Brondilat, Cerrokast, Drimon, Ephyra, Inmunokast, Inuvic, Kastair, Kipres, Leucotren, Leukast, Lukasm, Lukast, Lukastab, Lumona, Luxat, M-kast, Mokast, Molly, Molus, Monas, Monkast, Monkasta, Monocast, Montair, Montegen, Montegen orifarm, Montek, Montelukast, Montelukastum, Montene, Montiget, Monukast, Nor-vento, Notta, Onceair, Profilax, Promonta, Provair, Reokast, Reversair, Rhinosingulair, Ventek, Ventilar, Xalar, Zespira

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Also known as:  Montelukast.


Target of Singulair is to treat symptoms of asthma, perennial and seasonal allergic rhinitis. Sometimes Singulair is taken to prevent exercise-induced bronchoconstriction in patients who take this medicine only for this condition.This remedy works by obstructing the activity of substances which cause symptoms of allergy and asthma. It is LTRA (leukotriene receptor antagonist).

Singulair is also known as Montelukast sodium, Montair, Montus, Romilast.


Take Singulair chewable tablets (4 mg, 5 mg, 10 mg), granules, film-coated tablets orally with water.

Usually Singulair is taken as a single dose at least two hours before you exercise. Do not take another dose of Singulair for at least 24 hours.

Usually Singulair is taken once a day in the evening with or without food.

Do not take Singulair for asthma attack treatment that has already begun.

If you want to achieve most effective results do not stop taking Singulair suddenly.


If you overdose Singulair and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Singulair overdosage: stomach pain, agitation, insomnia, thirst, migraine, vomiting.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep this medicine in the original bottle. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Singulair 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 Singulair if you are allergic to its components or to aspirin.

Do not take Singulair if you use Singulair while you are pregnant or have nurseling.

You should not use Singulair for exercise-induced bronchoconstriction if you already take Singulair to prevent symptoms of allergy or asthma.

Try to be careful using Singulair if you take phenobarbital (such as Solfoton, Luminal), rifampin (such as Rifamate, Rifadin, Rimactane, Rifater).

It can be dangerous to use Singulair if you suffer from or have a history of phenylketonuria, liver disease.

Avoid any activities such as driving or operating machinery while taking Singulair.

It can be dangerous to stop Singulair taking suddenly.

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Open-label, cross-over, single-centre trial. Twenty-four 6 to 18-year-old children and adolescents, with reversible and stable airway obstruction, baseline FEV1 > or = 70%, predicted and proven EIA (i.e. a maximum decrease of FEV1 by > or = 20% compared with baseline) were treated with MON, orally for 3 days in the evening, or one single inhalation of DSCG/REP 20 min before the exercise challenge. The treatment sequence was randomised. The exercise test on a treadmill was performed under standardised conditions.

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Analysis of data from a placebo-controlled, cross-over study in which combination preventive therapy was demonstrated to be superior in reducing both early and late allergen-induced inflammatory response when compared with placebo and each component.

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Montelukast therapy was associated with less air trapping, hyperinflation, and Raw and better Sgaw compared with placebo. Lower serum ECP levels, a surrogate measure of airway inflammation, were associated with improvements in lung function.

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Cold urticaria is characterized by the development of urticaria, usually superficial and/or angioedematous reaction after cold contact. It was found predominantly in young women. The diagnosis is based on the history and ice cube test. Patients with a negative ice cube test may have represented systemic cold urticaria (atypical acquired cold urticaria) induced by general body cooling. The pathogenesis is poorly understood. Cold urticaria can be classified into acquired and familial disorders, with an autosomal dominant inheritance. Idiopathic cold urticaria is most common type but the research of a cryopathy is necessary. Therapy is often difficult. It is essential that the patient be warned of the dangers of swimming in cold water because systemic hypotension can occur. H1 antihistamines can be used for treatment of cold urticaria but the clinical responses are highly variable. The combination with an H2 antagonists is more effective. Doxepin may be useful in the treatment. Leukotriene receptor antagonists may be a novel, promising drug entity. In patients who do not respond to previous treatments, induction of cold tolerance may be tried.

