- Email: [email protected]
Goji berry: A potential new player in latex-food syndrome
206
Letters / Ann Allergy Asthma Immunol 110 (2013) 204e212
a higher-volume AIT practice may yield a larger number of errors, allowing for a more powerful analysis. In conclusion, we found that AIT administration errors occur between 0.1 and 0.2% in our practice and that the rate depends on the reporting mechanism. We identified 2 common situations that increased error rates for AIT administration based on our analysis: atypical dosing protocols and bottle changes. In attempts to eliminate the latter as a source of errors, we since have implemented a standard reduction in scheduled dose by (50%) for any new extract (new bottle or new lot), with the goal of reducing administration errors. Sujan Patel, MD Kari L. Rossow, PA-C Brandon J. Williams, MHA, CSSBB
James T. Li, MD, PhD Matthew A. Rank, MD Mayo Clinic Rochester, Minnesota [email protected]
References [1] Aaronson DW, Gandhi TK. Incorrect allergy injections: Allergists’ experiences and recommendations for prevention. J Allergy Clin Immunol. 2004;113:1117e1121. [2] Amin HS, Liss GM, Bernstein DI. Evaluation of near-fatal outcomes to allergy immunotherapy injections: States that 25% of near fatal reactions were due to dosing errors. J Allergy Clin Immunol. 2006;117:169e175. [3] To err is human. Building a safer health system. Washington, DC: National Academy Press; 2000.
Goji berry: A potential new player in latex-food syndrome The goji berry (Lycium barbarum), also known as wolfberry, is a berry member of the Solanaceae family. Goji berry has long been recognized in traditional Chinese medicine for various therapeutic properties based on its antioxidant and immune-modulating effects. In the last years, because of descriptions of their beneficial properties, the consumption of Goji berry has rapidly grown in occidental countries. Only a single report describing 2 cases of Goji allergy has been published,1 but the prevalence of this allergy is growing because of increased Goji consumption. It is important to describe new allergen sources and identify the allergens that could be responsible for cross-reactivity, such as occurs in latexefruit syndrome.2 Since the first description of a systemic reaction induced by plant-derived food in a patient allergic to latex,3 several reports of cross-reactivity between latex, fruits, and vegetables have been described. We report the case of a 40-year-old woman who presented with immediate pharyngeal pruritus after Goji berry ingestion. She had previously been diagnosed with rhinoconjuntivitis caused by grass, and she had experienced allergy (pruritus and hives) to fruits, latex, king prawn, and nuts. She also reported problems after eating salad containing lettuce, escarole, and soy. Skin prick tests were performed with a thorough battery of foods, including shellfish, tomato, potato, courgette, fruits, a panel of common inhalant allergens, and also latex, the panallergens lipid transfer protein (0.1 mg/mL), and Profilin (50 mg/mL) (ALK-Abelló, Madrid, Spain). Positive results were obtained for pollens, fruits, vegetables, nuts, LTP, and Profilin. Total immunoglobulin E (IgE; 222 kU/L) and triptase (2.29 kU/L) were measured. Also, serum specific IgE against commercial extracts (Phadia CAP System) were performed, being positive to fruits (0.53e1.39 kU/L), nuts (0.47e1.08 kU/L), and latex (1.87 kU/L). Also, serum specific IgE against latex component rHev b8 was positive (4.66 kUA/L). Prick by prick skin tests with Goji berries extract were positive (9 mm 5 mm); in 3 healthy controls the same test were negative. A protein extract from Goji berry was prepared following a previously described methodology4 with some modifications. Briefly, Goji proteins were extracted by magnetic stirring (16 hours at 4 C) in phosphate-saline buffer pH 7.5, at 10% w/v. The extract was clarified by centrifugation and dialyzed against distilled water. The dialyzed extract was filtered and freeze-dried. Protein concentration was estimated according to the method of Bradford.5 The protein profile was analyzed by sodium dodecyl
Disclosures: Authors have nothing to disclose. Funding Sources: This study was supported by Mutua Madrileña and CIBERES (CIBER de Enfermedades Respiratorias).
