Alexander S. Kim

Group 2 innate lymphoid cells are recruited to the nasal mucosa in patients with aspirin-exacerbated respiratory disease

Background Aspirin‐exacerbated respiratory disease (AERD) is characterized by tissue eosinophilia and mast cell activation, including abundant production of prostaglandin D2 (PGD2). Group 2 innate lymphoid cells (ILC2s), which promote tissue eosinophilia and mast cell responses, undergo chemotaxis and cytokine production in response to PGD2, but it is unknown whether ILC2s are active in patients with AERD. Objective We sought to determine whether ILC2 numbers change in peripheral blood and the nasal mucosa during COX‐1 inhibitor–induced reactions in patients with AERD. Methods Blood and nasal scrapings were collected at baseline, during reactions, and after completion of ketorolac/aspirin challenge/desensitization in 12 patients with AERD. ILC2s and eosinophils were quantitated by means of flow cytometry. Urine was also collected, and quantification of PGD2 metabolite and leukotriene E4 levels was done by using ELISA. Baseline and nonsteroidal anti‐inflammatory drug reaction clinical data were correlated with cell changes. Results ILC2 numbers significantly increased in nasal mucosal samples and decreased in blood at the time of COX‐1 inhibitor reactions in 12 patients with AERD. These changes were not observed in 2 patients without AERD. Furthermore, eosinophil numbers decreased in blood concurrently with significant increases in urinary PGD2 metabolite and leukotriene E4 levels. The magnitude of increases in nasal mucosal ILC2 numbers positively correlated with maximum symptom scores during challenges. Furthermore, blood ILC2 numbers during the reaction correlated with time for the reaction to resolve, possibly reflecting reaction severity. Conclusions ILC2s are recruited to the nasal mucosa during COX‐1 inhibitor–induced reactions in patients with AERD, correlating with enhanced production of prostaglandins and leukotrienes.

New and emerging therapies for asthma

A 34-year-old woman with severe persistent asthma, atopic dermatitis and allergic rhinitis presents for evaluation of asthma refractory to conventional therapy. The patient has a history of asthma commencing in early childhood, with progression to uncontrolled disease in the last two years. Allergen skin prick testing in childhood was positive to dust mites, cat and dog dander, as well as multiple pollens. Her principle triggers are inhaled allergens, especially animal dander, as well as irritants including tobacco smoke. Despite compliance with maximal dose inhaled corticosteroid/long acting beta agonist (ICS/LABA), leukotriene receptor antagonist, nasal corticosteroid and avoidance measures, she continues to experience nightly wheezing and chest tightness that requires daily beta-agonist inhalations. Furthermore, in the last year she has been hospitalized twice for asthma exacerbations following viral infections and has received five courses of oral corticosteroids. Her Asthma Control Test (ACT) score at initial consultation is 7. Physical exam is notable for bilateral expiratory wheezes in the lower lung fields. Total IgE level is 650 IU/mL and previous allergen sensitivities are confirmed. Lung function testing reveals a baseline FEV1 of 50% of predicted by age, improving to 66% post-bronchodilator administration (460cc increase). Fraction of exhaled nitric oxide levels (FeNO) is 125 and her peripheral eosinophils are elevated at 1350 cells per microliter. Additionally, the patient’s inhaler technique is assessed and she demonstrates excellent technique with both controller and rescue devices. Further questioning addresses any gaps in her asthma management. The patient has excellent medication compliance corroborated by her significant other, has installed dust-mite covers, and denies first or second-hand smoking or furry animal ownership or exposure. A recently performed pregnancy test is negative, and she denies a history chronic sinus disease including nasal polyposis, aspirin/NSAID sensitivity, occupational exposures or gastroesophogeal reflux disease. There are no socioeconomic or psychological stressors identified as possible contributors to her uncontrolled asthma and no clinical evidence to support paradoxical vocal fold motion. Evaluations for Eosinophilic Granulomatosis with Polyangiitis (EGPA) and Allergic Bronchopulmonary Aspergillosis (ABPA) are negative. What therapeutic strategies (present and future) can be utilized to optimize her severe uncontrolled asthma?

Mango: pulp fiction?

Keywords: contact dermatitis; cross-reactivity; delayed hypersensitivity; mango; patch testing; urushiol

Acquired Donor Peanut Allergy from Lung Transplantation resulting in Respiratory Failure: A Case Report

This case report describes a patient who acquired a donor peanut allergy after lung transplantation. A 53-year-old woman with alpha-1 antitrypsin deficiency underwent left-sided lung transplant from a donor with a history of anaphylaxis to peanut. Two weeks after the transplant, the patient developed acute respiratory failure immediately after consuming a peanut butter and jelly sandwich. The donors serum confirmed high titers of peanut-specific immunoglobulin E (IgE). The recipient patient had never had allergies to peanuts or other nuts before her transplant. After the transplant, she had negative serology but positive skin testing to peanuts. This case illustrates the importance of considering donor food allergies when caring for solid organ transplant recipients.