Facial Angioedema Research Articles

Hypersensibilité immédiate allergique au paracétamol

IntroductionParacetamol is an analgesic used in the general population with few side-effects. However, rare anaphylactic reactions to this molecule have been reported, for which allergy workups were usually negative, in contrast with our case. Case reportA 19-year-old atopic male patient presented generalized urticaria with facial angioedema, dyspnea and loss of consciousness in November 2017, one hour after ingestion of a single dose of paracetamol 1000mg. Symptoms improved within 30min under oral antihistamine and prednisolone. Before and since this reaction, nonsteroidal anti-inflammatory drugs were tolerated by the patient. In October 2018, an immediate-reading prick-test (10mg/mL) and an intradermal test (IDT) 10−2 (0.1mg/mL) performed with paracetamol were negative. Oral intake of paracetamol 50mg was well tolerated. A second series of skin tests was performed one month later and a paracetamol prick-test and IDT were positive. A basophil activation test (BAT) was positive at 40% in the presence of paracetamol (negative control 2% and positive control 93%). The BAT was negative in a control patient. In February 2019, a third series of skin tests with paracetamol was performed: a prick-test and IDT 10−2 were negative, but an IDT 10−1 (1mg/mL) was positive. A labial challenge paracetamol test using paracetamol prick solution was well tolerated. One hour after an oral drug challenge with 1000mg, the patient developed chest urticaria and cough with no other systemic symptoms. He recovered rapidly with intravenous antihistamine (dexchlorpheniramine). Serum tryptase was normal at 90min. DiscussionAllergic hypersensitivity to paracetamol was diagnosed and future intake of paracetamol was contraindicated. The absence of severe symptoms could account for the normal serum tryptase value during the last reaction. ConclusionWe report herein a rare case of immediate allergic hypersensitivity to paracetamol with a positive IDT and basophil activation test. BAT for paracetamol could be a reliable diagnostic tool in conjunction with skin tests and clinical history.

Ceftriaxone Induced Unilateral Facial Angioedema

We report a case receiving treatment with diclofenac sodium and ceftriaxone, who presented with facial unilateral angioedema attacks twice. Unilateral angioedema is a rare adverse reaction after NSAID usage. There is no previous report in the literature about ceftriaxone induced unilateral facial angioedema. To our knowledge this is the first reported case of unilateral facial angioedema following ceftriaxone treatment.

Characteristics Of Facial Angioedema In The Emergency Department

Characteristics Of Facial Angioedema In The Emergency Department

Probable “Escitalopram induced” angioedema in a patient with hereditary angioedema

Hereditary angioedema (HAE) is an autosomal dominant disorder. Considerable rate of mortality determines the importance of disease. In this paper, a patient with HAE who developed severe facial angioedema after the first dose of an antidepressant (Escitalopram) prescribed by a psychiatrist because of diagnosis of depression, was presented and discussed. In the presented case, severe facial angioedema was not found to be clearly associated with a particular cause. There were possibilities such as sporadic/idiopathic attack or depression related attack. However, occurrence of an acute attack soon after a newly started drug had to draw attention to Escitalopram. So, in patients with HAE under an antidepressant treatment, antidepressant related angioedema must be kept in mind when the HAE control deteriorated.

