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Abstracts: Medically Challenging Cases / Ann Allergy Asthma Immunol 121 (2018) S63−S134
Discussion: Aspirin desensitization and maintenance therapy can be considered in nursing AERD patients after careful assessment of risks and benefits along with pediatric consultation. It can potentially alleviate symptoms of rhinosinusitis, asthma, and nasal polyps.
M358 OTIC AND NASAL POLYPS WITH PERIPHERAL EOSINOPHILIA AND BILATERAL HEARING LOSS L. Tuong*, R. Khianey, R. Jyung, Newark, NJ Introduction: Refractory otitis media (OM) in adults is challenging as misdiagnosis can lead to permanent sensorineural hearing loss. OM in the presence of peripheral eosinophilia and atopic history should warrant alternative treatment rather than antibiotics and topical steroids. Case Description: A 71-year-old female with asthma, nasal polyps and allergic rhinitis presented with two years of bilateral hearing loss. She had multiple episodes of recurrent otitis media treated with topical and systemic steroids along with antibiotics without improvement. Physical exam was significant for hypertrophied turbinates and anterior rhinoscopy showed a large polyp in the right middle meatus. Otoendoscopy showed a right tympanic membrane with chronic myringitis, central perforation with polypoid changes to the middle ear mucosa. Left tympanic membrane had central perforation and polypoid tissue (Figure 1). Labs were significant for peripheral eosinophilia of 1.3 £ 103 eosinophils/mL (16.7%) and IgE level of 1065 IU/mL. A diagnosis of presumed eosinophilic otitis media was made. Discussion: Eosinophilic otitis media (EOM) is a rare disorder of intractable bilateral otitis media. Diagnosis can be made using the major criteria of eosinophils in the middle ear mucosa or its effusion, along with two or more items of the minor criteria (association with asthma, nasal polyposis, chronic rhinosinusitis, resistance to conventional treatment for otitis media, and a highly viscous middle ear effusion). The differential should exclude disorders such as eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome. Treatment of EOM includes removal of eosinophilic middle ear effusion and suppression with steroids.
Figure 1. Left tympanic membrane with central perforation and polypoid tissue.
M359 UNUSUAL CASE OF EOSINOPHILIC ASCITES AND PERIPHERAL EOSINOPHILIA S. Knox*, D. Patadia, Cleveland, OH Introduction: Drug reactions and atopic disease are common etiologies of peripheral eosinophilia in the United States, while helminthic infections, malignancy and hypereosinophilic syndrome (HES) are rare. Here we describe a patient with an unusual etiology for peripheral eosinophilia. Case Description: 24-year old previously healthy female presented with acute abdominal pain, distension and diarrhea. She had traveled
to Brazil and Italy in the previous three years. Initial peripheral absolute eosinophil count (AEC) was 4.67 k/uL. Abdominal ultrasound showed moderate ascites. Paracentesis yielded 2.3L of ascites fluid; analysis showed 3165 WBC with 92% eosinophils. Stool culture grew few Blastocystis hominis. Pathology showed 12 esophageal and >100 colonic eosinophils/hpf without significant abnormality in the stomach or duodenum. Bone marrow biopsy did not show evidence of malignancy. Allergy skin testing demonstrated sensitization to several aeroallergens. HES workup was normal. Gastroenterology considered treatment for eosinophilic gastroenteritis versus parasite infection. She was treated with metronidazole for Blastocystis, and symptoms improved over the following 8 weeks. Peripheral AEC decreased to 0.48 k/uL by 12 weeks post-treatment, without return of symptoms. Discussion: Blastocystis hominis is a protozoan parasite rarely implicated in human disease or peripheral eosinophilia. It can be found in stool of healthy individuals, though gastrointestinal symptoms may require treatment. Eosinophilic ascites has been associated with eosinophilic gastroenteritis, which may self-resolve or require corticosteroid treatment. Steroid treatment during parasitic infection, however, can lead to disseminated disease. In this case, where etiology of the eosinophilia was unclear, it was important to treat a possible parasitic infection prior to considering corticosteroid treatment.
M360 ERRONEOUS DIAGNOSIS OF PENICILLIN ALLERGY BASED ON MOLD HYPERSENSITIVITY TESTING COMPLICATING TREATMENT OF RHEUMATIC FEVER K. Vanijcharoenkarn*, G. Lee, Atlanta, GA Introduction: The penicillin allergy label puts a patient at risk for higher mortality and increased rates of severe infections. We present a case of treatment for rheumatic fever with Sydenham chorea complicated by erroneously labeled penicillin allergy due to mold hypersensitivity. Case Description: A 12-year old female became unable to stand from full-body choreiform movements and was found to have rheumatic fever. Her echocardiogram showed: “rheumatic carditis, thickened mitral valve leaflets.” Two months prior, she had group A streptococcus pharyngitis treated with cephalexin due to a label of penicillin allergy. Skin testing performed by her local ENT physician had been positive to penicillium mold and she was counseled to avoid all penicillin antibiotics. Penicillin antibiotic was not tested, and she had never had penicillin. She passed a penicillin oral challenge and was transitioned to monthly intramuscular penicillin G benzathine. Discussion: An erroneous penicillin allergy label prevented prompt treatment of this patient’s condition with gold standard therapy. Despite optimal adherence, oral prophylaxis options show increased rheumatic fever recurrence compared to parenteral therapy. Alternative medications such as sulfadiazine can have severe side effects including hepatitis and agranulocytosis. This case emphasizes the need to educate patients and providers that hypersensitivity to penicillium mold does not equate hypersensitivity with the penicillin antibiotic it secretes. Furthermore, authentication of a penicillin allergy label continues to be of utmost importance in allowing patients to receive optimal therapy.
M361 SYSTEMIC MASTOCYTOSIS WITH NORMAL BIOMARKERS. HOW VALUABLE ARE MAST CELL MEDIATORS IN IDENTIFYING DISEASE? J. Murillo*, J. Lewis, Scottsdale, AZ