sulfate polyacrylamide gel electrophoresis (SDS-PAGE) under reducing conditions, and protein bands were detected with colloidal Coomassie blue. Different protein bands ranging from 12 to 150 kDa were visualized in extracts (Fig 1A), the most prominent of which were at 17, 25, 35, 38, 44, 60 to 75, and 150 kDa approximately (Fig 1A). An immunodetection was performed to determine which proteins are able to bind IgE from patient serum. For these purpose, 20 mg Goji extract was loaded per line in an SDS-PAGE under reducing conditions. Briefly, the separated protein bands were electrophoretically transferred onto a 0.45mm nitrocellulose membrane (Bio-Rad, Richmond, California) and was blocked with 0.25% gelatin in NET (Tris HCl 0.5 M pH 7.5, NaCl 1.5 M, ethylenediaminetetra-acetic acid 0.05 M, X-100 Triton 0.5%). Membranes were incubated overnight with sera from the patient diluted 1:3 at 4 C, followed by rabbit anti-human IgE (1:10,000) (DakoCytomation, Glostrup, Denmark) peroxidase conjugate incubation and detected by the enhanced chemiluminescence method as recommended by the manufacturer (Amersham Biosciences, Buckinghamshire, United Kingdom). Specific IgE-binding bands were obtained, with an apparent molecular weight of 35 and 60 kDa from Goji extract (Fig 1B). The immunoreactive proteins were excised from the colloidal Coomassie blueestained gel, digested with trypsin, and the resulting peptide mixture was analyzed by Matrix-Assisted Laser Desorption Ionization-Time-of-Flight Mass Spectrometry. Identification of proteins by MALDI-TOF MS was performed as previously described.4 We identified 2 novel allergens in Goji berries. The protein of 60 kDa was identified as a b-glucosidase (Mowse score 82, P < .05), and the 35 kDa protein was identified as an enolase (Mowse score 156, P < .05). These 2 proteins had been identified previously as allergens in latex allergy.6,7 To explore potential cross-reactivity between Goji and latex, we have performed an immunoblot against latex antigen, and several bands were recognized by patient serum (Fig 1B). True cross-reactivity, however, must be demonstrated with inhibition assays. In summary, we report a new case of Goji allergy not attributable to the LTP as has been previously reported. The 2 new allergens identified in Goji extract are a b-glucosidase and an enolase, and they could be the responsible factors in latexefruit syndrome. Cristina Gámez, BS* Eva Marchán, MDy Lizette Miguel, MDy Veronica Sanz, Tch* Victoria del Pozo, PhD*
Letters / Ann Allergy Asthma Immunol 110 (2013) 204e212
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Figure 1. (A) SDS-PAGE of Goji berry protein extract. (B) IgE immunoblot with Goji berry protein extract. Arrows represent IgE-bands recognized by patient. 1: Serum sample from patient; 2: Serum sample from nonallergic donor. C: SDS-PAGE of latex protein extract and IgE immunoblot with latex extract. 1: Latex extract; 2: Serum sample from patient; 3: Serum sample from nonallergic donor. MK: molecular markers (kDa). *Immunology
Department IIS-Fundación Jiménez-Díaz Madrid, Spain y Allergy Department Complejo Hospitalario de Toledo Toledo, Spain [email protected] References [1] Monzón Ballarín S, López-Matas MA, Sáenz Abad D, Pérez-Cinto N, Carnés J. Anaphylaxis associated with the ingestion of Goji berries (Lycium barbarum). J Invest Allergol Clin Immunol. 2011;21:567e570.
[2] Blanco C, Carrillo T, Castillo R, Quiralte J, Cuevas M. Latex allergy: clinical features and cross-reactivity with fruits. Ann Allergy. 1994;73:309e314. [3] M’Raihi L, Charpin D, Pons A, Bongrand P, Vervloet D. Cross-reactivity between latex and banana. J Allergy Clin Immunol. 1991;87:129e130. [4] Luengo O, Mollá R, Gámez C, et al. Allergenicity and cross-reactivity of Senecio pollen: identification of novel allergens using the immunoproteomics approach. Clin Exp Allergy. 2008;38:1048e1060. [5] Bradford MM. A rapid and sensitive method for quantitation of micrograms quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248e254. [6] Yagami T, Sato M, Nakamura A, et al. Plant defense-related enzymes as latex antigens. J Allergy Clin Immunol. 1998;101:379e385. [7] Posch A, Chen Z, Wheeler C, Dunn MJ, Raulf-Heimsoth M, Baur X. Characterization and identification of latex allergens by two- dimensional electrophoresis and protein microsequencing. J Allergy Clin Immunol. 1997;99:385e395.