GADOLINIUM-INDUCED ANAPHYLAXIS: NOT ALL CONTRAST AGENTS ARE CREATED EQUAL

Introduction Hypersensitivity reactions to gadolinium-based contrast agents (GBCAs) are uncommon but anaphylaxis and fatalities have occurred. Case Description A 40-year-old woman with a past medical history of hypertension and chronic urticaria developed facial urticaria, flushing, angioedema, and presyncope within minutes of undergoing a gadobenate-based Magnetic Resonance Imaging (MRI) to detect breast cancer. The procedure was stopped, and her condition improved after treatment with IM dyphenhydramine. Tryptase was not obtained. Six-weeks later, undiluted skin prick tests (SPTs) and intradermal testing were performed using 1:1000, 1:100 and 1:10 dilution of the suspected and alternative GBCAs. SPT was positive to gadobenate and gadoterate meglumine (Figure 1), while the alternative GBCAs were negative (gadobutrol, gadodiamide, and gadoxetrate). Baseline tryptase was within normal limits (2.7; ref Discussion In patients with a history of gadolinium-induced anaphylaxis SPT may offer a viable option to select an alternative agent. There are few studies which investigate SPTs which can detect the presence of IgE thus predicting reactions to GBCAs. In our case, SPTs were utilized to avoid certain agents, while a subsequent graded dose challenge further helped identify gadobutrol as a safe agent. Hypersensitivity reactions to gadolinium-based contrast agents (GBCAs) are uncommon but anaphylaxis and fatalities have occurred. A 40-year-old woman with a past medical history of hypertension and chronic urticaria developed facial urticaria, flushing, angioedema, and presyncope within minutes of undergoing a gadobenate-based Magnetic Resonance Imaging (MRI) to detect breast cancer. The procedure was stopped, and her condition improved after treatment with IM dyphenhydramine. Tryptase was not obtained. Six-weeks later, undiluted skin prick tests (SPTs) and intradermal testing were performed using 1:1000, 1:100 and 1:10 dilution of the suspected and alternative GBCAs. SPT was positive to gadobenate and gadoterate meglumine (Figure 1), while the alternative GBCAs were negative (gadobutrol, gadodiamide, and gadoxetrate). Baseline tryptase was within normal limits (2.7; ref In patients with a history of gadolinium-induced anaphylaxis SPT may offer a viable option to select an alternative agent. There are few studies which investigate SPTs which can detect the presence of IgE thus predicting reactions to GBCAs. In our case, SPTs were utilized to avoid certain agents, while a subsequent graded dose challenge further helped identify gadobutrol as a safe agent.

ACQUIRED ANGIOEDEMA – AN UNUSUAL PRESENTATION OF SYSTEMIC LUPUS ERYTHEMATOSUS

Introduction Acquired angioedema requires evaluation for underlying etiologies including lymphoproliferative processes and autoimmune conditions. We present a patient with recurrent angioedema that was found to have systemic lupus erythematosus (SLE). Angioedema was her only presenting symptom. She denied other common signs and symptoms of SLE. Case Description The patient is a 30-year old Hispanic female with obesity and 3-4 episodes of facial angioedema in the past 6 months. She was hospitalized for severe acute abdominal pain and emesis with no other associated symptoms. The patient was not on ACEI and has no family history of angioedema. Physical examination revealed diffuse abdominal tenderness. Imaging showed small bowel edema. Laboratory evaluation revealed leukocytosis and mild elevation of transaminases. Due to history of recurrent facial angioedema, further work-up was done that showed low C1 esterase inhibitor levels and decreased function, low C1q, low C3 and C4, positive antinuclear antibodies (ANA) and Anti- SSA/Anti-SSB antibodies, suggesting underlying SLE. She denied any previous diagnosis of SLE and no signs/symptoms consistent with autoimmune conditions. She was started on C1 esterase inhibitor replacement prophylactically and has icatibant for acute attacks. She was also started on hydroxychloroquine for the underlying SLE. Discussion Acquired C1 esterase deficiency should prompt a broad evaluation for an underlying disorder. Our case suggests the consideration of an autoimmune disorder in the differential diagnosis, especially in young women who have no other supporting features.

DRESS TO TEN: IS THIS A CONTINUUM?

