- Email: [email protected]
Anti–thyroid peroxidase IgE in patients with chronic urticaria
Letters to the Editor 467
J ALLERGY CLIN IMMUNOL VOLUME 108, NUMBER 3
10. Parnes SM, Chuma AV. Acute effects of antileukotrienes on sinonasal polyposis and sinusitis. ENT J 2000;79:18-25. 11. Dahlen B, Nizankowska E, Szczeklik A, Zetterstrom O, Bochenek G, Kumlin M, et al. Benefits from adding the 5-lipoxygenase inhibitor zileuton to conventional therapy in aspirin-intolerant asthmatics. Am J Respir Crit Care Med 1998;157:1187-94. 12. Khan DA, Cody TC III, George TJ, Gleich GJ, Leiferman KM. Allergic fungal sinusitis: an immunohistologic analysis. J Allergy Clin Immunol 2000;106:1096-101.
A
1/8/117592 doi:10.1067/mai.2001.117592
Anti–thyroid peroxidase IgE in patients with chronic urticaria
B
FIG 2. Sinus CT scan shows clearing of disease after 1 month of montelukast treatment. Residual nasal septal bowing to the left persists. A, Image taken through the maxillary sinuses. B, Image taken through the ethmoid and sphenoid sinuses.
31 W Camelback Rd Phoenix, AZ 85013 REFERENCES 1. deShazo RD, Swain RE. Diagnostic criteria for allergic fungal sinusitis. J Allergy Clin Immunol 1995;96:24-35. 2. Schubert MS, Goetz DW. Evaluation and treatment of allergic fungal sinusitis. I. Demographics and diagnosis. J Allergy Clin Immunol 1998;102:387-94. 3. Kupferberg SB, Bent JP. Allergic fungal sinusitis in the pediatric population. Arch Otolaryngol Head Neck Surg 1996;122:1381-4. 4. Mabry RL, Marple BF, Folker RJ, Mabry CS. Immunotherapy in the treatment of allergic fungal sinusitis: three years’ experience. Otolaryngol Head Neck Surg 1998;119:648-51. 5. Schubert MS, Goetz DW. Evaluation and treatment of allergic fungal sinusitis. II. Treatment and follow-up. J Allergy Clin Immunol 1998;102:395-402. 6. Schubert MS. Medical treatment of allergic fungal sinusitis. Ann Allergy Asthma Immunol 2000;85:90-101. 7. Hamilos DL. Chronic sinusitis. J Allergy Clin Immunol 2000;106:21327. 8. Ogino S, Irifune M, Harada T, Kikumori H, Matsunaga T. Arachidonic acid metabolites in human nasal polyps. Acta Otolaryngol Suppl 1993;501:85-7. 9. Georgitis JW, Matthews BL, Stone B. Chronic sinusitis: characterization of cellular influx and inflammatory mediators in sinus lavage fluid. Int Arch Allergy Immunol 1995;106:416-21.