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Asthma patients who continue to experience symptoms despite taking regular inhaled corticosteroids represent a management challenge. Leukotrienes play a key role in asthma pathophysiology, and since pro-inflammatory leukotrienes are poorly suppressed by corticosteroids it seems rational to add a leukotriene receptor antagonist (LTRA) when a low to moderate dose of inhaled corticosteroids does not provide sufficient disease control. Long acting beta2-agonist (LABA) treatment represents an alternative to LTRAs and both treatment modalities have been shown to provide additional disease control when added to corticosteroid treatment. To compare the relative clinical benefits of adding either a LTRA or a LABA to asthma patients inadequately controlled by inhaled corticosteroids, a randomized, double-blind, multi-centre, 48-week study will be initiated at approximately 120 centres throughout Europe, Latin America, Middle East, Africa and the Asia-Pacific region in early 2000. The study will compare the oral LTRA montelukast with the inhaled LABA salmeterol, each administered on a background of inhaled fluticasone, on asthma attacks, quality of life, lung function, eosinophil levels, healthcare utilization, and safety, in approximately 1200 adult asthmatic patients. The requirements for study enrollment include a history of asthma, FEV1 or PEFR values between 50% and 90% of the predicted value together with > or = 12% improvement in FEV1 after beta-agonist administration, a minimum pre-determined level of asthma symptoms and daily beta-agonist medication. The study will include a 4-week run-in period, during which patients previously taking inhaled corticosteroids are switched to open-label fluticasone (200 microg daily), followed by a 48-week double-blind, treatment period in which patients continuing to experience abnormal pulmonary function and daytime symptoms are randomized to receive montelukast (10 mg once daily) and salmeterol placebo, or inhaled salmeterol (100 microg daily) and montelukast placebo. All patients will continue with inhaled fluticasone (200 microg daily). During the study, asthma attacks, overnight asthma symptoms, and morning peak expiratory flow rate will be assessed using patient diary cards; quality of life will also be assessed using an asthma-specific quality-of life questionnaire. The results of this study are expected to provide physicians with important clinical evidence to help them make a rational and logical treatment choice for asthmatic patients experiencing breakthrough symptoms on inhaled corticosteroids.

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Montelukast and Hypericum perforatum significantly reduced malondialdehyde levels and increased glutathione levels compared to the I/R group (P < 0.008). A statistically significant difference was also found between the I/R group and MIR and HPIR groups in terms of myelqperoxidase levels (P < 0.008). The MIR and HPIR groups showed increased cardiotrophin- 1 levels compared to the control and I/R groups (P < 0.008 for all). The MIR and HPIR groups showed significantly lower histological scores compared to the I/R group (P = 0.03 and P = 0.007, respectively).

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Sixty subjects were recruited and 54 completed the study. The treatment groups were well matched for disease severity at baseline (SASSAD scores were 25 and 29 in the montelukast and placebo groups, respectively). There were no significant differences between the treatment groups in any of the parameters used to assess treatment response. The improvement in mean SASSAD score from baseline (visit 2) to the end of treatment was marginally superior in the placebo group, 1.41 points on montelukast vs. 1.76 on placebo, a difference of 0.35 (95% confidence interval -6.1 to 6.8). Adverse events were generally of a mild nature except for a brief septicaemic illness in one subject receiving montelukast.

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Montelukast is a potent cysteinyl leukotriene-1 receptor antagonist possessing some anti-inflammatory effects although the molecular mechanism of these anti-inflammatory effects is unknown. In this study, we aimed to investigate the effect of montelukast on nuclear factor (NF)-kappaB-associated histone acetylation activity in phorbol myristate acetate (PMA)-differentiated U937 cells.

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Airway remodeling in bronchial asthma results from chronic, persistent airway inflammation. The effects of the reversal of airway remodeling by drug interventions remain to be elucidated. We investigated the effects of ONO-1301, a novel prostacyclin agonist with thromboxane inhibitory activity, on the prevention and reversibility of airway remodeling in an experimental chronic asthma model. Mice sensitized and challenged to ovalbumin (OVA) three times a week for 5 consecutive weeks were administered ONO-1301 or vehicle twice a day from the fourth week of OVA challenges. Twenty-four hours after the final OVA challenge, airway hyperresponsiveness (AHR) was assessed, and bronchoalveolar lavage was performed. Lung specimens were excised for staining to detect goblet-cell metaplasia, airway smooth muscle, and submucosal fibrosis. Mice administered ONO-1301 showed limited increases in AHR compared with mice administered the vehicle. The histological findings of airway remodeling were improved in ONO-1301-treated mice compared with vehicle-treated mice. Presumably, these therapeutic effects of ONO-1301 are attributable to the up-regulation of production of hepatocyte growth factor (HGF) in lung tissue, because the neutralization of HGF by antibodies prevented the effects of ONO-1301 on AHR and airway remodeling. Mice administered ONO-1301 showed similar levels of AHR and airway remodeling as mice administered montelukast, a cysteinyl-leukotriene-1 receptor antagonist, and lower levels were observed in mice administered dexamethasone. These data suggest that ONO-1301 exerts the effect of reversing airway remodeling, at least in part through an elevation of HGF in the lungs, and may be effective as an anti-remodeling drug in the treatment of asthma.