Introduction Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) is a potentially life-threatening severe cutaneous adverse drug reaction (SCAR) that can be triggered by medications. Toxic Epidermal Necrolysis (TEN) is also a type of SCAR. To the best of our knowledge, we present a first known clear case of DRESS which progressed to clinical TEN and was successfully treated. Case Description A 17-year old female was started on Lamotrigine and Escitalopram for a mood disorder. One week later, she developed tender cervical lymphadenopathy, fevers, and abdominal discomfort. About 2.5 weeks after starting these two medications, she developed a raised, pruritic, erythematous rash on her arms. Although the medication was discontinued, she failed to improve and developed facial angioedema, hepatic failure, eosinophilia and atypical lymphocytosis - all concerning signs for DRESS. Skin biopsy confirmed perivascular lymphocytic infiltrate with scattered eosinophils supporting DRESS. She was treated with intravenous immunoglobulin and eventually discharged home with a resolving rash. As Prednisone was tapered, the patient was readmitted with concerns for relapsing DRESS. She went on to develop TEN with mucosal involvement as well as greater than 30 percent skin involvement. She was successfully treated with a combination of Cyclosporine and high dose Prednisone. Discussion There is paucity of literature on SCAR overlap syndromes and we acknowledge the ambiguity and difficulty with this diagnosis given the overlapping presentation with SCAR syndromes. Although the mortality rate tends to be quite high for SCAR overlap syndromes, our patient was successfully treated with a combination of IVIG, steroids and Cyclosporine. Progression towards TEN. Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) is a potentially life-threatening severe cutaneous adverse drug reaction (SCAR) that can be triggered by medications. Toxic Epidermal Necrolysis (TEN) is also a type of SCAR. To the best of our knowledge, we present a first known clear case of DRESS which progressed to clinical TEN and was successfully treated. A 17-year old female was started on Lamotrigine and Escitalopram for a mood disorder. One week later, she developed tender cervical lymphadenopathy, fevers, and abdominal discomfort. About 2.5 weeks after starting these two medications, she developed a raised, pruritic, erythematous rash on her arms. Although the medication was discontinued, she failed to improve and developed facial angioedema, hepatic failure, eosinophilia and atypical lymphocytosis - all concerning signs for DRESS. Skin biopsy confirmed perivascular lymphocytic infiltrate with scattered eosinophils supporting DRESS. She was treated with intravenous immunoglobulin and eventually discharged home with a resolving rash. As Prednisone was tapered, the patient was readmitted with concerns for relapsing DRESS. She went on to develop TEN with mucosal involvement as well as greater than 30 percent skin involvement. She was successfully treated with a combination of Cyclosporine and high dose Prednisone. There is paucity of literature on SCAR overlap syndromes and we acknowledge the ambiguity and difficulty with this diagnosis given the overlapping presentation with SCAR syndromes. Although the mortality rate tends to be quite high for SCAR overlap syndromes, our patient was successfully treated with a combination of IVIG, steroids and Cyclosporine. Progression towards TEN.

CATAMENIAL ANAPHYLAXIS PRESENTING PRIOR TO ONSET OF MENSES

Introduction Catamenial anaphylaxis is an uncommon, heterogeneous disorder related to type 1 hypersensitivity to endogenous progesterone. We report a twelve-year old premenstrual female who presented with recurrent episodes of anaphylaxis with improvement after starting an oral contraceptive. Case Description A twelve-year old female presented with six episodes of anaphylaxis that occurred monthly. Her symptoms included nausea, vomiting, diarrhea, urticaria, dizziness, and facial angioedema all requiring hospitalization. She was treated with intramuscular epinephrine, antihistamines, and systemic steroids. Her third episode occurred thirty-six hours after she had received her first dose of omalizumab. Her symptoms were uncontrolled despite treatment with prednisone, cromolyn, ketotifen, anti-leukotrienes and antihistamines. Her work-up for anaphylactic triggers, systemic mastocytosis, and carcinoid syndrome was negative. Her lab-work showed an elevated tryptase to 13.2 ug/L from a baseline of 2.0 ug/L. There was concern for catamenial anaphylaxis given the cyclical nature of her symptoms, however the patient had not started menstruation. She underwent an oral challenge with progesterone with no reaction. She was started on low-ogestrel and did not have any subsequent episodes of anaphylaxis. Discussion Catamenial anaphylaxis is described as recurrent episodes of multi-system allergic reactions occurring around the time of menstruation. This case is the first description of a premenstrual female who presented with catamenial anaphylaxis. The patient had no further episodes of anaphylaxis following initiation of an oral contraceptive as opposed to previous therapies. It is important to consider catamenial anaphylaxis in the differential diagnosis of idiopathic anaphylaxis prior to the onset of menses.