To the Editor: The demonstration of a serologic mediator of whealing1 has led to the classification of chronic idiopathic urticaria as an “autoreactive” disorder in a significant proportion of cases (20% to 50%, according to Greaves2 and judging from our personal experience3). Hide et al4 demonstrated that the serum of many patients with autoreactive urticaria can induce in vitro histamine release from basophils of healthy subjects, and this histamine-releasing activity was shown to be related to (1) IgG autoantibodies directed against the IgE high-affinity receptor (FcεRI), (2) IgG against IgE, or (3) asyet-undefined histamine-releasing factors. An association of chronic urticaria with thyroid autoimmunity has been reported by several authors.5 Furthermore, a remission of urticarial symptoms has been observed in patients with chronic urticaria and autoimmune thyroiditis who were treated with thyroxine.6 Bar-Sela et al7 detected the presence of anti–thyroid peroxidase (TPO) IgE in a patient with chronic urticaria and suggested that these IgE autoantibodies might play a pathogenetic role in urticarial symptoms, sensitizing mast cells and inducing degranulation after exposure to the specific circulating antigen (released as a result of autoimmune thyroid damage). It has been also hypothesized that anti-TPO IgE could cross-react with peroxidase contained in vegetables and that the ingestion of some peroxidase-containing vegetables could trigger urticaria. To assess the potential role of specific anti-TPO IgE in inducing urticaria, we examined sera from 38 patients with chronic urticaria with or without thyroid autoimmunity. Chronic idiopathic urticaria was diagnosed on the basis of urticarial wheals persisting for at least 6 weeks; known causes of urticaria, such as food allergy, additive intolerance, parasitoses, and systemic diseases, were excluded by appropriate investigations. Each patient underwent an intradermal test with autologous serum,1 readings being taken at 15 and 40 minutes. Intradermal injection of saline solution and skin prick testing with histamine (10 mg/mL) were used as controls. All intradermal tests were performed at least 5 days after the ingestion of the last antihistamine tablet (cetirizine 10 mg, fexofenadine 180 mg, or loratadine 10 mg in every case). Serum histamine-releasing activity was assessed by in vitro stimulation of dextran-sedimented leukocytes obtained from 2 normal donors; the basophils of these 2 subjects had previously been shown to release 30% of total histamine content on challenge with an optimal dose of polyclonal anti-IgE (10 µg/mL; Sigma Chemical, St Louis, Mo). Histamine release in the cell supernatant was evaluated through use of an automated fluorometric method; net histamine release was calculated as percent of total histamine content after subtraction of spontaneous release. A 5% release cutoff value was used. Serum anti-TPO IgG values were measured by means of a commercially available radioimmunoassay (Pharmacia Cap-System, Uppsala, Sweden); the same kit was used to detect anti-TPO IgE with radiolabeled mouse monoclonal anti–human IgE antibodies (instead of anti-IgG) as a second antibody. Sera from 23 patients with chronic urticaria contained anti-TPO IgG, but no patient was positive for anti-TPO IgE. Twenty-one (91%) of the 23 patients had positive autologous serum skin test results, and 9 (47%) of 19 were positive on in vitro basophil histamine release assay. Anti-TPO IgE antibodies were not detected in 15 of 15 patients with chronic urticaria without anti-TPO IgG antibodies; 7 (46.6%) of 15 had positive intradermal test results with autol-
468 Letters to the Editor
J ALLERGY CLIN IMMUNOL SEPTEMBER 2001
ogous serum, and 4 (26.6%) of 15 had positive basophil histamine release assay results. Finally anti-TPO IgE antibodies were not detected in 11 of 11 subjects without chronic urticaria (of whom 1 had autoimmune thyroiditis and 2 had allergic rhinitis); none of these subjects had positive intradermal test results with autologous serum. Taken all together, these results indicate that the detection of IgE specific for TPO is an occasional finding and that these antibodies are unlikely to play a pathogenic role in most cases of chronic urticaria. Alberto Tedeschi, MDa Maurizio Lorinia Riccardo Asero, MDb aAllergy and Immunopharmacology Unit, First Division of Medicine IRCCS Ospedale Maggiore Policlinico 20122-Milan Italy bAllergy Unit, Ospedale Caduti Bollatesi 2021-Bollate (Milan) Italy REFERENCES 1. Grattan CE, Wallington TB, Warin RP, Kennedy CT, Bradfield JW. A serological mediator in chronic idiopathic urticaria: a clinical, immunological and histological evaluation. Br J Dermatol 1986;114:583-90. 2. Greaves M. Chronic urticaria. J Allergy Clin Immunol 2000;105:664-72. 3. Asero R, Lorini M, Tedeschi A, Miadonna A. In vivo and in vitro diagnostic methods in autoimmune chronic urticaria [abstract]. J Allergy Clin Immunol 2000;105:S268. 4. Hide M, Francis DM, Grattan CEH, Hakimi J, Kochan JP, Greaves MW. Autoantibodies against the high affinity IgE receptor as a cause of histamine release in chronic urticaria. N Engl J Med 1993;328:1599-604. 5. Leznoff A, Susman GL. Syndrome of idiopathic chronic urticaria and angioedema with thyroid autoimmunity: a study of 90 patients. J Allergy Clin Immunol 1989;84:66-71. 6. Rumbyrt JS, Katz JL, Schocker AL. Resolution of chronic urticaria in patients with thyroid autoimmunity. J Allergy Clin Immunol 1995;96:901-5. 7. Bar-Sela S, Reshef T, Mekori Y. IgE antithyroid microsomal antibodies in a patient with chronic urticaria. J Allergy Clin Immunol 1999;103:1216-7.
