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Seeming Tongue Swelling Responding To Nebulized Ipratropium In An Individual With A Diagnosis Of Type III HAE (Hereditary Angioedema) Ms. Jennifer Vegh1, Dr. Arthur B. Vegh, MD, FAAAAI2, Ms. Nicholette Butler1; 1none, Tacoma, WA, 2University of Washington, Tacoma, WA. RATIONALE: When a patient presentation doesn’t conform, reassessment of mechanisms and dx need be done. We present a case of type III hereditary angioedema who self-induced what appeared to be tongue swelling. METHODS: Critical direct evaluation of an acute attack. referred for HAE. She presented 3 1/2years ago with a 9 RESULTS: 31 yS yr h/o repeated episodes of swellings of the abdomen, tongue, and throat. This included ‘‘dozens’’ of intubations, a 3 month hospitalization and tracheostomy at a midwest university, a dx of HAE at Mayo Clinic despite unremarkable complement studies. Three months before seeing us, JM suffered repeated ED visits and 5 hospitalizations for swellings. Treatments: multiple different pain medications, IV corticosteroids, antihistamines with inadequate benefit. Pt claimed, however, immediate IV diphenhydramine benefit. Fresh frozen plasma gave seemingly mild benefit in 3 hours. Examination: VS nl. Pulm: minimal course breath sounds. Her abdomen was moderately distended and tender to mild palpation. Complement studies unremarkable. PFTs: NS improvement with BD but symptomatic benefit. Initial treatments: amitriptyline, albuterolHFA prn, tapering chronic narcotics. C1 esterase inhibitor infusions and prn ecallantide with partial benefit. Witnessing a tongue swelling, with the above h/o immediate diphen response (anticholinergic effect), neb. ipratropium was administered with rapid resolution of tongue and throat swelling. With inhaled cs, tiotropium, her throat and tongue swellings have almost resolved. CONCLUSIONS: We present a case of an individual with a dx of HAE with recurrent atypical bronchospasm giving a sensation of throat swelling and causing the patient to induce what appears to be tongue angioedema.
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Cytokine Expression In a Case Of Cutaneous Mastocytosis With An Unusual Presentation Prof. Young Min Ahn, MD1, Prof. sang-Hoon Kim, Prof. Ho-jung Lee2, Prof. Jai Youl Ro, PhD3; 1Department of Pediatrics, South Korea, Department of Internal Medicine, South Korea, 2Department of Pathology, Eulji University School of Medicine, South Korea, 3Sungkyunkwan University School of Medicine, South Korea. RATIONALE: We experienced the case of a 10-year-old girl who presented with angioedma and facial nerve palsy possibly associated with the cutaneous mastocytosis. Her recurrent angioedema has presented since 4 year of age which was exacerbated by spicy foods or certain drugs. Therefore this study aims to investigate the relationship between cutaneous mastocytosis and patient serum cytokine expression during the episode of angioedema. METHODS: Serum tryptase was checked. Skin biopsy was taken from the scalp and trunk lesions for histological examination. The immunofluorescence stain with CD 117 and genetic examination of KIT mutation was done on the infiltrating cells in the dermis. Individual cytokines were determined by human ELISA kit. RESULTS: Serum tryptase levels were elevated at 4, 9, and 10 years old respectively (51.5, 72.9, and 30 ng/mL). Mast cells densely infiltrated entire dermis , extending into subcutaneous fat. C-KIT mutation at codon 816 was negative. MRI showed possible involvement of facial nerve course in both side in temporal bone and no evidence of neurogenic tumor along 7th and 8thcranial nerve. Expression of inflammatory cytokines, such as TNF-a, TGF-b, IL-4, IL-5, IL-6, IL-13, was remarkably increased in patient’s serum versus those in normal serum and anti-inflammatory cytokine IL-10 was remarkably decreased in patient’s serum versus that in normal serum. CONCLUSIONS: Magnetic resonance image suggests that transient facial palsy is possibly caused by soft tissue swelling on parotid gland area associated with mastocytosis. And that cutaneous mastocytosis may be induced through down-regulating the expression of anti-inflammatory cytokine IL-10 and up-regulating the expression of various inflammatory cytokines.