A RARE CAUSE OF ANGIOEDEMA WITH TREATMENT LEADING TO RESOLUTION OF CUTANEOUS SYMPTOMS

Introduction Urticarial vasculitis (UV) manifestations range from urticaria to systemic vasculitis. Serious cases are associated with hypocomplementemia in which immune complexes deposit in multiple sites called Hypocomplementemic Urticarial Vasculitis Syndrome (HUVS). Case Description A 63-year-old female presented to our medical center for evaluation of intermittent facial angioedema and urticaria occurring over five years without known trigger. These episodes prompted evaluation in local emergency departments for acute treatment. Instructions provided from previous allergy evaluation included initiation of daily antihistamines; however, intermittent episodes continued. Urticaria was not associated with burning, pain, or bruising. Past medical history was notable for stable chronic kidney disease, hypertension, diabetes, and polymyalgia rheumatica. Laboratory evaluation revealed reduced serum C4 with negative work-up for hereditary and acquired angioedema. Additional studies for thyroid dysfunction, mast cell disorder, and systemic inflammation were negative. Increased but stable serum creatinine was noted on metabolic profile. She was diagnosed with idiopathic urticaria–angioedema and advised to quadruple her antihistamine regimen. One year later, she was admitted for acute renal failure with increased serum creatinine. Lab-work revealed worsened hypocomplementemia with elevated ANCA (1:10240), urine eosinophilia, and proteinuria. Renal biopsy confirmed pauci-immune necrotizing glomerulonephritis. She was treated with rituximab and a taper of oral prednisone. Since treatment, she has been without recurrence of angioedema, and kidney function has returned to baseline. Discussion HUVS with glomerulonephritis is rare with few reported cases. This patient experienced years of angioedema prior to diagnosis with resolution of complaints after rituximab and prednisone treatment, demonstrating the need for a comprehensive evaluation and exploration of therapeutic options.

¿Son seguros los productos naturales analgésicos en los pacientes con alergia a los antiinflamatorios no esteroideos?

Nonsteroidal anti-inflammatory drugs (NSAID)-induced hypersensitivity reactions can be clinically apparent with asthma, rhinosinusitis, anaphylaxis or rash. Although natural anti-inflammatory products can have similar components, they are not subjected to rigorous quality control standards. The case is presented of a 22-year-old female with NSAID allergy who attended with facial and laryngeal angioedema associated with pruritus in eyelids and pharynx. She developed these symptoms fifteen minutes after taking an over-the-counter (OTC) natural anti-inflammatory product. She received treatment with epinephrine, antihistamines and corticosteroids. Different natural anti-inflammatory products are freely available both OTC and online. Some contain dangerous substances that can cause important, and even lethal. side effects. Allergologists, dermatologists and general practitioners should be able to recognize that the consumption of these products, which is widely spread, can cause angioedema.