1/8/117792 doi:10.1067/mai.2001.117792
Manufacturing and labeling issues for commercial products: Relevance to food allergy To the Editor: Food allergy affects more than 6 million Americans1 who must avoid potentially life-threatening allergens that appear in commercial food products. For these individuals, successful avoidance requires clear and accurate food processing and labeling practices. In January 2001, the US Food and Drug Administration reported an investigation of food companies in which it was found that 25% of products contained undeclared allergenic ingredients, often from cross-contamination.2 Ingredient statements such as “May contain peanut” are presumably helpful, but they are in fact poorly correlated with actual risks for contamination3 and are therefore frustrating to consumers. There have been no reports to determine the impact of food labeling procedures (undeclared allergens, label terminology, etc) on food-allergic individuals and their families. We analyzed unsolicited calls from consumers to the Food Allergy and Anaphylaxis Network (FAAN) alerting FAAN of allergic reactions from incorrectly labeled commercial products or providing “Good Samaritan” notification of labeling issues. Over a period of 24 months, 319 calls were logged. Ninety-eight calls were eliminated from analysis for the following reasons: repeat calls for the same issue (32), no clear follow-up or investigation of the concern (48), lack of details (4), concern shown to be incorrect (14). This left 221 calls for further analysis. Seventy (32%) of the calls were associated with reactions due to ingestion of a product; the remainder were to pose questions or provide information concerning labeling changes/errors. The implicated food proteins included milk (84), peanut (60), nuts (31), egg (14), seeds (5), wheat (2), and mixed or other allergens (25).
TABLE I. Types of problems/label issues reported Percent (n = 206)
Cross-contaminated by unlabeled allergen Visible ingredient, not disclosed on label Allergen newly disclosed on label Completely wrong contents in package Outer package label different from individual package label inside Ambiguous terminology (“spices,” “natural flavors”) Reaction from milk in product labeled “Pareve” Label in English placed over a foreignlanguage label Different package sizes of same product have different ingredients
28 26 22 7 6 5 3 1.5 1.5
Eleven complaints pertained to products that are not ingested, such as cosmetics. Four products were from in-store supermarket bakeries. A variety of issues were reported in connection with the 206 remaining commercial food products, as delineated in Table I. Among episodes of cross-contamination, 65% were called to FAAN’s attention because of otherwise unexplained reactions to the product and 35% were based on consumer-initiated calls to the manufacturer. The potential for error was confirmed by the company in 88% of these incidents (eg, shared processing equipment). A large number of calls (22%) were made to alert FAAN that a new allergen had been added to a commercial product; this underscores the need for reading the label on every item purchased, even when the product is familiar. Because members of FAAN are provided with lists of words that signify common allergens (eg, casein and whey indicate cow’s milk protein, and natural flavors might indicate a food allergen), we suspect that problems caused by these ambiguous terms were underreported. In conclusion, current labeling and manufacturing procedures present an enormous variety of challenges for food-allergic individuals and their families. We suggest that simple language be used (eg, the term milk should be used in place of the term casein), that allergens be declared when they are present in spices or natural flavors, and that precautionary statements such as “May contain . . .” not be used unless it is clear that there are no viable methods of preventing contamination despite good manufacturing practices. Implementation of allergen prevention plans is needed for industry to reduce the introduction of unintended allergens and to ensure accurate labeling. Finally, continued patient education regarding careful label-reading is paramount. Aimee S. Altschul, MDa Debbie L. Scherrer, BAb Anne Muñoz-Furlong, BAb Scott H. Sicherer, MDa aDepartment of Pediatric Allergy, Jaffe Food Allergy Institute Mount Sinai School of Medicine New York, NY bThe Food Allergy and Anaphylaxis Network Fairfax, Va REFERENCES 1. Sampson HA. Food allergy. Part 1: immunopathogenesis and clinical disorders. J Allergy Clin Immunol 1999;103:717-28. 2. US Food and Drug Administration, Center for Food Safety and Applied Nutrition, Office of Scientific Analysis and Support. Food allergen partnership. January 2001. Available at: www.cfsan.fda.gov/~dms/alrgpart.html. Accessed April 18, 2001. 3. Niemann LM, Hlywka JJ, Hefle SL. Immunochemical analysis of retail foods labeled as “May contain peanut” or other similar declaration: implications for food allergic individuals [abstract]. J Allergy Clin Immunol 2000;105:S188.
