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1.
Anti-inflammatory medications for the treatment of pediatric obstructive sleep apnea.
Kuhle, S, Urschitz, MS
Paediatric respiratory reviews. 2020;:35-36
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2.
Efficacy of Montelukast in Allergic Rhinitis Treatment: A Systematic Review and Meta-Analysis.
Krishnamoorthy, M, Mohd Noor, N, Mat Lazim, N, Abdullah, B
Drugs. 2020;(17):1831-1851
Abstract
BACKGROUND In treating allergic rhinitis, montelukast has the potential to be used as an alternative or addition to an oral antihistamine or intranasal corticosteroid. OBJECTIVE The objective of this systematic review was to assess the effectiveness of montelukast in treating allergic rhinitis. METHODS An electronic literature search was performed using the Cochrane Central Register of Controlled Trials, EMBASE, and MEDLINE from 1966 to 21 January 2019. The eligibility criteria were randomized controlled trials comparing montelukast with placebo or other standard treatments. The primary outcomes assessed were daytime nasal symptom score (DNS) and night-time nasal symptom score (NNS). The secondary outcomes assessed were composite nasal symptom score (CSS), daytime eyes symptom score (DES), and rhinoconjunctivitis quality-of-life questionnaires (RQLQ). The meta-analysis was conducted using Review Manager 5.3 software based on the random-effects model. RESULTS Fifteen studies of 10387 participants met the inclusion criteria. Montelukast was more effective than placebo in improving DNS (mean difference [MD] - 0.12, 95% confidence interval [CI] - 0.15 to - 0.08; p < 0.001), NNS (MD - 0.09, 95% CI - 0.13 to - 0.05; p < 0.001), CSS (MD - 0.08, 95% CI - 0.11 to - 0.06; p < 0.001), DES (MD - 0.17, 95% CI - 0.33 to - 0.02; p < 0.030), and RQLQ (MD - 0.34, 95% CI - 0.49 to - 0.20; p < 0.001). Oral antihistamine was superior to montelukast in improving DNS (MD 0.08, 95% CI 0.03-0.13; p = 0.002), CSS (MD 0.03, 95% CI - 0.02 to 0.07; p = 0.27), DES (MD 0.06, 95% CI 0-0.12; p = 0.040), and RQLQ (MD 0.03, 95% CI - 0.05 to 0.12; p = 0.430). Montelukast was superior to oral antihistamine in improving NNS (MD -0.03, 95% CI - 0.08 to 0.03; p = 0.330). Intranasal fluticasone spray was superior to montelukast in improving DNS (MD 0.71, 95% CI 0.44-0.99; p < 0.001) and NNS (MD 0.63, 95% CI 0.29-0.97; p < 0.001). Combined montelukast and oral antihistamine was superior to oral antihistamine in improving DNS (MD - 0.15, 95% CI - 0.27 to - 0.03; p = 0.010), NNS (MD - 0.16, 95% CI - 0.28 to - 0.05; p = 0.006), CSS (MD - 0.12, 95% CI - 0.25 to - 0.01; p = 0.070), DES (MD - 0.12, 95% CI - 0.30 to 0.06; p = 0.180), and RQLQ (MD - 0.10, 95% CI - 0.28 to 0.08; p = 0.290). Combined montelukast and OAH was superior to montelukast in improving DNS (MD 0.15, 95% CI 0.08-0.21; p < 0.001), NNS (MD 0.05, 95% CI - 0.09 to 0.19; p = 0.510), CSS (MD 0.1, 95% CI 0.03-0.17; p = 0.007), DES (MD 0.18, 95% CI 0-0.36; p = 0.050), and RQLQ (MD 0.07 95% CI - 0.15 to 0.29; p = 0.530). CONCLUSIONS Montelukast is more effective than placebo in treating the overall symptoms of allergic rhinitis while the combined therapy of montelukast and an oral antihistamine is superior to either montelukast or an oral antihistamine alone.
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3.
Airway mechanics after withdrawal of a leukotriene receptor antagonist in children with mild persistent asthma: Double-blind, randomized, cross-over study.