Hereditary angioedema attack – case presentation

Hereditary angioedema, or inherited C1-inhibitor esterase deficiency, is a rare genetic disorder, characterized by recurrent episodes of isolated angioedema, which most often affect the skin or mucosal tissues of the upper respiratory and gastrointestinal tracts. Although swelling resolves spontaneously in two to five days in the absence of treatment, angioedema is often temporarily debilitating, and laryngeal angioedema may cause fatal asphyxiation. Dental surgery and intubation are the major triggers for hereditary angioedema attacks. Typically, laryngeal edema develops 24 to 48 hours after the onset of prodromal signs. However, rapidly evolving, fulminant laryngeal edema cases have been described. We present the case of a 42-year-old male patient, with a medical history of hereditary angioedema, included in the National Program of Hereditary Angioedema, who was referred to the Allergy Department of the „Prof. Dr. Octavian Fodor“ Institute of Gastroenterology and Hepatology, Cluj-Napoca, for dysphagia, dysphonia, facial and right laterocervical edema, events that started about one hour after a dental surgery for which he received premedication with a C1-inhibitor esterase recombinant. Physical examination revealed facial and right laterocervical angioedema, edema of the oral and pharyngeal mucosa, dysphonia, tachycardia, and decreased SaO2. Subcutaneous administration of icatibant significantly improved the signs and symptoms. Laryngeal edema is a life-threatening complication of hereditary angioedema attacks. Dental surgery and tracheal intubation are major risk factors for attacks. Although premedication with C1-inhibitor esterase recombinant appears to have prevented such events, this was not the case for our patient. Also, hereditary angioedema signs and symptoms typically consolidate in one up to two days after the prodromal phase. In the present case, the clinical picture had a rapid evolution. The treatment with bradikinin B2 receptor antagonists brought rapid efficient clinical benefit.

P178 Severe chronic idiopathic urticaria and angioedema with an elevated anti-IgE IgG level

Chronic idiopathic urticaria (CIU) is characterized by pruritic urticarial lesions, but the underlying mechanism is not understood. Proposed etiologies have implicated autoantibodies, cellular mast cell and/or basophil defects. The symptoms experienced by patients with CIU may cause significant morbidity, especially if facial and oropharyngeal angioedema occur. Here, we discuss a patient with CIU, recurrent angioedema and an elevated anti-IgE IgG.

Angioedema como única manifestación inicial de hipogammaglobulinemia

Common variable immunodeficiency is characterized by hypogammaglobulinemia and the inability to respond to vaccines. Patients mostly manifest infections, however only less than 5 % have pathological conditions as autoimmunity, granulomatous inflammation, and splenomegaly or lymphoproliferative disease among others, without showing infections. We report the case of a woman who debuted with localized cutaneous affection, facial angioedema, without other early symptoms. After diagnosis splenomegaly and bronchiectasis were documented. Angioedema and bronchiectasis responded with IVIG replacement. We also review the dermatological manifestations associated with CVID.

Recurrent elevated liver transaminases and acute liver failure in two siblings with novel bi-allelic mutations of NBAS

BackgroundAcute liver failure (ALF) in children can be life-threatening. Although many causes are known, ALF remains unexplained in about half of the cases. Recently, bi-allelic mutations in NBAS were reported to underlie recurrent episodes of elevated liver transaminases (ELT) and ALF in the context of diverse extrahepatic phenotypes. Methods and ResultsWe here describe two sisters, born to non-consanguineous Portuguese parents, who had short stature and presented with recurrent episodes of severe ELT triggered by febrile respiratory viral infections since early childhood. Patient 1 had mild facial dysmorphism and died during the second ELT crisis at 3–11/12 years of age. Patient 2, currently 9 years old, had multiple episodes of ELT (>30), twice with ALF, often accompanied by extensive urticaria and facial angioedema. Whole-exome and Sanger sequencing revealed that both patients carried previously undescribed compound heterozygous mutations of NBAS (NM_015909.3): c.680A > C (p.His227Pro), affecting an evolutionarily conserved residue, and c.1749G > A (p.Trp583*), causing a premature stop codon. Both mutations are predicted to be highly damaging. The parents and two younger siblings are healthy and heterozygous for one or another mutant allele. ConclusionThe multiplex kindred reported herein expands the genotypic and phenotypic spectrum of this recently described clinical syndrome due to autosomal recessive NBAS deficiency.

