- Email: [email protected]
Anaphylaxis following cilantro ingestion
Letters / Ann Allergy Asthma Immunol 109 (2012) 470e475
period, significant decreases in tree nutespecific IgE might be seen. Future studies will need to incorporate entry challenges to tree nuts, periodic challenges while on therapy, and long-term follow-up. Avoidance of the allergenic food and treatment of a reaction with auto-injectable epinephrine is still considered the standard therapy for food allergy.7 As new treatment options emerge, clinicians must be mindful of the implications of each treatment for the multi-food-allergic person. The data from this report do not support the notion that cross-reactive allergens may be treated with peanut OIT. Regardless of the modality of therapy used, if the therapy is only allergen-specific, the benefit of protection against 1 allergen while remaining allergic to other allergens must be considered. Tree nuteallergic individuals receiving peanut OIT should continue strict avoidance of tree nuts and should carry selfinjectable epinephrine in case of accidental ingestion. Acknowledgment We are grateful to Rong Huang, MS, Children’s Medical Center, Dallas, Texas, for biostatistical assistance. J. Andrew Bird, MD* Michael Kulis, PhDy Caitlin M. Burk, BAz Brian P. Vickery, MDz Stacie M. Jones, MDx Wesley Burks, MDy *Department of Pediatrics Division of Allergy and Immunology
471
UT Southwestern Medical Center Dallas, Texas y University of North Carolina Chapel Hill, North Carolina z Duke University Medical Center Durham, North Carolina x University of Arkansas for Medical Sciences Little Rock, Arkansas [email protected]
References [1] Jones SM, Pons L, Roberts JL, et al. Clinical efficacy and immune regulation with peanut oral immunotherapy. J Allergy Clin Immunol. 2009;124:292e300.e97. [2] Varshney P, Jones SM, Scurlock AM, et al. A randomized controlled study of peanut oral immunotherapy: clinical desensitization and modulation of the allergic response. J Allergy Clin Immunol. 2011;127:654e660. [3] Maloney JM, Rudengren M, Ahlstedt S, Bock SA, Sampson HA. The use of serum-specific IgE measurements for the diagnosis of peanut, tree nut, and seed allergy. J Allergy Clin Immunol. 2008;122:145e151. [4] de Leon MP, Glaspole IN, Drew AC, Rolland JM, O’Hehir RE, Suphioglu C. Immunological analysis of allergenic cross-reactivity between peanut and tree nuts. Clin Exp Allergy. 2003;33:1273e1280. [5] Beyer K, Bardina L, Grishina G, Sampson HA. Identification of sesame seed allergens by 2-dimensional proteomics and Edman sequencing: seed storage proteins as common food allergens. J Allergy Clin Immunol. 2002;110: 154e159. [6] Ball H, Luyt D, Bravin K, Kirk K. Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets. Pediatr Allergy Immunol. 2011;22:808e812. [7] Boyce JA, Assa’ad A, Burks AW, et al. Guidelines for the Diagnosis and Management of Food Allergy in the United States: Summary of the NIAIDSponsored Expert Panel Report. J Allergy Clin Immunol. 2010;126:1105e1118.
Anaphylaxis following cilantro ingestion A 52-year-old white male presented for evaluation of a systemic reaction that occurred after ingesting fresh bruschetta bread with coriander (cilantro) leaves. On the first occasion, he developed diffuse urticaria that was self-limited. On the second occasion, he developed severe angioedema of the face, urticaria, and laryngeal edema with wheezing. He presented to the emergency room and was treated with intravenous methylprednisolone, diphenhydramine, and famotidine, and was discharged with a prescription for an EpiPen (epinephrine auto-injector). The patient recognized that the only common ingestion with the episodes was cilantro. He introduced the foods eaten on both occasions without cilantro and no reaction occurred. The patient then purposely consumed the same food with minute amounts of cilantro, but quickly stopped the meal when he developed mild itching of the face with angioedema of the face and lips that did not progress. The patient reported a history of persistent allergic rhinitis treated with intranasal steroids. The patient denied any history of food allergy, drug allergy, asthma, urticaria, angioedema, latex sensitivity, allergic contact dermatitis, or other forms of atopic disease. His medical history included mild obstructive sleep apnea, type 2 diabetes mellitus, essential hypertension, exogenous obesity, and erectile dysfunction. His medications were aspirin, sitagliptin, glipizide, vardenafil, atorvastatin, lisinopril, repaglinide/metformin, and mometasone nasal spray. Skin prick testing revealed negative reactions to all foods consumed during the allergic reaction. Environmental testing revealed a reaction to dust mite, and intradermal
Disclosures: Authors have nothing to disclose.
