Abstract
Objective:To determine the role of montelukast – a leukotriene receptor antagonist (LTRA) – in improving the quality of life (QOL) and asthma control of adult patients with mild to moderate persistent asthma.Methods:Randomized, double-blind, placebo-controlled, non-crossover trial was conducted from March 2017 till November 2018 in three hospitals of Karachi and Hyderabad. Adults of age 15 years or more with mild to moderate persistent asthma. Treatment group was administered tablet montelukast 10mg once daily; the other group was given a similar looking placebo; as an adjuvant to the current medication. QOL was assessed with Asthma Quality of Life Questionnaire – Standard (AQLQ-S) before and after the treatment. Asthma control was monitored via Asthma Control Test (ACT).Results:After 4 weeks, the mean ± SD of overall QOL on AQLQ-S improved from 3.74±0.88 to 5.06±0.89 for montelukast group and from 3.58±0.92 to 4.71±0.97 for placebo group (p=0.02). The improvement in sub-domains of symptoms, activity, and emotional functions was not significant; however, the sub-domain “environmental stimuli” significantly improved with 5.06±0.89 for montelukast group and 4.71±0.97 for placebo group (p=0.02). The mean ± SD of ACT, after four weeks, for montelukast group was 18.19±2.91 and for placebo group 17.28±3.36. Only on ACT, Montelukast did not show any statistically insignificant results.Conclusion:The role of montelukast in improving QOL of adult patients with mild to moderate persistent asthma is quite beneficial. It improves patient quality of life. It has the ease of once daily oral administration and also eradicates side effects associated with long-term adherence to steroids.
Highlights
Asthma is the complex, chronic, immunologically mediated condition characterized by imbalance in the normal airway repair mechanism leading to airway inflammation, edema, obstruction, remodeling, and hyper-responsiveness
This allergen is first endocytosed by the antigen presenting cells (APCs); which process it and present to naïve the T cells, which in turn, stimulate the respiratory epithelium to secrete inflammatory mediators such as thymic stromal lymphopoietin (TSLP) which recruit leukocytes and dendritic cells (DC)
Under the influence of DCs, T cells are differentiated into T-helper 2 (Th2) and Th17 cells via stimulation of interleukin 4 (IL-4) and IL-13
Summary
Chronic, immunologically mediated condition characterized by imbalance in the normal airway repair mechanism leading to airway inflammation, edema, obstruction, remodeling, and hyper-responsiveness. As the respiratory mucosa is exposed to an allergen, which maybe an environmental trigger or a microbe, a cascade of inflammatory response is initiated. This allergen is first endocytosed by the antigen presenting cells (APCs); which process it and present to naïve the T cells, which in turn, stimulate the respiratory epithelium to secrete inflammatory mediators such as thymic stromal lymphopoietin (TSLP) which recruit leukocytes and dendritic cells (DC). IL-5, produced from Th2 cells, increases eosinophil levels which release inflammatory mediators These chemicals, along with those released from T cells, macrophages, and neutrophils damage the airway, cause smooth muscle contraction, stimulate inflammatory pathways, and result in airway remodeling. Th2 cells induce production of immunoglobulin E (IgE) antibody which binds to mast cells and basophils to release histamine, cysteinylleukotrienes (CysLTs) and other mediators.[2]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