A case of recurrent facial angioedema associated with elevated tree pollen counts

A case of recurrent facial angioedema associated with elevated tree pollen counts

Angioedema Without Urticaria In The Emergency Department

M O N D A Y 643 Profile of Seasonal Differences in Angioedema Presenting to an Inner City Hospital Karyn Winkler, MD, Tukisa Smith, MD, Ashlei Mathew, MD, Rauno Joks, MD; Center for Allergy and Asthma Research, SUNY Downstate Medical Center. RATIONALE: We have previously reported there is a significant increase in angioedema, but not urticaria, in the summer months. In order to further understand this increase, we have investigated the difference in the clinical profiles of patients who are diagnosed in summer months vs. those treated in the winter months. METHODS: A retrospective EMR chart review of the cases of patients treated for angioedema from 2007 to 2012 in either summer (June, July, August) or winter (December, January, February). Data gathered included probable triggers (medication, food, or unknown), body location (face, lips, mouth/throat, and/or extremities/other), duration of symptoms before seeking medical care, and AM or PM presentation at the hospital. Statistical methods included Chi-square test, Fisher’s Exact test, and Mann-Whitney test. RESULTS: A total of 96 cases of angioedema were diagnosed in summer, vs. 65 in winter (p50.015).There was no significant difference in associated triggers between the two seasons (p50.186). There was a significant increase in facial edema occurring with winter presentation (24/ 65) vs. summer (19/65) (p50.016). There was no difference in AM vs. PM presentation (AM summer 49/88 (59%) vs AM winter 34/63 (41%), p50.87) or duration of symptoms (mean6 SD: summer: 2.06 2.2 hours vs. winter 1.6 6 1.6 hours) before presentation (0.09). CONCLUSIONS: Seasonal influence on angioedema includes increase in frequency in summer months and increased facial angioedema in winter months.

Anaphylaxis induced by proton pump inhibitors

Anaphylaxis induced by proton pump inhibitors

A lurking threat: transfer of peanut allergy through peripheral blood stem cell transplantation

Background There exist several reports of atopy and allergen-specific IgE-mediated hypersensitivity transferred by bone marrow transplantation, and it has been concluded that the transfer of allergic reactivity results from adoptive transfer of IgE-producing donor-derived B- and/or plasma cells. To the best of our knowledge we report the first case of peanut allergy after PBSCT.Case presentation A 55-year-old anciently non allergic man with secondary acute myeloid leukemia (AML) received an allogeneic peripheral blood stem cell transplantation from a matched unrelated donor following reduced-intensity conditioning. On day 32 after PBSCT, while still on prophylactic systemic immunosuppression, the patient noticed a first episode of angioedema with swelling of the nasal and oral mucosa 30 min after consuming peanut puffs. In a second episode, eight months after PBSCT, he again developed angioedema, generalized pruritus and nausea within minutes after eating biscuits containing hazelnut and peanut. Moreover, after topical application of a peanut oil-containing ointment, the patient experienced facial erythema and angioedema. Nine months after PBSCT an evaluation for peanut allergy revealed a highly increased specific IgE to peanut of 75.9 kU/l. Accordingly, skin prick tests for peanut extract were also positive. In consequence, the patient was counseled to strictly avoid peanut-related products, and provided with an emergency set. No adverse allergic events have occurred since for an observation time of 15 months after PBSCT. The stem cell donor was contacted and confirmed intolerance to peanuts. His specific serum IgE pattern nine month after PBSCT harvest was analysed and showed similar sensitization profiles compared to those of the transplant recipient.Conclusions Because of the close temporal association between the onset of allergic symptoms in the PBSC recipient it is reasonable to assume that the acquired peanut allergy had been transferred from the donor to the recipient by the PBSC graft.

Eosinophilic esophagitis: a matter of flavoring

Eosinophilic esophagitis (EoE) is an inflammatory disease characterized by eosinophilic infiltration of the esophageal wall. It is an increasingly recognized disease that affects mostly caucasian males in two peaks of incidence: 5-10/20-40 years. Studies show that more than 90% of this patients are sensitized to mite or polens, 50% to food, and that the contact with them exacerbates the disease. We aim to present a 30 years old caucasian male patient with a previous history of rhinitis, sent in 2012 to our immunoallergology department by urticaria, intermittent dysphagia and food impactation for 10 years. First impactation occurred in 2008 and the upper gastrointestinal endoscopy (UGIE) revealed annular strictures, longitudinal grooves and the respective biopsy showed eosinophilic inflammatory infiltrate. In the Gastroenterology department started a proton pump inhibitor and later topical corticosteroids for 3 months. In January 2012 after the intake of dried pumpkin seeds the patient had an episode of generalized urticaria plus facial angioedema without other systemic involvement; this episode occurred again after consumption of dried flavored cashews. In August 2012 a new food impactation occurred. (1) Skin prick tests (mm):