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Lung parenchymal strips isolated from ovalbumin-sensitized rats manifest a mast cell-dependent, biphasic contraction when challenged with allergen. The first phase is mediated by the release of preformed 5-HT while the second phase is dependent on de novo synthesis of leukotrienes. Sphingosine 1-phosphate (S1P) is a sphingolipid metabolite which is readily generated in mast cells and has been demonstrated to be an important regulator of allergen-induced mast cell activation. We have used the parenchymal strip to explore the role of sphingosine 1-phosphate and the S1P(2) receptor in the two components of the acute response to allergen. Lung parenchymal strips were prepared from Brown Norway rats actively sensitized to ovalbumin. The strips were set up in organ baths and contractile responses measured isometrically. The inhibitors of sphingosine kinase, D-erythro-NN-dimethylsphingosine (dimethylsphingosine) and 4-[4-(4-chloro-phenyl)-thiazol-2-ylamino]-phenol (SKI-II) inhibited concentration-dependently both phases of the contractile response induced by 0.1 microg ml(-1) ovalbumin. The effects were seen at concentrations similar to those which inhibit the purified enzyme and were selective in that neither the contractile response to adenosine nor that to 5-hydroxytryptamine was affected. JTE-013 (a selective S1P(2) receptor antagonist) also blocked the response to ovalbumin (0.1 microg ml(-1)). However, the concentrations of JTE-013 required (microM) were substantially higher than its affinity for the S1P(2) receptors (nM). However, when tested against a lower concentration of ovalbumin (0.03 microg ml(-1)), JTE-013 inhibited the response with nM potency. These data demonstrate the importance of S1P and the S1P(2) receptor as regulators of allergen-induced activation of mast cells in their natural environment in the rat lung.

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Chronic liver disease is characterized by inflammation and fibrosis. Angiogenesis which leading to new vasculature may have prognostic value in disease progression. This study examined the implication of 5-lipoxygenase pathway and angiogenic factors in hepatic fibrosis progression and whether, the inhibition of arachidonic acid cascade product (cysteinyl leukotrienes) can represent a potential target for therapy. Cholestasis and subsequent fibrosis was induced by common bile duct ligation and resection (BDL) for 5 weeks in rats. After surgery, Cysteinyl leukotrienes antagonist (montelukast) was orally and daily administrated (10 mg/kg) for 34 days. Sham operated and drug control groups received either saline or montelukast immediately after operation. BDL significantly increased liver hydroxyproline (Hp), nuclear factor kappa B (NF-(k )ss), transforming growth factor beta (TGF-ss), tissue inhibitor metalloproteinase (TIMP-1), vascular endothelial growth factor (VEGF), and reduced the level of matrix metalloproteinase 9 (MMP-9). On the other hand, montelukast treatment reversed all these biochemical parameters and ameliorated histopathological changes which previously induced by BDL. Findings of the present study suggest that montelukast treatment may favor collagenolytic activity through modulating hepatic expression of TGFss-, NF-(k)ss, and MMP-9/TIMP-1 ratio. Amelioration of necroinflammatory liver injury and fibrogenesis may support such assumption.

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Nasal AEC were collected by brushings from subjects with a history of stable (no exacerbations or change in medication for ≥ 1 month) physician confirmed mild/moderate asthma whose asthma symptoms were documented to benefit from Diflucan Dosing Uti Montelukast treatment (NCT01230437). Release of the following mediators by nasal AEC were measured: IL-8, IL-6, IL-10, GM-CSF, RANTES, eotaxin and IFN-γ. Nasal AEC were cultured before and one week after withdrawal of their Montelukast treatment.

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Montelukast sodium (Singulair, Merck) is a selective and orally-active leukotriene-receptor antagonist (LTRA) that inhibits the cysteinyl leukotriene 1 (CysLT1) receptor. Montelukast is Xenical Online Usa an effective and well-tolerated preventative treatment for asthma and allergic rhinitis in adults and children. The upper and lower airway show similar inflammatory responses to allergen challenge. Leukotrienes are inflammatory mediators that are known as the slow-reacting substance of anaphylaxis produced by a number of cell types including mast cells, eosinophils, basophils, macrophages and monocytes. Synthesis of these mediators results from the cleavage of arachidonic acid in cell membranes and they exert their biological effects by binding and activating specific receptors. This occurs in a series of events that lead to contraction of the human airway smooth muscle, chemotaxis and increased vascular permeability. These effects have led to their important role in the diseases of asthma and allergic rhinitis. As these agents lead to the production of symptoms in patients that are asthmatic or allergic, the use of LTRAs, particularly montelukast, may seem appropriate. Clinical trials have shown that montelukast is effective and safe in the treatment of patients with asthma, allergic rhinitis or both diseases.

