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Risk factors – Treatable traits
Published in Vibeke Backer, Peter G. Gibson, Ian D. Pavord, The Asthmas, 2023
Vibeke Backer, Peter G. Gibson, Ian D. Pavord
The evidence base to guide treatment decisions for smokers with asthma is limited because of their exclusion from many clinical trials. The overall assessment is that approved medications for nonsmokers with asthma are also effective for smokers with asthma. However, because of reduced corticosteroid sensitivity, it may be necessary to use higher doses of ICS in treating asthmatics who smoke. Montelukast, a leukotriene receptor antagonist is also effective in these patients. Low-dose theophylline and biologics, such as omalizumab, mepolizumab and dupilumab, may improve clinical outcomes in smokers with asthma, although never tested due to tobacco often is an exclusion criteria in RCT studies.
Compatibility of commonly used drugs in lactation
Published in Amy Brown, Wendy Jones, A Guide to Supporting Breastfeeding for the Medical Profession, 2019
Leukotriene receptor antagonists: Montelukast – PPB 99%, oral bioavailability 64%, RID 0.68%. Used in children. Zafirlukast– PPB >99%, oral bioavailability poor, RID 0.7%. Absorption slowed with food. Used in children > 12 years.
Medical Management for Rhinosinusitis
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Montelukast, a leukotriene receptor antagonist has been investigated in studies primarily as an adjunct to steroid treatment inpatients with CRSwNP and asthma. There is one positive single-blinded placebo controlled cross-over study with methodological problems, that shows benefit over placebo, while three other randomized trials were negative for change in polyp scores, although there were some benefits on some symptoms including sneezing and facial pain.27 Most studies found greater benefit in patients with associated nasal allergy. There is the definite possibility of leukotriene receptor antagonists assisting with concomitant allergic rhinitis symptom control in these patients and may be the mechanism of effect as many of these patients have both conditions. This is also the basis of some benefit seen and reported by studies on immunotherapy and CRS.28
Ragweed allergy immunotherapy tablet MK-3641 (Ragwitek®) for the treatment of allergic rhinitis
Published in Expert Review of Clinical Immunology, 2018
To assess the efficacy of medication approved in the United States for treatment of allergic rhinitis, a systematic review was conducted of randomized, controlled trials through November 2008[16]. A total of 54 articles, including more than 14,000 adults and 1,580 children with AR met the criteria for review. Of these, 29 included oral antihistamines (OAH), 7 included nasal antihistamines (INAH), and 17 included intranasal corticosteroids (INCS). Thirty-eight studies were conducted in patients with seasonal allergic rhinitis (SAR) compared with 12 studies in patients with perennial allergic rhinitis (PAR). The mean improvements from baseline in total nasal symptom score in the SAR studies were: INAHs −22.2%, OAHs −23.5%, INCSs −40.7%, and placebo −15%[15]. Another systematic review assessed the effectiveness of leukotriene receptor antagonists (LRAs) in allergic rhinitis[17]. Eleven studies on SAR were used in the analysis. LRAs reduced the mean daily rhinitis symptom scores 5% more than placebo compared to 7% for OAHs and 17% for INCSs.
Emerging drugs for eosinophilic esophagitis
Published in Expert Opinion on Emerging Drugs, 2018
Robert D. Pesek, Sandeep K. Gupta
As described earlier, there are limited treatment options currently available for EoE. Food-elimination diets or medical management including use of PPIs or swallowed corticosteroids are the mainstay of treatment (Table 1). Other treatments that target allergic pathways have also been investigated including the use of leukotriene receptor antagonists and mast-cell stabilizers. Use of montelukast, a leukotriene D4 receptor antagonist, was studied in 12 adult patients with EoE. After 4 months of therapy at a dose of 20–40 mg/day, half of the subjects had improvement in clinical symptoms but there was no change in numbers of esophageal eosinophils [25]. In a study by Lucendo et al. [26], montelukast was also ineffective at maintaining pathologic and histologic remission as well as symptom improvements in 11 adults with EoE who were previously treated with swallowed fluticasone. A randomized study of montelukast for EoE was performed by Alexander et al. in 2017 and concluded that montelukast was not effective in preventing symptomatic recurrence compared to placebo [27]. Cromolyn sodium, a mast-cell stabilizer, was utilized in a study of 14 children with EoE over 4 weeks, but no improvement was seen in the number of esophageal eosinophils or clinical symptoms after treatment [28]. Systemic corticosteroids and immune-modulating drugs such as 6-mercaptopurine have also been investigated in small cohorts. Both classes of medications are effective in reducing esophageal eosinophilia but may have significant systemic side effects that preclude their use in most patients [28–30].
Mepolizumab for the treatment of eosinophilic granulomatosis with polyangiitis
Published in Expert Opinion on Biological Therapy, 2019
Daniel Ennis, Jason Kihyuk Lee, Christian Pagnoux
Our understanding of the pathophysiology of EGPA continues to evolve. As described in many rheumatic disorders, EGPA may develop in a genetically predisposed individual with relevant exposures and triggering factors. A single inciting trigger for the disease has not yet been identified. Possible culprits have been suggested, including environmental and chemical allergens (silica, diesel dust, pigeon droppings, farming), infections (Aspergillus sp.), medications (leukotriene receptor antagonists [LTRAs], omalizumab, carbamazepine), vaccinations (hepatitis B, influenza virus), and desensitization treatment [46–49]. The specific contribution of leukotriene receptor antagonists to the development of EGPA has received particular scrutiny given its frequent use in the early 2000s in the treatment of asthma. A number of theories have been put forth to explain this association. The most prevalent is the ‘unmasking’ hypothesis, in which the use of LTRAs for asthma allowed for a tapering of GCs, which eventually exposed the underlying vasculitis, as LTRAs are not effective enough at preventing or treating vasculitis. Similarly, omalizumab is also thought to ‘unmask’ EGPA with a withdrawal of GCs in patients who were previously on chronic therapy [50]. Nevertheless, omalizumab has been successfully used in patients with EGPA for their asthma without worsening of EGPA [50,51]. In the widely debated ‘worsening’ or ‘causative’ hypothesis, LTRAs, added in order to control progressive asthma, provoke the development of EGPA possibly through a leukotriene profile imbalance [52–56].