1/8/117794 doi:10.1067/mai.2001.117794
J ALLERGY CLIN IMMUNOL VOLUME 108, NUMBER 3
10. Parnes SM, Chuma AV. Acute effects of antileukotrienes on sinonasal polyposis and sinusitis. ENT J 2000;79:18-25. 11. Dahlen B, Nizankowska E, Szczeklik A, Zetterstrom O, Bochenek G, Kumlin M, et al. Benefits from adding the 5-lipoxygenase inhibitor zileuton to conventional therapy in aspirin-intolerant asthmatics. Am J Respir Crit Care Med 1998;157:1187-94. 12. Khan DA, Cody TC III, George TJ, Gleich GJ, Leiferman KM. Allergic fungal sinusitis: an immunohistologic analysis. J Allergy Clin Immunol 2000;106:1096-101.
A
1/8/117592 doi:10.1067/mai.2001.117592
Anti–thyroid peroxidase IgE in patients with chronic urticaria
B
FIG 2. Sinus CT scan shows clearing of disease after 1 month of montelukast treatment. Residual nasal septal bowing to the left persists. A, Image taken through the maxillary sinuses. B, Image taken through the ethmoid and sphenoid sinuses.
31 W Camelback Rd Phoenix, AZ 85013 REFERENCES 1. deShazo RD, Swain RE. Diagnostic criteria for allergic fungal sinusitis. J Allergy Clin Immunol 1995;96:24-35. 2. Schubert MS, Goetz DW. Evaluation and treatment of allergic fungal sinusitis. I. Demographics and diagnosis. J Allergy Clin Immunol 1998;102:387-94. 3. Kupferberg SB, Bent JP. Allergic fungal sinusitis in the pediatric population. Arch Otolaryngol Head Neck Surg 1996;122:1381-4. 4. Mabry RL, Marple BF, Folker RJ, Mabry CS. Immunotherapy in the treatment of allergic fungal sinusitis: three years’ experience. Otolaryngol Head Neck Surg 1998;119:648-51. 5. Schubert MS, Goetz DW. Evaluation and treatment of allergic fungal sinusitis. II. Treatment and follow-up. J Allergy Clin Immunol 1998;102:395-402. 6. Schubert MS. Medical treatment of allergic fungal sinusitis. Ann Allergy Asthma Immunol 2000;85:90-101. 7. Hamilos DL. Chronic sinusitis. J Allergy Clin Immunol 2000;106:21327. 8. Ogino S, Irifune M, Harada T, Kikumori H, Matsunaga T. Arachidonic acid metabolites in human nasal polyps. Acta Otolaryngol Suppl 1993;501:85-7. 9. Georgitis JW, Matthews BL, Stone B. Chronic sinusitis: characterization of cellular influx and inflammatory mediators in sinus lavage fluid. Int Arch Allergy Immunol 1995;106:416-21.