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Montelukast seems be a very useful product in the treatment of the bronchial asthma in children since generates a Daily Valtrex Cost saving of corticoids and longtime beta 2 in the mild or moderate asthma, associate or not with the inmunoterapia.

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To evaluate the Epivir 10 Mg treatment outcomes of leukotriene receptor antagonists (LTRA) as monotherapy or combined with the second-generation oral H1-histamines in the treatment of allergic rhinitis (AR), and to provide a basis for optimizing clinical therapeutic strategies.

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In all, 107 patients completed the trial medication. At the end of 4 weeks, the UAS score Epivir Mg as a response to treatment was 23.3% for Group A, 63.3% for Group B, 53.3% for Group C, and no real change for the placebo treatment group.

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In this study, the perceptions of asthmatics to change in their disease was associated with observed changes in clinical asthma measures, in order to identify the threshold Altace Drug Interactions where changes in clinical asthma measures are perceivable by patients. The study included 281 asthmatic patients, aged 18-63 yrs, in a randomized, placebo-controlled clinical trial of a leukotriene antagonist. Changes were related in: 1) asthma symptom scores; 2) inhaled beta-agonist use; 3) forced expiratory volume in one second (FEV1); and 4) peak expiratory flow (PEF) to a global question that queried overall change in asthma since starting the study drug. Additional analyses examined differences in the group reporting minimal improvement by treatment (active treatment versus placebo), sex and age groups. The average minimal patient perceivable improvement for each measure was: 1) -0.31 points for the symptom score on a scale of 0-6; 2) -0.81 puffs x day(-1) for inhaled beta-agonist use; 3) 0.23 L for FEV1; and 4) 18.79 L x min(-1) for PEF. In general placebo-treated patients and older patients, who reported minimal improvement, experienced less mean improvement from baseline than active-treated patients and younger patients, who reported minimal improvement. Determining the minimal patient perceivable improvement value for a measure may be helpful to interpret changes. However, interpretation should be carried out cautiously when reporting a single value as a clinically important change.

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To analyze the trend of use of new drugs for the treatment of chronic obstructive pulmonary disease in primary Omnicef O Tab care of Madrid (Spain) between 1996 and 2005, and to evaluate its impact in terms of supply, use and costs.

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Predictors of a larger placebo response were generally markers of less severe asthma and/or EIB. This may be related to EIB variability, spontaneous improvement, or the extent of placebo response relative to the outcomes in less severe patients.

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A simple, semi-automated, protein precipitation assay for the determination of montelukast (SINGULAIR, MK-0476) in human plasma has been developed. Montelukast is a potent and selective antagonist of the cysteinyl leukotriene receptor used for the treatment of asthma. A Packard MultiPROBE II EX is used to transfer 300 microl of plasma from sample, standard, and QC sample tubes to a microtiter plate (96-well). After addition of the internal standard by a repeating pipettor, a Tomtec QUADRA 96 adds 400 microl of acetonitrile to all plasma sample wells, simultaneously, in the microtiter plate. The Tomtec is also used to transfer the acetonitrile supernatant from the plasma protein precipitation step, batchwise, to another microtiter plate for analysis by HPLC with fluorescence detection. This assay has been validated and implemented for a clinical study of over 1300 plasma samples and is comparable to manual assays in the LLOQ (lower limit of quantitation, 3 ng/ml) and in stability. This is the first semi-automated protein precipitation assay published for the analysis of montelukast in human plasma and it results in significant time savings over the manual methods, both in sample preparation and in HPLC run time.

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Eosinophilic esophagitis (EE) is a clinicopathologic syndrome comprising isolated eosinophilic inflammation of the esophagus, with symptoms of dysphagia, and possibly, reflux. It was initially described in children, and in recent years, there is a heightened awareness in adults. The etiology is not completely understood. The treatments include dietary manipulation, topical corticosteroids, systemic corticosteroids, Montelukast, and endoscopic dilation. In adults, there are no randomized trials demonstrating the efficacy of any particular treatment, and no prospective studies describing the natural history of the disease following treatment.

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Aspirin-induced asthma is a challenging issue. Rhinitis is a major feature of discomfort. Following montelukast administration, we noted an improvement in the QOL and rhinitis subjective parameters, and an objective improvement in spirometrical measurements and in the doses of oral corticosteroids.

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These results confirm that LTD4 directly induces activation of eosinophils via the cysLT1 receptor. Furthermore, the results suggest that a beta2-agonist has no effect on eosinophil adhesion and activation induced by cysLTs. These results explain the differential effects of an LTRA and a beta2-agonist in the treatment of eosinophilic inflammation in asthma.