Kim, JH, Lee, S, Shin, YH, Ha, EK, Lee, SW, Kim, MA, Yoon, JW, Baek, HS, Choi, SH, Han, MY
Pediatric pulmonology. 2020;(12):3279-3286
Abstract
BACKGROUND To determine the response of airway mechanics and the changes in asthma symptoms to stepping down of leukotriene receptor antagonist (LTRA) therapy. METHODS Thirty children (mean age: 7.1 years) with mild, well-controlled, and persistent asthma who took LTRA as maintenance treatment were randomized into a double-blind, placebo-controlled, cross-over study. Each group received an LTRA (montelukast) or placebo daily for 2 weeks, followed by a 1-week washout period, and then the alternate treatment for 2 weeks. Spirometry and impulse oscillation system (IOS) measurements before and after four puffs of salbutamol inhalation, fractional exhaled nitric oxide (FeNO), and the childhood asthma control test (C-ACT) were evaluated at baseline, the end of placebo treatment, and the end of LTRA treatment. RESULTS Changes of FEV1 /FVC (p = .113) and FEV1 (p = .109) from baseline to posttreatment did not differ significantly between the placebo and montelukast groups. In the placebo group, prebronchodilator (pre-) FEV1 /FVC was decreased (83% vs. 86%) and bronchodilator response (BDR) in FEV1 was diminished (10.7% vs. 6.4%) at posttreatment compared with baseline. However, the montelukast group had no significant changes in pre-FEV1 /FVC (p = .865) and BDR in FEV1 (p = .461). In addition, compared with the montelukast group, the placebo group showed no significant changes in Rrs5 (total airway resistance), Rrs5-20 (peripheral airway resistance), FeNO, and symptoms by the C-ACT. CONCLUSION In children with well-controlled mild persistent asthma, changes in spirometry, IOS, FeNO, and C-ACT results did not differ between the placebo and montelukast groups within 2 weeks.
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4.
Effect of montelukast combined with methylprednisolone for the treatment of mycoplasma pneumonia.
Wu, H, Ding, X, Zhao, D, Liang, Y, Ji, W
The Journal of international medical research. 2019;(6):2555-2561
Abstract
OBJECTIVE To study the effect of the leukotriene receptor agonist montelukast combined with methylprednisolone on inflammatory response and peripheral blood lymphocyte subset content in children with mycoplasma pneumonia. METHODS Seventy-four children were enrolled and randomly divided into a standard treatment group and a montelukast plus methylprednisolone group. Serum levels of inflammatory cytokines and corresponding cytokines of T lymphocyte subsets were measured, and peripheral blood was collected to determine the T cell subset content. RESULTS At 3 days and 7 days after treatment, serum MCP-1, PCT, ICAM-1, CXCL8, CRP, IFN-γ, and IL-17 levels and peripheral blood Th1 and Th17 content were significantly decreased in both groups, while serum IL-4 and TGF-β levels and peripheral blood Treg and Th2 content were significantly increased. However, serum MCP-1, PCT, ICAM-1, CXCL8, CRP, IFN-γ, and IL-17 levels and peripheral blood Th1 and Th17 content were significantly lower while serum IL-4 and TGF-β levels and peripheral blood Treg and Th2 content were significantly higher in the montelukast plus methylprednisolone group compared with the control group. CONCLUSION Montelukast combined with methylprednisolone for the treatment of mycoplasma pneumonia can inhibit inflammatory responses and regulate levels of Th1/Th2 and Th17/Treg cells.
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5.
Combination therapy with montelukast and loratadine alleviates pharyngolaryngeal symptoms related to seasonal allergic rhinitis.
Imoto, Y, Takabayashi, T, Sakashita, M, Tokunaga, T, Morikawa, T, Ninomiya, T, Okamoto, M, Narita, N, Fujieda, S
The journal of allergy and clinical immunology. In practice. 2019;(3):1068-1070.e3
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6.
Mast Cell Activation Syndrome and Mastocytosis: Initial Treatment Options and Long-Term Management.
Castells, M, Butterfield, J
The journal of allergy and clinical immunology. In practice. 2019;(4):1097-1106
Abstract
Patients with clonal mast cell activation syndromes (MCAS) including cutaneous and systemic mastocytosis (SM) may present with symptoms of mast cell activation, but in addition can have organ damage from the local effects of tissue infiltration by clonal mast cells. Patients with nonclonal MCAS may have chronic or episodic mast cell activation symptoms with an increase in serum tryptase and/or urinary metabolites of histamine, prostaglandin D2, and leukotrienes. Symptoms of MCAS and SM can be managed by blockade of mediator receptors (H1 and H2 antihistamines, leukotriene receptor blockade), inhibition of mediator synthesis (aspirin, zileuton), mediator release (sodium cromolyn), anti-IgE therapy, or a combination of these approaches. Acute episodes of mast cell activation require epinephrine, and prolonged episodes may be addressed with corticosteroids. Patients with clonal mast cell syndromes may need a reduction in the number of mast cells to prevent severe symptoms including anaphylaxis and/or progression to aggressive diseases.
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7.
Asthma pharmacotherapy: an update on leukotriene treatments.