Stevens-Johnson syndrome: A review of 14 adult cases with one fatal outcome Introduction Stevens-Johnson Syndrome (SJS) is one of the most severe of a large spectrum of drug-induced cutaneous reactions.1 It is characterized by a prodrome of fever, malaise, and myalgias with subsequent eruption of erythematous or purpuric macules and patches, which can then progress into epidermal sloughing of 10% or less of body surface area, most often including 2 or more mucosal surfaces. Drugs are the causative agent in most cases.1,2 The incidence has been reported to be between 1 and 7 cases per million person-years.3 Diagnosis of SJS is solely clinical, and confirmation is made by skin biopsy.2,4 Treatment is an issue of contention; 2 basic principles are removal of the offending agent and the administration of supportive care, ideally in a burn unit. Beyond this, there are no universally accepted treatment standards.3,5 We conducted a retrospective case series evaluation of electronic medical records of patients seen in Kingston General Hospital, Kingston, Ontario, Canada, from January 1, 2002 to January 1, 2010, with ICD-9 codes (or equivalent) of L511 bullous erythema multiforme, L512 toxic epidermal necrolysis, and L519 unspecified
Disclosures: Authors have nothing to disclose.
erythema multiforme to case find for SJS. Details regarding patient sex, age, inciting agent, symptoms, management, illness duration, and outcomes were recorded for qualitative/descriptive analysis. A total of 14 cases of SJS were found; summarized in Table 1. Average age was 51.4 years, ranging from 27 to 82 years. All but one (case 7) were drug-induced; the remainder had a negative infectious work-up. Average time from initiation of the culprit agent to onset of eruption was 15 days, (range 1 to 34 ), excluding case 3, where the patient had been taking allopurinol for many years. Ten patients had a documented prodrome, of which nine included fever. Six cases had eruptions typical of SJS where the eruption progressed to vesicles/bullae and skin sloughing. Six cases had involvement of one mucosal surface, six involved two surfaces, one case with three surfaces. Two cases were identified as partial DRESS overlap syndromes given the presence of peripheral Eosinophilia and mild liver dysfunction. Extended laboratory testing is summarized in eTable1. Combination treatment with IVIG and corticosteroids was implemented in three patients, three were treated with IVIG alone, four with corticosteroids alone, and four with only supportive therapy. All but one patient survived. Hospital stay ranged from two to 65 days, with all but two patients hospitalized for less than two weeks.
Letters / Ann Allergy Asthma Immunol 110 (2013) 204e212
a higher-volume AIT practice may yield a larger number of errors, allowing for a more powerful analysis. In conclusion, we found that AIT administration errors occur between 0.1 and 0.2% in our practice and that the rate depends on the reporting mechanism. We identified 2 common situations that increased error rates for AIT administration based on our analysis: atypical dosing protocols and bottle changes. In attempts to eliminate the latter as a source of errors, we since have implemented a standard reduction in scheduled dose by (50%) for any new extract (new bottle or new lot), with the goal of reducing administration errors. Sujan Patel, MD Kari L. Rossow, PA-C Brandon J. Williams, MHA, CSSBB
James T. Li, MD, PhD Matthew A. Rank, MD Mayo Clinic Rochester, Minnesota [email protected]
References [1] Aaronson DW, Gandhi TK. Incorrect allergy injections: Allergists’ experiences and recommendations for prevention. J Allergy Clin Immunol. 2004;113:1117e1121. [2] Amin HS, Liss GM, Bernstein DI. Evaluation of near-fatal outcomes to allergy immunotherapy injections: States that 25% of near fatal reactions were due to dosing errors. J Allergy Clin Immunol. 2006;117:169e175. [3] To err is human. Building a safer health system. Washington, DC: National Academy Press; 2000.