testing yielded positive results to tree mix, cat, dog, mixed feathers, mixed ragweed, and cockroach. Skin prick testing with fresh cilantro leaf was negative. Allergen-specific IgE testing was performed using the ImmunoCAP(R) FEIA methodology, which has been shown to have a very high antigen-binding capacity and has minimal nonspecific binding with high total IgE. Laboratory immunoassay for IgE antibody to coriander (cilantro) seed was 0.99 Ku/L (reference range, <0.35). Food-induced anaphylactic reaction (FIAR) accounts for approximately 125,000 emergency department visits per year in the United States resulting from immunoglobulin E (IgE) and non-IgE mechanisms.1 Food-induced anaphylactic reaction is most commonly the result of peanuts and tree nut ingestion in the United States.1 In 1 study of food allergy in adults, spice allergy was found in 2% of patients.1 There is little in the literature on food-induced anaphylactic reaction secondary to cilantro. Cilantro (the Spanish term for coriander) is a member of the Apiaecea family and refers to the entire plant, both leaves and seeds. The allergens are present in both the leaves and the seeds.2 It is the leaf of Coriandrum sativum L. and is a commonly used spice found in Mexican and eastern Indian, Chinese, and Thai cuisines. Dating back to 5000 B.C., cilantro was used by Hippocrates. The herb was known to the Egyptians as the “spice of happiness,” because it was purported to be an aphrodisiac.2 Commercially, the herb is used as a flavoring agent in a number of products such as tobacco, meat sauce, alcoholic beverages, candies, and perfumes.2 Cilantro is thought to have disease-modifying effects in patients with rheumatoid arthritis.3 Most data on spice allergy are limited to the adult literature, because spice consumption is uncommon in children. Exposure to
472
Letters / Ann Allergy Asthma Immunol 109 (2012) 470e475
spices can occur through a variety of mechanisms such as ingestion (most common), inhalation, or direct skin exposure.4 Reactions are classified as non-IgE (irritant cutaneous) or IgE-mediated (urticaria, angioedema, airway compromise).5 In the case of spices, Bet V1 (pathogenesis-related protein) and Bet v2 (profilins) are commonly found allergen structures responsible for allergic reactions to spices.4 Patients with birch pollenosis may demonstrate cross-reactivity with such foods as apple, cherry, or pears, which are members of the family Rosaceae, or celery, caraway seeds, fennel seeds, aniseed, parsley, or carrots, which are members of the family Apiaceae.5, 6 Quirce et al7 reported 2 cases of carrot-induced asthma after consumption of cooked carrots or parsley.7 Patients may also experience cross-reactivity to members of the families Solanaceae (paprika, tomato, nicotine, alkaloids, capsaicin, petunia, nightshade), Piperaceae (peppercorns including black pepper), Anacardiaceae (cashew, pistachio, mango, poison ivy), and Liliaceae (garlic, onion, tulips, tiger lilies).6 Differing in etiology from oral allergy syndrome, because of prior sensitization to aeroallergens such as weed and tree pollens, these patients may hypothetically benefit from pollen allergen immunotherapy.6 Because commercially available, reliable standardized extracts are unavailable for skin prick testing, allergy is based on history, immunoassay testing, and food challenge. Spice allergy and cross-reactivity of foods in patients with pollenosis is an increasing concern. This case describes foodinduced anaphylactic reaction secondary to coriander (cilantro) allergy and underscores the need for a detailed history of aeroallergen sensitivity and consideration for associated botanical cross-reactivity. David W. Unkle, MSN, APN, FCCM* Anthony J. Ricketti, MD, FCCPy,z Peter A. Ricketti, DOx Dennis J. Cleri, MD, FACP{ John R. Vernaleo, MDjj
