IgE Specific to Oxycodone Identified by ELISA Inhibition in a Young Woman with Symptoms of Anaphylaxis Following Oral Ingestion: First Case Report of Oxycodone-Mediated Anaphylaxis

Abstract

RationaleReactions to opioid analgesics are rarely IgE mediated but usually the result of histamine release. Morphine, codeine, pethidine, fentanyl, and tramadol have been implicated in case reports of Type I IgE-mediated reactions. Here we present a young woman with anaphylaxis and specific IgE to oxycodone.MethodsOxycodone ELISA inhibition study against patient serum and controls by Wilford Hall Allergy Clinic Laboratory.ResultsThis patient with a history of chronic lower back pain and asthma ingested one dose of Percocet (acetaminophen 325mg, oxycodone 5mg). Within 60 minutes, she developed generalized urticaria, dysphonia, and dyspnea. She denied wheezing and her characteristic symptoms of asthma exacerbation. In the ED she had increasing tongue swelling, decreased respiratory effort, and muffled voice; symptoms worsened despite epinephrine 0.3mg intramuscular then 0.1mg intravenous, dexamethasone 10mg IV, diphenhydramine 25mg IV, and ranitidine 50mg IV. She was intubated by anesthesiology for airway protection and transferred to the ICU. Patient extubated 12 hours after intubation, discharged within 48 hours with an Epipen, diagnosed with Percocet allergy, and instructed to avoid all opiates. Serum tryptase (8 hrs after exposure) 3ng/mL, C1 esterase inhibitor 95%, C3 99.6mg/dL, C4 16.17mg/dL, and IgG 831mg/dL. ELISA for oxycodone was run with 100μg oxycodone per well and found an average 47% inhibition of IgE binding with 100μg/100μL of a 1:3 dilution of serum.ConclusionsWe believe this is the first reported case of Type I IgE-mediated anaphylaxis to oxycodone. The use of ELISA to detect oxycodone IgE may be instructional for other diagnostic studies of suspected opioid anaphylaxis. RationaleReactions to opioid analgesics are rarely IgE mediated but usually the result of histamine release. Morphine, codeine, pethidine, fentanyl, and tramadol have been implicated in case reports of Type I IgE-mediated reactions. Here we present a young woman with anaphylaxis and specific IgE to oxycodone. Reactions to opioid analgesics are rarely IgE mediated but usually the result of histamine release. Morphine, codeine, pethidine, fentanyl, and tramadol have been implicated in case reports of Type I IgE-mediated reactions. Here we present a young woman with anaphylaxis and specific IgE to oxycodone. MethodsOxycodone ELISA inhibition study against patient serum and controls by Wilford Hall Allergy Clinic Laboratory. Oxycodone ELISA inhibition study against patient serum and controls by Wilford Hall Allergy Clinic Laboratory. ResultsThis patient with a history of chronic lower back pain and asthma ingested one dose of Percocet (acetaminophen 325mg, oxycodone 5mg). Within 60 minutes, she developed generalized urticaria, dysphonia, and dyspnea. She denied wheezing and her characteristic symptoms of asthma exacerbation. In the ED she had increasing tongue swelling, decreased respiratory effort, and muffled voice; symptoms worsened despite epinephrine 0.3mg intramuscular then 0.1mg intravenous, dexamethasone 10mg IV, diphenhydramine 25mg IV, and ranitidine 50mg IV. She was intubated by anesthesiology for airway protection and transferred to the ICU. Patient extubated 12 hours after intubation, discharged within 48 hours with an Epipen, diagnosed with Percocet allergy, and instructed to avoid all opiates. Serum tryptase (8 hrs after exposure) 3ng/mL, C1 esterase inhibitor 95%, C3 99.6mg/dL, C4 16.17mg/dL, and IgG 831mg/dL. ELISA for oxycodone was run with 100μg oxycodone per well and found an average 47% inhibition of IgE binding with 100μg/100μL of a 1:3 dilution of serum. This patient with a history of chronic lower back pain and asthma ingested one dose of Percocet (acetaminophen 325mg, oxycodone 5mg). Within 60 minutes, she developed generalized urticaria, dysphonia, and dyspnea. She denied wheezing and her characteristic symptoms of asthma exacerbation. In the ED she had increasing tongue swelling, decreased respiratory effort, and muffled voice; symptoms worsened despite epinephrine 0.3mg intramuscular then 0.1mg intravenous, dexamethasone 10mg IV, diphenhydramine 25mg IV, and ranitidine 50mg IV. She was intubated by anesthesiology for airway protection and transferred to the ICU. Patient extubated 12 hours after intubation, discharged within 48 hours with an Epipen, diagnosed with Percocet allergy, and instructed to avoid all opiates. Serum tryptase (8 hrs after exposure) 3ng/mL, C1 esterase inhibitor 95%, C3 99.6mg/dL, C4 16.17mg/dL, and IgG 831mg/dL. ELISA for oxycodone was run with 100μg oxycodone per well and found an average 47% inhibition of IgE binding with 100μg/100μL of a 1:3 dilution of serum. ConclusionsWe believe this is the first reported case of Type I IgE-mediated anaphylaxis to oxycodone. The use of ELISA to detect oxycodone IgE may be instructional for other diagnostic studies of suspected opioid anaphylaxis. We believe this is the first reported case of Type I IgE-mediated anaphylaxis to oxycodone. The use of ELISA to detect oxycodone IgE may be instructional for other diagnostic studies of suspected opioid anaphylaxis.