Goji berry: A potential new player in latex-food syndrome The goji berry (Lycium barbarum), also known as wolfberry, is a berry member of the Solanaceae family. Goji berry has long been recognized in traditional Chinese medicine for various therapeutic properties based on its antioxidant and immune-modulating effects. In the last years, because of descriptions of their beneficial properties, the consumption of Goji berry has rapidly grown in occidental countries. Only a single report describing 2 cases of Goji allergy has been published,1 but the prevalence of this allergy is growing because of increased Goji consumption. It is important to describe new allergen sources and identify the allergens that could be responsible for cross-reactivity, such as occurs in latexefruit syndrome.2 Since the first description of a systemic reaction induced by plant-derived food in a patient allergic to latex,3 several reports of cross-reactivity between latex, fruits, and vegetables have been described. We report the case of a 40-year-old woman who presented with immediate pharyngeal pruritus after Goji berry ingestion. She had previously been diagnosed with rhinoconjuntivitis caused by grass, and she had experienced allergy (pruritus and hives) to fruits, latex, king prawn, and nuts. She also reported problems after eating salad containing lettuce, escarole, and soy. Skin prick tests were performed with a thorough battery of foods, including shellfish, tomato, potato, courgette, fruits, a panel of common inhalant allergens, and also latex, the panallergens lipid transfer protein (0.1 mg/mL), and Profilin (50 mg/mL) (ALK-Abelló, Madrid, Spain). Positive results were obtained for pollens, fruits, vegetables, nuts, LTP, and Profilin. Total immunoglobulin E (IgE; 222 kU/L) and triptase (2.29 kU/L) were measured. Also, serum specific IgE against commercial extracts (Phadia CAP System) were performed, being positive to fruits (0.53e1.39 kU/L), nuts (0.47e1.08 kU/L), and latex (1.87 kU/L). Also, serum specific IgE against latex component rHev b8 was positive (4.66 kUA/L). Prick by prick skin tests with Goji berries extract were positive (9 mm 5 mm); in 3 healthy controls the same test were negative. A protein extract from Goji berry was prepared following a previously described methodology4 with some modifications. Briefly, Goji proteins were extracted by magnetic stirring (16 hours at 4 C) in phosphate-saline buffer pH 7.5, at 10% w/v. The extract was clarified by centrifugation and dialyzed against distilled water. The dialyzed extract was filtered and freeze-dried. Protein concentration was estimated according to the method of Bradford.5 The protein profile was analyzed by sodium dodecyl
Disclosures: Authors have nothing to disclose. Funding Sources: This study was supported by Mutua Madrileña and CIBERES (CIBER de Enfermedades Respiratorias).
sulfate polyacrylamide gel electrophoresis (SDS-PAGE) under reducing conditions, and protein bands were detected with colloidal Coomassie blue. Different protein bands ranging from 12 to 150 kDa were visualized in extracts (Fig 1A), the most prominent of which were at 17, 25, 35, 38, 44, 60 to 75, and 150 kDa approximately (Fig 1A). An immunodetection was performed to determine which proteins are able to bind IgE from patient serum. For these purpose, 20 mg Goji extract was loaded per line in an SDS-PAGE under reducing conditions. Briefly, the separated protein bands were electrophoretically transferred onto a 0.45mm nitrocellulose membrane (Bio-Rad, Richmond, California) and was blocked with 0.25% gelatin in NET (Tris HCl 0.5 M pH 7.5, NaCl 1.5 M, ethylenediaminetetra-acetic acid 0.05 M, X-100 Triton 0.5%). Membranes were incubated overnight with sera from the patient diluted 1:3 at 4 C, followed by rabbit anti-human IgE (1:10,000) (DakoCytomation, Glostrup, Denmark) peroxidase conjugate incubation and detected by the enhanced chemiluminescence method as recommended by the manufacturer (Amersham Biosciences, Buckinghamshire, United Kingdom). Specific IgE-binding bands were obtained, with an apparent molecular weight of 35 and 60 kDa from Goji extract (Fig 1B). The immunoreactive proteins were excised from the colloidal Coomassie blueestained gel, digested with trypsin, and the resulting peptide mixture was analyzed by Matrix-Assisted Laser Desorption Ionization-Time-of-Flight Mass Spectrometry. Identification of proteins by MALDI-TOF MS was performed as previously described.4 We identified 2 novel allergens in Goji berries. The protein of 60 kDa was identified as a b-glucosidase (Mowse score 82, P < .05), and the 35 kDa protein was identified as an enolase (Mowse score 156, P < .05). These 2 proteins had been identified previously as allergens in latex allergy.6,7 To explore potential cross-reactivity between Goji and latex, we have performed an immunoblot against latex antigen, and several bands were recognized by patient serum (Fig 1B). True cross-reactivity, however, must be demonstrated with inhibition assays. In summary, we report a new case of Goji allergy not attributable to the LTP as has been previously reported. The 2 new allergens identified in Goji extract are a b-glucosidase and an enolase, and they could be the responsible factors in latexefruit syndrome. Cristina Gámez, BS* Eva Marchán, MDy Lizette Miguel, MDy Veronica Sanz, Tch* Victoria del Pozo, PhD*
Letters / Ann Allergy Asthma Immunol 110 (2013) 204e212
207
Figure 1. (A) SDS-PAGE of Goji berry protein extract. (B) IgE immunoblot with Goji berry protein extract. Arrows represent IgE-bands recognized by patient. 1: Serum sample from patient; 2: Serum sample from nonallergic donor. C: SDS-PAGE of latex protein extract and IgE immunoblot with latex extract. 1: Latex extract; 2: Serum sample from patient; 3: Serum sample from nonallergic donor. MK: molecular markers (kDa). *Immunology
Department IIS-Fundación Jiménez-Díaz Madrid, Spain y Allergy Department Complejo Hospitalario de Toledo Toledo, Spain [email protected] References [1] Monzón Ballarín S, López-Matas MA, Sáenz Abad D, Pérez-Cinto N, Carnés J. Anaphylaxis associated with the ingestion of Goji berries (Lycium barbarum). J Invest Allergol Clin Immunol. 2011;21:567e570.