*Department
of Family Medicine School of Osteopathic Medicine University of Medicine & Dentistry of New Jersey Stratford, New Jersey y Section of Allergy and Immunology, and Internal Medicine Residency St. Francis Medical Center Trenton, New Jersey z Seton Hall University School of Health and Medical Sciences South Orange, New Jersey x Internal Medicine University of Medicine & Dentristry of New Jersey Newark, New Jersey { Internal Medicine Residency St. Francis Medical Center Trenton, New Jersey jj Wyckoff Heights Medical Center Brooklyn, New York [email protected]
References [1] Rudders SA, Banerji A, Vassallo MF, Clark S, Camargo CA Jr. Trends in pediatric emergency department visits for food-induced anaphylaxis. J Allergy Clin Immunol.. 2010;126:385e388. [2] Burdock GA, Carabin IG. Safety assessment of coriander (Coriandrum sativum L.) essential oil as a food ingredient. Food Chem Toxicol.. 2009;47:22e34. [3] Nair V, Singh S, Gupta YK. Evaluation of disease modifying activity of Coriandrum sativum in experimental models. Indian J Med Res.. 2012;135: 240e245. [4] Chen JL, Bahna SL. Spice allergy. Ann Allergy Asthma Immunol.. 2011;107: 191e199. [5] Konstantinou GN, Grattan CEH. Food contact hypersensitivity syndrome: the mucosal contact urticarial paradigm. Clin Exp Dermatol.. 2008;33:383e389. [6] Egger M, Mutschlechner S, Wopfner N, Gadermaier G, Briza P, Ferreira F. Pollenfood syndromes associated with weed pollinosis: an update from the molecular point of view. Allergy.. 2006;61:461e476. [7] Quirce S, Blanco R, Diez-Gomez ML, Cuevas M, Eiras P, Losada E. Carrot-induced asthma: immunodetection of allergens. J Allergy Clin Immunol.. 1997;99: 718e719.
Food protein-induced enterocolitis syndrome triggered by orange juice Food proteineinduced enterocolitis syndrome (FPIES) is a none immunoglobulin E (IgE)-mediated gastrointestinal disorder triggered by ingestion of certain foods. Often a delay in diagnosis occurs because patients have nonspecific symptoms and can be mismanaged as acute gastrointestinal illness, intussusception, or sepsis.1 The most common offending foods include cow’s milk, soy, and rice; however, other foods have been identified as causative agents.2 Review of the literature revealed 1 case report of fruitinduced FPIES diagnosed by open food challenge (OFC) to mixed fruit including apple, pear, and banana,3 as well as 3 documented cases of FPIES to banana.4,5 We describe the first report to our knowledge of FPIES to orange juice. Recently we managed a 2-year-old white boy with repetitive emesis, dehydration, and lethargy occurring on 5 separate occasions. His first reaction occurred at 10 months of age with approximately 10 episodes of emesis with no fever, diarrhea, rash, angioedema, or respiratory symptoms. The boy was admitted to our hospital and returned to baseline shortly after intravenous fluid replacement. One week later, he developed multiple episodes of emesis and was treated in the emergency department for viral gastroenteritis. At approximately 11 months of age, he had 2
Disclosures: Authors have nothing to disclose.