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Aerochambers and Asthmatics: Do No Harm? Dr. Jack Leon-Max Mutnick, MD; Stevens Community Medical Center, Morris, MN. RATIONALE: Spacers added to metered-dose inhalers improve delivery of medication to lung tissue, but are spacers a harbinger for infection, especially in asthmatic patients already combatting inflammation in the lung? METHODS: In a single blind randomized pilot study patients diagnosed with asthma, according to current guidelines, were recruited to determine if the Advantage OptichamberÒ is a harbinger of microbial or fungal organisms. Patients are started on a metered-dose inhaler (Mometasone/ Formoterol) with the Advantage OptichamberÒ and are having the ‘‘spacer’’ cultured at three sites for bacterial/fungal organisms. Sensitivity of the organisms to antibiotics or antifungal medications is also being evaluated. Culture and sensitivity results are being accumulated at months 1, 4, and 10. RESULTS: Early results show that after 1 month of therapy, cultures of the Advantage OptichamberÒ show organisms including Methicillin-resistant Staphylococcus epidermidis, Micrococcus luteus, Streptococcus parasanguinis, and gram positive rods. Staphylococcus epidermidis (Methicillin-resistant or –sensitive) shows almost a complete classresistance to the fluoroquinolones. Fungal results show rare alternaria species isolated. CONCLUSIONS: As we develop improved therapies to treat and control asthma, we must look beyond the ‘‘mouthpiece’’ and consider the risks that aerochambers present to our patients. Asthma exacerbations are serious and not without complications, and one must question if aerochamber devices should be impregnated with antibacterial/antifungal chemicals or if these devices should also have a ‘‘shelf-life’’ considering the hazards posed to patients, especially the concern for pulmonary infections due to these devices.
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Characterizing The Severe Asthma Population In The United States: Claims-Based Analysis Of Three Treatment Cohorts In The Year Prior To Treatment Escalation Dr. Patrick W. Sullivan, PhD1, Dr. Jon Campbell, PhD2, Dr. Vahram Ghushchyan, PhD2, Dr. Gary Globe, PhD3, Dr. Jeff Lange, PhD3, Dr. J Michael Woolley, PhD3; 1Regis University, 2University of Colorado Denver, 3Amgen, Inc., Thousand Oaks, CA. RATIONALE: To describe demographics, employment, insurance, medication adherence and healthcare utilization of patients with severe asthma. METHODS: This was an asthma cohort study (age 12-75 years) requiring three initial claims within three months for omalizumab, high-intensity _1000 mg/day fluticasone equivalent or oral corticosteroids (HICS; > _500 to <1000 prednisone), or high-dose inhaled corticosteroid (HDICS; > mg/day fluticasone equivalent) from 2002-2011.Adherence was assessed using the annualized Medication Possession Ratio (MPR: % of year taking medication). RESULTS: Of 70,343 patients, 1,046 initiated omalizumab, 24,319 initiated HICS, and 44,978 initiated HDICS. More severe cohorts (omalizumab, HICS, and HDICS, respectively) had higher pre-index mean values for medical expenditures ($14,071; $12,030 and $7570), utilization (27 outpatient and 10 specialty care visits; 19 outpatient and 2 specialty; 15 outpatient and 2 specialty), asthma-related prescription drugs (11.74; 7.8; 5.17) and chronic comorbidities (2.68; 2.67 and 2.19). In the year prior to omalizumab treatment: 72% of patients were taking HICS (MPR 30%), 64% oral corticosteroids (MPR 13%), 33% HDICS (MPR 40%), 63% leukotrienes (MPR 54%) and 69% short-acting beta agonists (29%); these patients were more likely to be salaried, full-time employees with commercial PPO/POS insurance. CONCLUSIONS: Categorizing severe asthma patients by treatment cohorts provides more granular focus augmenting GINA categorization. Increased severity was associated with higher baseline healthcare expenditures and utilization. Prior to omalizumab treatment, most patients were taking high doses of corticosteroids. The high utilization and polypharmacy burden may reflect failures in standard of care and its treatment options prior to titrating to the next step of therapy.
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Abstracts AB41
J ALLERGY CLIN IMMUNOL VOLUME 133, NUMBER 2