Ousama Rachid 1,*, Mutasem Rawas-Qalaji 2,* and Keith J. Simons 3
Epinephrine is a life-saving treatment in anaphylaxis. In community settings, a first-aid dose of epinephrine is injected from an auto-injector (EAI). Needle phobia highly contributes to EAI underuse, leading to fatalities—especially in children. A novel rapidly-disintegrating sublingual tablet (RDST) of epinephrine was developed in our laboratory as a potential alternative dosage form.
Background: Allergic rhinitis is estimated to affect 20–25% of Canadians and has a significant impact on quality of life, with many patients reporting inadequate control of their symptoms . Mainstays of treatment for allergic rhinitis include avoidance, intranasal steroids, oral antihistamines and leukotriene receptor antagonists . Specific immunotherapy offers disease-modifying treatment for those uncontrolled by, intolerant to, or averse to pharmacotherapy .
Yukako Seo,1Manabu Nonaka,1Yukie Yamamura,1Ruby Pawankar,2 and Etsuko Tagaya3
1Department of Otolaryngology, Tokyo Women’s Medical University, Tokyo 162-8666, Japan.
2Department of Pediatrics, Nippon Medical School, Tokyo 113-0022, Japan.
3First Department of Medicine, Tokyo Women’s Medical University, Tokyo 162-8666, Japan.
Correspondence to: Manabu Nonaka. Department of Otolaryngology, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan. Tel: +81-3-3353-8111 (ext. 28531), Fax: +81-3-5269-7617, Email: firstname.lastname@example.org
Eosinophilic otitis media (EOM) is often associated with comorbid asthma. The middle ear cavity is part of the upper airway. Therefore, EOM and asthma can be considered to be a crucial part of the “one airway, one disease” phenomenon. Based on the concept of one airway, one disease in the context of allergic rhinitis and asthma, optimal level of inhalation therapy for better asthma control leads to improvement in allergic rhinitis.
Bronchial asthma is characterized by persistent cough, increased sputum, and repeated wheezing. The pathophysiology underlying these symptoms is the hyper-responsiveness of the airway along with chronic airway inflammation. Repeated injury, repair, and regeneration of the airway epithelium following exposure to environmental factors and inflammation results in histological changes and functional abnormalities in the airway mucosal epithelium; such changes are believed to have a significant association with the pathophysiology of asthma. Damage to the barrier functions of the airway epithelium enhances mucosal permeability of foreign substances in the airway epithelium of patients with asthma. Thus, epithelial barrier fragility is closely involved in releasing epithelial cytokines (e.g., TSLP, IL-25, and IL-33) because of the activation of airway epithelial cells, dendritic cells, and innate group 2 innate lymphoid cells (ILC2). Functional abnormalities of the airway epithelial cells along with the activation of dendritic cells, Th2 cells, and ILC2 form a single immunopathological unit that is considered to cause allergic airway inflammation. Here we use the latest published literature to discuss the potential pathological mechanisms regarding the onset and progressive severity of asthma with regard to the disruption of the airway epithelial function.