similar episodes, with resolution of symptoms after intravenous fluid replacement. His last reaction, occurring at 18 months of age, was more severe, with emesis, decreased urine output, hypotension, and lethargy. He was admitted to our hospital for dehydration with negative abdominal x-ray and stool culture. Because of concern for IgE-mediated food allergy, he was referred to our allergy clinic. In our clinic, on further history taking, the possibility of orange juice as a trigger for his reactions was identified. Emesis had occurred 1 to 2 hours after ingestion of orange juice in most of his reactions. No other specific foods or triggers could be elicited. His parents denied exposure to other citrus foods in the past. He was tolerating other fruits, including apples, pears, and bananas, thereby decreasing the likelihood of fructose intolerance. No history of atopy, including asthma, allergic rhinitis, eczema, or food allergy, was identified. The possibility of IgE-mediated food allergy was ruled out based on negative skin prick testing to orange extract and fresh orange juice. Additionally, specific IgE to orange was less than 0.1 kU/L. Given that most gastrointestinal food hypersensitivities are noneIgE-mediated and require elimination diets or food challenges for diagnosis,6 we elected to perform an oral food challenge (OFC). We followed the OFC protocol for FPIES outlined in “Work group report: oral food challenge testing,” by NowakWe˛grzyn et al.7 Based on his history of severe reactions, we used
period, significant decreases in tree nutespecific IgE might be seen. Future studies will need to incorporate entry challenges to tree nuts, periodic challenges while on therapy, and long-term follow-up. Avoidance of the allergenic food and treatment of a reaction with auto-injectable epinephrine is still considered the standard therapy for food allergy.7 As new treatment options emerge, clinicians must be mindful of the implications of each treatment for the multi-food-allergic person. The data from this report do not support the notion that cross-reactive allergens may be treated with peanut OIT. Regardless of the modality of therapy used, if the therapy is only allergen-specific, the benefit of protection against 1 allergen while remaining allergic to other allergens must be considered. Tree nuteallergic individuals receiving peanut OIT should continue strict avoidance of tree nuts and should carry selfinjectable epinephrine in case of accidental ingestion. Acknowledgment We are grateful to Rong Huang, MS, Children’s Medical Center, Dallas, Texas, for biostatistical assistance. J. Andrew Bird, MD* Michael Kulis, PhDy Caitlin M. Burk, BAz Brian P. Vickery, MDz Stacie M. Jones, MDx Wesley Burks, MDy *Department of Pediatrics Division of Allergy and Immunology
471
UT Southwestern Medical Center Dallas, Texas y University of North Carolina Chapel Hill, North Carolina z Duke University Medical Center Durham, North Carolina x University of Arkansas for Medical Sciences Little Rock, Arkansas [email protected]
References [1] Jones SM, Pons L, Roberts JL, et al. Clinical efficacy and immune regulation with peanut oral immunotherapy. J Allergy Clin Immunol. 2009;124:292e300.e97. [2] Varshney P, Jones SM, Scurlock AM, et al. A randomized controlled study of peanut oral immunotherapy: clinical desensitization and modulation of the allergic response. J Allergy Clin Immunol. 2011;127:654e660. [3] Maloney JM, Rudengren M, Ahlstedt S, Bock SA, Sampson HA. The use of serum-specific IgE measurements for the diagnosis of peanut, tree nut, and seed allergy. J Allergy Clin Immunol. 2008;122:145e151. [4] de Leon MP, Glaspole IN, Drew AC, Rolland JM, O’Hehir RE, Suphioglu C. Immunological analysis of allergenic cross-reactivity between peanut and tree nuts. Clin Exp Allergy. 2003;33:1273e1280. [5] Beyer K, Bardina L, Grishina G, Sampson HA. Identification of sesame seed allergens by 2-dimensional proteomics and Edman sequencing: seed storage proteins as common food allergens. J Allergy Clin Immunol. 2002;110: 154e159. [6] Ball H, Luyt D, Bravin K, Kirk K. Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets. Pediatr Allergy Immunol. 2011;22:808e812. [7] Boyce JA, Assa’ad A, Burks AW, et al. Guidelines for the Diagnosis and Management of Food Allergy in the United States: Summary of the NIAIDSponsored Expert Panel Report. J Allergy Clin Immunol. 2010;126:1105e1118.
Anaphylaxis following cilantro ingestion A 52-year-old white male presented for evaluation of a systemic reaction that occurred after ingesting fresh bruschetta bread with coriander (cilantro) leaves. On the first occasion, he developed diffuse urticaria that was self-limited. On the second occasion, he developed severe angioedema of the face, urticaria, and laryngeal edema with wheezing. He presented to the emergency room and was treated with intravenous methylprednisolone, diphenhydramine, and famotidine, and was discharged with a prescription for an EpiPen (epinephrine auto-injector). The patient recognized that the only common ingestion with the episodes was cilantro. He introduced the foods eaten on both occasions without cilantro and no reaction occurred. The patient then purposely consumed the same food with minute amounts of cilantro, but quickly stopped the meal when he developed mild itching of the face with angioedema of the face and lips that did not progress. The patient reported a history of persistent allergic rhinitis treated with intranasal steroids. The patient denied any history of food allergy, drug allergy, asthma, urticaria, angioedema, latex sensitivity, allergic contact dermatitis, or other forms of atopic disease. His medical history included mild obstructive sleep apnea, type 2 diabetes mellitus, essential hypertension, exogenous obesity, and erectile dysfunction. His medications were aspirin, sitagliptin, glipizide, vardenafil, atorvastatin, lisinopril, repaglinide/metformin, and mometasone nasal spray. Skin prick testing revealed negative reactions to all foods consumed during the allergic reaction. Environmental testing revealed a reaction to dust mite, and intradermal
Disclosures: Authors have nothing to disclose.