[2] Blanco C, Carrillo T, Castillo R, Quiralte J, Cuevas M. Latex allergy: clinical features and cross-reactivity with fruits. Ann Allergy. 1994;73:309e314. [3] M’Raihi L, Charpin D, Pons A, Bongrand P, Vervloet D. Cross-reactivity between latex and banana. J Allergy Clin Immunol. 1991;87:129e130. [4] Luengo O, Mollá R, Gámez C, et al. Allergenicity and cross-reactivity of Senecio pollen: identification of novel allergens using the immunoproteomics approach. Clin Exp Allergy. 2008;38:1048e1060. [5] Bradford MM. A rapid and sensitive method for quantitation of micrograms quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248e254. [6] Yagami T, Sato M, Nakamura A, et al. Plant defense-related enzymes as latex antigens. J Allergy Clin Immunol. 1998;101:379e385. [7] Posch A, Chen Z, Wheeler C, Dunn MJ, Raulf-Heimsoth M, Baur X. Characterization and identification of latex allergens by two- dimensional electrophoresis and protein microsequencing. J Allergy Clin Immunol. 1997;99:385e395.
Stevens-Johnson syndrome: A review of 14 adult cases with one fatal outcome Introduction Stevens-Johnson Syndrome (SJS) is one of the most severe of a large spectrum of drug-induced cutaneous reactions.1 It is characterized by a prodrome of fever, malaise, and myalgias with subsequent eruption of erythematous or purpuric macules and patches, which can then progress into epidermal sloughing of 10% or less of body surface area, most often including 2 or more mucosal surfaces. Drugs are the causative agent in most cases.1,2 The incidence has been reported to be between 1 and 7 cases per million person-years.3 Diagnosis of SJS is solely clinical, and confirmation is made by skin biopsy.2,4 Treatment is an issue of contention; 2 basic principles are removal of the offending agent and the administration of supportive care, ideally in a burn unit. Beyond this, there are no universally accepted treatment standards.3,5 We conducted a retrospective case series evaluation of electronic medical records of patients seen in Kingston General Hospital, Kingston, Ontario, Canada, from January 1, 2002 to January 1, 2010, with ICD-9 codes (or equivalent) of L511 bullous erythema multiforme, L512 toxic epidermal necrolysis, and L519 unspecified
Disclosures: Authors have nothing to disclose.
erythema multiforme to case find for SJS. Details regarding patient sex, age, inciting agent, symptoms, management, illness duration, and outcomes were recorded for qualitative/descriptive analysis. A total of 14 cases of SJS were found; summarized in Table 1. Average age was 51.4 years, ranging from 27 to 82 years. All but one (case 7) were drug-induced; the remainder had a negative infectious work-up. Average time from initiation of the culprit agent to onset of eruption was 15 days, (range 1 to 34 ), excluding case 3, where the patient had been taking allopurinol for many years. Ten patients had a documented prodrome, of which nine included fever. Six cases had eruptions typical of SJS where the eruption progressed to vesicles/bullae and skin sloughing. Six cases had involvement of one mucosal surface, six involved two surfaces, one case with three surfaces. Two cases were identified as partial DRESS overlap syndromes given the presence of peripheral Eosinophilia and mild liver dysfunction. Extended laboratory testing is summarized in eTable1. Combination treatment with IVIG and corticosteroids was implemented in three patients, three were treated with IVIG alone, four with corticosteroids alone, and four with only supportive therapy. All but one patient survived. Hospital stay ranged from two to 65 days, with all but two patients hospitalized for less than two weeks.