montelukast and azelastine

Allergic Rhinitis (AR) is a prevalent chronic inflammatory nasal condition with significant negative effects on the patients' quality of life. This study aimed to investigate the efficacy of Montelukast and intranasal antihistamine in combination with intranasal corticosteroid (INCS) in moderate to severe allergic rhinitis on the patients' quality of life and AR control.. This double-blind randomized clinical trial study was carried out on 66 moderate to severe AR patients referred to Namazi Hospital, Shiraz, Iran from 2020 to 2021, who were randomly divided into 3 groups. Group one received Montelukast add-on therapy and Budesonide nasal spray. The second group received intranasal antihistamine (Azelastine) add-on therapy and Budesonide nasal spray and the third group as the control group received intranasal Budesonide spray with a placebo tablet.To measure the impact of each medication on the patient's quality of life and AR control, we employed the Sino-Nasal Outcome Test-22 questionnaire (SNOT 22). We evaluated the symptoms and compared them at baseline, one and three months after the start of treatments. Spirometry was performed to investigate the possibility of co-morbid asthma at baseline and end of the study.. The patients' mean age was 30.13 ± 12.7 years. Most patients experienced perennial AR (65.2%). Reduction of mean scores SNOT22 was statistically different between groups (P-value < 0.001). Three months after treatment, the mean decrease of SNOT-22 in the Azelastine group was statistically significant compared to both Montelukast (P-value < 0.001) and control groups (P-value < 0.001). No significant difference was observed between the Montelukast and control groups (P-value = 0.142). 23 of 66 patients were diagnosed with asthma and asthma treatment was initiated. The amount of FEV1 change after AR treatment was not statistically significant between the groups in asthmatic patients (P-value = 0.351).. Based on our findings, we recommend Azelastine in conjunction with an intranasal corticosteroid for the treatment of moderate to severe allergic rhinitis. In moderate to severe AR or even asthma management, Montelukast has no greater impact than INCS.

Topics: Acetates; Administration, Intranasal; Adolescent; Adrenal Cortex Hormones; Adult; Asthma; Budesonide; Cyclopropanes; Double-Blind Method; Histamine Antagonists; Histamine H1 Antagonists; Humans; Nasal Sprays; Phthalazines; Quality of Life; Quinolines; Rhinitis, Allergic; Sulfides; Treatment Outcome; Young Adult

Histamine and cysteinyl leukotrienes play an important role in early (EAR) and late (LAR) allergen reactions. Although protection by anti-histamines and anti-leukotrienes has been studied extensively, little is known about the effect of their combination. We, therefore, assessed the effect of clinically recommended doses of azelastine and montelukast alone and in combination on EAR and LAR.. Seventeen patients (mean age 31 years, 14 m/3 f) with asthma and proven EAR and LAR received an oral dose of 4 mg azelastine twice daily, or 10mg montelukast once daily, or both for 1 week, in a double-blind, double-dummy, cross-over fashion. FEV(1) was measured after single-dose allergen challenges during EAR (0-2h) and LAR (2-9h).. Azelastine, montelukast and their combination protected against both EAR and LAR (p<0.004, each) by 46% and 43%, 76% and 59%, and 89% and 78%, respectively. Azelastine was not as effective during EAR but equally effective to montelukast during LAR. The combination was superior to each drug alone during both EAR and LAR (p<0.05, each).. The combination of azelastine and montelukast in clinically recommended doses has a greater effect in suppressing early and late allergen reactions than each drug alone.

Topics: Acetates; Adult; Anti-Allergic Agents; Asthma; Bronchial Provocation Tests; Bronchoconstriction; Cross-Over Studies; Cyclopropanes; Double-Blind Method; Drug Therapy, Combination; Female; Humans; Male; Middle Aged; Phthalazines; Quinolines; Respiratory Function Tests; Sulfides

Urocortin (UCN), a newly identified, 40-amino-acid, corticotropin-releasing hormone (CRH) structurally related peptide, has been demonstrated to be expressed in the central nervous system and many peripheral tissues of rats and man. This study aimed to investigate the expression profile of UCN in rat lung and the effect of UCN on lung vascular permeability. The expression of UCN mRNA was detected by reverse transcriptase PCR (RT-PCR). UCN peptide was measured by immunohistochemistry and Western blot analysis. We found that both UCN mRNA and peptide were obviously expressed in rat lung. Immunohistochemistry results showed that UCN peptide is mainly expressed in bronchial epithelium mucosa and alveolar epithelium. We also found that rats receiving inhalation aerosol of UCN had a significant elevation of lung vascular permeability compared with rats receiving vehicle and ovalbumin (OVA) by the Evans blue (EB) technique. UCN aerosol inhalation resulted in obvious pulmonary congestion and edema observed under light microscope by hematoxylin and eosin (HE) staining. The nonselective peptide CRH receptor antagonist astressin markedly reduced lung vascular permeability triggered by UCN. Enhanced pulmonary vascular permeability induced by UCN was markedly inhibited by pretreatment with the mast-cell stabilizer cromolyn and histamine-1 (H1) receptor antagonist azelastine respectively, but not by the leukotriene receptor antagonist montelukast. In summary, in the present study, we demonstrated for the first time that UCN is expressed in rat lung and contributes to an increase in lung vascular permeability through activation of CRH receptors. Mast cells and histamine may be involved in this effect of UCN. Peripherally produced UCN in lung may act as an autocrine and paracrine proinflammatory factor.

Topics: Acetates; Administration, Inhalation; Aerosols; Animals; Blotting, Western; Bronchi; Capillary Permeability; Corticotropin-Releasing Hormone; Cromolyn Sodium; Cyclopropanes; Epithelium; Histamine H1 Antagonists; Immunohistochemistry; Leukotriene Antagonists; Lung; Male; Mast Cells; Ovalbumin; Peptide Fragments; Phthalazines; Pulmonary Alveoli; Quinolines; Rats; Rats, Sprague-Dawley; Respiratory Mucosa; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sulfides; Urocortins