testing yielded positive results to tree mix, cat, dog, mixed feathers, mixed ragweed, and cockroach. Skin prick testing with fresh cilantro leaf was negative. Allergen-specific IgE testing was performed using the ImmunoCAP(R) FEIA methodology, which has been shown to have a very high antigen-binding capacity and has minimal nonspecific binding with high total IgE. Laboratory immunoassay for IgE antibody to coriander (cilantro) seed was 0.99 Ku/L (reference range, <0.35). Food-induced anaphylactic reaction (FIAR) accounts for approximately 125,000 emergency department visits per year in the United States resulting from immunoglobulin E (IgE) and non-IgE mechanisms.1 Food-induced anaphylactic reaction is most commonly the result of peanuts and tree nut ingestion in the United States.1 In 1 study of food allergy in adults, spice allergy was found in 2% of patients.1 There is little in the literature on food-induced anaphylactic reaction secondary to cilantro. Cilantro (the Spanish term for coriander) is a member of the Apiaecea family and refers to the entire plant, both leaves and seeds. The allergens are present in both the leaves and the seeds.2 It is the leaf of Coriandrum sativum L. and is a commonly used spice found in Mexican and eastern Indian, Chinese, and Thai cuisines. Dating back to 5000 B.C., cilantro was used by Hippocrates. The herb was known to the Egyptians as the “spice of happiness,” because it was purported to be an aphrodisiac.2 Commercially, the herb is used as a flavoring agent in a number of products such as tobacco, meat sauce, alcoholic beverages, candies, and perfumes.2 Cilantro is thought to have disease-modifying effects in patients with rheumatoid arthritis.3 Most data on spice allergy are limited to the adult literature, because spice consumption is uncommon in children. Exposure to
472
Letters / Ann Allergy Asthma Immunol 109 (2012) 470e475
spices can occur through a variety of mechanisms such as ingestion (most common), inhalation, or direct skin exposure.4 Reactions are classified as non-IgE (irritant cutaneous) or IgE-mediated (urticaria, angioedema, airway compromise).5 In the case of spices, Bet V1 (pathogenesis-related protein) and Bet v2 (profilins) are commonly found allergen structures responsible for allergic reactions to spices.4 Patients with birch pollenosis may demonstrate cross-reactivity with such foods as apple, cherry, or pears, which are members of the family Rosaceae, or celery, caraway seeds, fennel seeds, aniseed, parsley, or carrots, which are members of the family Apiaceae.5, 6 Quirce et al7 reported 2 cases of carrot-induced asthma after consumption of cooked carrots or parsley.7 Patients may also experience cross-reactivity to members of the families Solanaceae (paprika, tomato, nicotine, alkaloids, capsaicin, petunia, nightshade), Piperaceae (peppercorns including black pepper), Anacardiaceae (cashew, pistachio, mango, poison ivy), and Liliaceae (garlic, onion, tulips, tiger lilies).6 Differing in etiology from oral allergy syndrome, because of prior sensitization to aeroallergens such as weed and tree pollens, these patients may hypothetically benefit from pollen allergen immunotherapy.6 Because commercially available, reliable standardized extracts are unavailable for skin prick testing, allergy is based on history, immunoassay testing, and food challenge. Spice allergy and cross-reactivity of foods in patients with pollenosis is an increasing concern. This case describes foodinduced anaphylactic reaction secondary to coriander (cilantro) allergy and underscores the need for a detailed history of aeroallergen sensitivity and consideration for associated botanical cross-reactivity. David W. Unkle, MSN, APN, FCCM* Anthony J. Ricketti, MD, FCCPy,z Peter A. Ricketti, DOx Dennis J. Cleri, MD, FACP{ John R. Vernaleo, MDjj
*Department
of Family Medicine School of Osteopathic Medicine University of Medicine & Dentistry of New Jersey Stratford, New Jersey y Section of Allergy and Immunology, and Internal Medicine Residency St. Francis Medical Center Trenton, New Jersey z Seton Hall University School of Health and Medical Sciences South Orange, New Jersey x Internal Medicine University of Medicine & Dentristry of New Jersey Newark, New Jersey { Internal Medicine Residency St. Francis Medical Center Trenton, New Jersey jj Wyckoff Heights Medical Center Brooklyn, New York [email protected]