A Case of Coconut Anaphylaxis

Event Abstract Back to Event A Case of Coconut Anaphylaxis ANA M. ACEVEDO1, 2*, ANA M. CELIS1, 2 and RUTH H. RAMIREZ1, 2 1 Antioquia´s University, Allergy, Colombia 2 Grupo de Alergología Clínica y Experimental- (GACE), Colombia INTRODUCTION: The coconut is the fruit of monocot plant Cocosnucifera from the Arecaceae family. Few cases of allergy to coconuts have been reported, and most are mediated by specific immunoglobulin E. There are only two cases reported of anaphylaxis coconut in the pediatric population. The coconutis composed of 25% albumin and 75% globulin and are involved in the reactions to this fruit, asCocn2(7S globulin) and Cocn4(11S globulin). Cross-reactivity betweencoconut, walnuts, hazelnuts and lentils has been described.. OBJECTIVE:To describe a case of anaphylaxis coconut. METHODS: 9-yearold patient, from the Colombian Atlantic coast, with a history of asthma,rhinoconjunctivitis and atopic dermatitis since the early years of life, sensitized to dust mites, dogs and mosquitos; with clinical symptoms from 2 years life consisting of facial angioedema, throat and nasalocular itching within a few minutes of eating fresh coconut. Eating coconut again when 7 years old and there is immediate presence of facial and tongue angioedema, associated with itchy eyes, nasal, pharyngeal and respiratory distress, requiring emergency assistance service. After the last episode, the patient describes nasal ocular symptoms by inhaling vapors from cooking coconut, which are similar to the symptoms described after peanut and pineapple intake. In the diagnostic approach prick tests with coconut commercial extracts and prick-by-prick with fresh samples were performed in triplicate with positive and negative for almond, hazelnut, pistachio, lentils and pineapple. In addition to specific serum immunoglobulin E coconut performed: 23.2 Class 4, Class 312.2 peanuts, pineapple, 0.29 (negative). CONCLUSION: A case of anaphylaxis described by coconut in pediatric population so confirmed mediated Immunoglobulin E coconut and skin tests. Skin tests are useful tool in the diagnosis of this type of allergy. Besides, the use of fresh extract has been described in other studies to give better performance, with about 80.6% specificity and negative predictive value of 78.1% References AllergolImmunopathol (Madr). 2013 Allergy 2002: 57:182–183 Pediatr Allergy Immunol 2010: 21: 1114–1118 Keywords: Coconut, allergy, Anaphylaxis, Immunoglobulin E, Skin Tests Conference: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología, Medellin, Colombia, 13 Oct - 16 Oct, 2015. Presentation Type: Poster Presentation Topic: Allergy Citation: ACEVEDO AM, CELIS AM and RAMIREZ RH (2015). A Case of Coconut Anaphylaxis. Front. Immunol. Conference Abstract: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología. doi: 10.3389/conf.fimmu.2015.05.00267 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 29 May 2015; Published Online: 14 Sep 2015. * Correspondence: MD. ANA M ACEVEDO, Antioquia´s University, Allergy, Medellín, Colombia, anitaace@hotmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers ANA M ACEVEDO ANA M CELIS RUTH H RAMIREZ Google ANA M ACEVEDO ANA M CELIS RUTH H RAMIREZ Google Scholar ANA M ACEVEDO ANA M CELIS RUTH H RAMIREZ PubMed ANA M ACEVEDO ANA M CELIS RUTH H RAMIREZ Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.