A Retrospective Analysis of Esophageal Eosinophilia in Patients with Aspirin-exacerbated Respiratory Disease

Abstract

RATIONALE: About 10% of patients report allergy to penicillin. Of those patients evaluated with a penicillin skin test (ST) and challenge, 90-99% are able to tolerate penicillin, resulting in penicillin allergy de-labeling. However, while patients are often de-labeled in the short term, factors that predict the persistence of penicillin allergy de-labeling remain unknown. METHODS: A retrospective chart review was conducted on patients evaluated for penicillin allergy from 2012-2017(inpatient and outpatient). Data was collected from the electronic medical record (EMR), pharmacy records, as well as a follow-up telephone survey with patients. RESULTS: Thirty-three patients were successfully de-labeled of their penicillin allergy (negative ST and tolerated oral challenge). One-third of these patients had persistence of their penicillin allergy in the EMR (11/ 33), and 7 patients had persistence in their pharmacy records (21%). Persistence of the penicillin allergy label was not significantly associated with age (p50.73), gender (p50.35), or whether the evaluation was done inpatient or outpatient (p50.88). Follow-up telephone survey was done with 24 patients (nine patients were unavailable for follow-up), and 96% (n523) recalled the results of their allergy evaluation correctly. Despite accurate recall, 3 patients continued to avoid penicillin for fear of a possible reaction. CONCLUSIONS: This study found that while penicillin allergy delabeling is safe and effective, there is a discrepancy between the allergy evaluation and the appropriate removal of the penicillin allergy from the EMR and pharmacy records, which may include patient apprehension as a cause. Neither age, gender, nor place of evaluation predicted persistence of the penicillin allergy label.

Major complications of aspirin desensitization and maintenance therapy in aspirin‐exacerbated respiratory disease

“…AERD patients with a history of eosinophilic esophagitis should avoid aspirin therapy because of the potential for exacerbation of gastrointestinal symptoms. 16 Given the retrospective nature of our study, there are inherent limitations to our study design, including selection bias. To minimize this limitation, outcomes were focused on analyzing objective data only, such as the maintenance dose of aspirin therapy during ATAD, as well as the percentage of AERD patients who discontinued therapy following an aspirin-related complication.…”

“…If an AERD patient's asthma is poorly controlled, AD with ATAD should be delayed until symptoms are optimized so as to prevent further exacerbation of the patient's asthma. AERD patients with a history of eosinophilic esophagitis should avoid aspirin therapy because of the potential for exacerbation of gastrointestinal symptoms 16 …”

The role of aspirin desensitization followed by oral aspirin therapy in managing patients with aspirin-exacerbated respiratory disease: A Work Group Report from the Rhinitis, Rhinosinusitis and Ocular Allergy Committee of the American Academy of Allergy, Asthma & Immunology

“…Patients with a history of eosinophilic esophagitis might be at risk for worsening gastrointestinal symptoms on initiation of aspirin therapy. 77 Although evidence is lacking, it is possible that some of these patients may tolerate aspirin therapy if concomitantly treated with agents targeting IL-5 or IL-4/13.…”

“…137 Esophageal eosinophilia has also been described after aspirin desensitization. 77,138 Approach to silent desensitizations A clinical dilemma can exist if a patient with an excellent history and sinonasal polyposis does not ''react'' during the desensitization despite the fact that clinical criteria for AERD are met. One strategy that is frequently used in a patient who undergoes a nonreactive challenge would be to assume that they do have AERD and experienced a ''silent desensitization'' 139 related to the use of LTMDs during the desensitization or recent FESS.…”

Eosinophilic esophagitis—established facts and new horizons

“…Although most connective tissue diseases, such as eosinophilic granulomatosis with polyangiitis, lupus erythematodes, rheumatoid arthritis, systemic sclerosis, Sjögren syndrome, or scleromyositis may cause tissue eosinophilia in the GI tract, it occurs mostly in the small bowel, stomach, or colon [135, Peripheral blood eosinophils > 1500 cells/ml without secondary causes and evidence of an eosinophil-mediated end organ manifestation Atopic diseases (Asthma, aspirin-exacerbated respiratory disease, IgE mediated food allergy) [152,153] Extraintestinal manifestations Drug hypersensitivity and pill esophagitis Medical history Radiofrequency ablation for Barrett's esophagus [154][155][156] Typically without dysphagia Graft-versus-host disease [157] Eosinophil density correlates with GvHR Oral immunotherapy [158] Mostly transient and without symptoms Asymptomatic esophageal eosinophilia [159][160][161][162] Exclusive diagnosis 136]. An esophageal involvement is a rarity [136,137] and as opposed to EoE, most patients are female, have no atopy, and present with peripheral eosinophilia [136].…”