References [1] Rudders SA, Banerji A, Vassallo MF, Clark S, Camargo CA Jr. Trends in pediatric emergency department visits for food-induced anaphylaxis. J Allergy Clin Immunol.. 2010;126:385e388. [2] Burdock GA, Carabin IG. Safety assessment of coriander (Coriandrum sativum L.) essential oil as a food ingredient. Food Chem Toxicol.. 2009;47:22e34. [3] Nair V, Singh S, Gupta YK. Evaluation of disease modifying activity of Coriandrum sativum in experimental models. Indian J Med Res.. 2012;135: 240e245. [4] Chen JL, Bahna SL. Spice allergy. Ann Allergy Asthma Immunol.. 2011;107: 191e199. [5] Konstantinou GN, Grattan CEH. Food contact hypersensitivity syndrome: the mucosal contact urticarial paradigm. Clin Exp Dermatol.. 2008;33:383e389. [6] Egger M, Mutschlechner S, Wopfner N, Gadermaier G, Briza P, Ferreira F. Pollenfood syndromes associated with weed pollinosis: an update from the molecular point of view. Allergy.. 2006;61:461e476. [7] Quirce S, Blanco R, Diez-Gomez ML, Cuevas M, Eiras P, Losada E. Carrot-induced asthma: immunodetection of allergens. J Allergy Clin Immunol.. 1997;99: 718e719.
Food protein-induced enterocolitis syndrome triggered by orange juice Food proteineinduced enterocolitis syndrome (FPIES) is a none immunoglobulin E (IgE)-mediated gastrointestinal disorder triggered by ingestion of certain foods. Often a delay in diagnosis occurs because patients have nonspecific symptoms and can be mismanaged as acute gastrointestinal illness, intussusception, or sepsis.1 The most common offending foods include cow’s milk, soy, and rice; however, other foods have been identified as causative agents.2 Review of the literature revealed 1 case report of fruitinduced FPIES diagnosed by open food challenge (OFC) to mixed fruit including apple, pear, and banana,3 as well as 3 documented cases of FPIES to banana.4,5 We describe the first report to our knowledge of FPIES to orange juice. Recently we managed a 2-year-old white boy with repetitive emesis, dehydration, and lethargy occurring on 5 separate occasions. His first reaction occurred at 10 months of age with approximately 10 episodes of emesis with no fever, diarrhea, rash, angioedema, or respiratory symptoms. The boy was admitted to our hospital and returned to baseline shortly after intravenous fluid replacement. One week later, he developed multiple episodes of emesis and was treated in the emergency department for viral gastroenteritis. At approximately 11 months of age, he had 2
Disclosures: Authors have nothing to disclose.
similar episodes, with resolution of symptoms after intravenous fluid replacement. His last reaction, occurring at 18 months of age, was more severe, with emesis, decreased urine output, hypotension, and lethargy. He was admitted to our hospital for dehydration with negative abdominal x-ray and stool culture. Because of concern for IgE-mediated food allergy, he was referred to our allergy clinic. In our clinic, on further history taking, the possibility of orange juice as a trigger for his reactions was identified. Emesis had occurred 1 to 2 hours after ingestion of orange juice in most of his reactions. No other specific foods or triggers could be elicited. His parents denied exposure to other citrus foods in the past. He was tolerating other fruits, including apples, pears, and bananas, thereby decreasing the likelihood of fructose intolerance. No history of atopy, including asthma, allergic rhinitis, eczema, or food allergy, was identified. The possibility of IgE-mediated food allergy was ruled out based on negative skin prick testing to orange extract and fresh orange juice. Additionally, specific IgE to orange was less than 0.1 kU/L. Given that most gastrointestinal food hypersensitivities are noneIgE-mediated and require elimination diets or food challenges for diagnosis,6 we elected to perform an oral food challenge (OFC). We followed the OFC protocol for FPIES outlined in “Work group report: oral food challenge testing,” by NowakWe˛grzyn et al.7 Based on his history of severe reactions, we used