Trinh, HKT, Lee, SH, Cao, TBT, Park, HS
Expert review of respiratory medicine. 2019;(12):1169-1178
Abstract
Introduction: Asthma is a chronic inflammatory disease of the airways with a large heterogeneity of clinical phenotypes. There has been increasing interest regarding the role of cysteinyl leukotriene (LT) and leukotriene receptor antagonists (LTRA) in asthma treatment.Areas covered: This review summarized the data (published in PubMed during 1984-2019) regarding LTRA treatment in asthma and LTs-related airway inflammation mechanisms. Involvement of LTs C4/D4/E4 has been demonstrated in the several aspects of airway inflammation and remodeling. Novel pathways related to LTE4, the most potent mediator, and its respective receptors have recently been studied. Antagonists against cysteinyl leukotriene receptor (CysLTR) type 1, including montelukast, pranlukast and zafirlukast, have been widely prescribed in clinical practices; however, some clinical trials have shown insignificant responses to LTRAs in adult asthmatics, while some phenotypes of adult asthma showed more favorable responses to LTRAs including aspirin-exacerbated respiratory disease, elderly asthma, asthma associated with smoking, obesity and allergic rhinitis.Expert opinion: Further investigations are needed to understand the role of LTs in airway inflammation and remodeling of the asthmatic airways. There is a lack of biomarkers to predict responsiveness to LTRA, especially in adult asthmatics. Besides CysLTR1 antagonists, targets aiming other LT pathways should be considered.
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8.
Effects of Medical Therapy on Mild Obstructive Sleep Apnea in Adult Patients.
Smith, DF, Sarber, KM, Spiceland, CP, Ishman, SL, Augelli, DM, Romaker, AM
Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2019;(7):979-983
Abstract
STUDY OBJECTIVES Patients with obstructive sleep apnea (OSA) have been shown to have high levels of inflammatory markers. Anti-inflammatory treatment with montelukast and intranasal steroids have demonstrated efficacy for mild OSA in children; this has not been fully evaluated in adults. This study investigated the response of mild OSA in adults to anti-inflammatory medical therapy. METHODS Adults aged ≥ 21 years with an apnea-hypopnea index (AHI) ≤ 15 events/h on polysomnography (PSG) were recruited to a prospective double-blind, randomized control trial. Patients were treated for 12 weeks with montelukast and fluticasone or placebo. All underwent a pretreatment and posttreatment PSG. Epworth Sleepiness Scale (ESS) score was obtained pretreatment and at 6 and 12 weeks posttreatment. RESULTS A total of 26 patients completed the study with 13 in each group. Mean age in the treatment and placebo groups were 58.3 ± 10.3 and 54.8 ± 14 years, respectively. There was no significant difference between groups reporting nasal congestion (P = .186), rhinitis (P = .666), or snoring (P = .177). There was no difference in the pretreatment ESS score (P = .077), body mass index (P = .173), or AHI (P = .535). The posttreatment PSG in the treatment group demonstrated a significant increase in total sleep time (P = .02) and percent of stage R sleep (P = .05). Neither group showed significant change in AHI. In patients in the treatment group, the 6- and 12-week follow-up ESS scores were not significantly different from pretreatment scores (P = .37-.46). CONCLUSIONS Intranasal steroids and montelukast did not decrease AHI; however, total sleep time and percent of stage R sleep significantly increased. Self-reported improvement could be explained by observed changes in sleep parameters. Larger prospective studies could help elucidate the effects of medical therapy on adult patients with OSA. CLINICAL TRIAL REGISTRATION Registry: ClinicalTrials.gov; Title: Montelukast and Nasa ICS for Treatment of Mild Obstructive Sleep Apnea in Adults; Identifier: NCT01089647; URL: https://clinicaltrials.gov/ct2/show/record/NCT01089647.
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9.
Phenotyping patients with chronic cough: Evaluating the ability to predict the response to anti-inflammatory therapy.
Sadeghi, MH, Wright, CE, Hart, S, Crooks, M, Morice, A
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology. 2018;(3):285-291
Abstract
BACKGROUND Whether the fraction of exhaled nitric oxide (FeNO) measurement can predict the response to anti-inflammatory treatment in chronic cough is unknown. OBJECTIVE To explore whether the effectiveness of treatment with 10 mg of montelukast or 20 mg of prednisolone in patients with chronic cough is predicted by FeNO level. METHODS In this randomized, open-label, controlled pilot study conducted in the Clinical Trial Unit in Castle Hospital in the United Kingdom, 50 nonsmoking patients with a cough that lasted more than 8 weeks were sequentially enrolled in the study. Thirty patients with high FeNO levels (≥30 ppb) were randomized in a 1:1 ratio to receive 10 mg of montelukast or 20 mg of prednisolone for 2 weeks followed by 10 mg of montelukast for 2 weeks. Twenty patients with a low FeNO level (≤20 ppb) received 10 mg of montelukast. The primary objective was to determine the effectiveness of treatment on 24-hour cough counts. RESULTS The 24-hour cough counts decreased in both groups by approximately 50% (P < .005), indicating that FeNO did not predict treatment response. However, it was a good marker for eosinophilic inflammation with a high degree of correlation with blood and sputum eosinophilia (P < .001). CONCLUSION These results suggest that prior investigation may not predict response to anti-inflammatory treatment, which may be consequent on localized leukotriene-mediated inflammation. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT02479074.
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10.
Question 2: Is there a role for Montelukast in the management of viral-induced wheeze in preschool children?
Burman, A
Archives of disease in childhood. 2018;(5):519-520