To the Editor: The demonstration of a serologic mediator of whealing1 has led to the classification of chronic idiopathic urticaria as an “autoreactive” disorder in a significant proportion of cases (20% to 50%, according to Greaves2 and judging from our personal experience3). Hide et al4 demonstrated that the serum of many patients with autoreactive urticaria can induce in vitro histamine release from basophils of healthy subjects, and this histamine-releasing activity was shown to be related to (1) IgG autoantibodies directed against the IgE high-affinity receptor (FcεRI), (2) IgG against IgE, or (3) asyet-undefined histamine-releasing factors. An association of chronic urticaria with thyroid autoimmunity has been reported by several authors.5 Furthermore, a remission of urticarial symptoms has been observed in patients with chronic urticaria and autoimmune thyroiditis who were treated with thyroxine.6 Bar-Sela et al7 detected the presence of anti–thyroid peroxidase (TPO) IgE in a patient with chronic urticaria and suggested that these IgE autoantibodies might play a pathogenetic role in urticarial symptoms, sensitizing mast cells and inducing degranulation after exposure to the specific circulating antigen (released as a result of autoimmune thyroid damage). It has been also hypothesized that anti-TPO IgE could cross-react with peroxidase contained in vegetables and that the ingestion of some peroxidase-containing vegetables could trigger urticaria. To assess the potential role of specific anti-TPO IgE in inducing urticaria, we examined sera from 38 patients with chronic urticaria with or without thyroid autoimmunity. Chronic idiopathic urticaria was diagnosed on the basis of urticarial wheals persisting for at least 6 weeks; known causes of urticaria, such as food allergy, additive intolerance, parasitoses, and systemic diseases, were excluded by appropriate investigations. Each patient underwent an intradermal test with autologous serum,1 readings being taken at 15 and 40 minutes. Intradermal injection of saline solution and skin prick testing with histamine (10 mg/mL) were used as controls. All intradermal tests were performed at least 5 days after the ingestion of the last antihistamine tablet (cetirizine 10 mg, fexofenadine 180 mg, or loratadine 10 mg in every case). Serum histamine-releasing activity was assessed by in vitro stimulation of dextran-sedimented leukocytes obtained from 2 normal donors; the basophils of these 2 subjects had previously been shown to release 30% of total histamine content on challenge with an optimal dose of polyclonal anti-IgE (10 µg/mL; Sigma Chemical, St Louis, Mo). Histamine release in the cell supernatant was evaluated through use of an automated fluorometric method; net histamine release was calculated as percent of total histamine content after subtraction of spontaneous release. A 5% release cutoff value was used. Serum anti-TPO IgG values were measured by means of a commercially available radioimmunoassay (Pharmacia Cap-System, Uppsala, Sweden); the same kit was used to detect anti-TPO IgE with radiolabeled mouse monoclonal anti–human IgE antibodies (instead of anti-IgG) as a second antibody. Sera from 23 patients with chronic urticaria contained anti-TPO IgG, but no patient was positive for anti-TPO IgE. Twenty-one (91%) of the 23 patients had positive autologous serum skin test results, and 9 (47%) of 19 were positive on in vitro basophil histamine release assay. Anti-TPO IgE antibodies were not detected in 15 of 15 patients with chronic urticaria without anti-TPO IgG antibodies; 7 (46.6%) of 15 had positive intradermal test results with autol-
468 Letters to the Editor
J ALLERGY CLIN IMMUNOL SEPTEMBER 2001
ogous serum, and 4 (26.6%) of 15 had positive basophil histamine release assay results. Finally anti-TPO IgE antibodies were not detected in 11 of 11 subjects without chronic urticaria (of whom 1 had autoimmune thyroiditis and 2 had allergic rhinitis); none of these subjects had positive intradermal test results with autologous serum. Taken all together, these results indicate that the detection of IgE specific for TPO is an occasional finding and that these antibodies are unlikely to play a pathogenic role in most cases of chronic urticaria. Alberto Tedeschi, MDa Maurizio Lorinia Riccardo Asero, MDb aAllergy and Immunopharmacology Unit, First Division of Medicine IRCCS Ospedale Maggiore Policlinico 20122-Milan Italy bAllergy Unit, Ospedale Caduti Bollatesi 2021-Bollate (Milan) Italy REFERENCES 1. Grattan CE, Wallington TB, Warin RP, Kennedy CT, Bradfield JW. A serological mediator in chronic idiopathic urticaria: a clinical, immunological and histological evaluation. Br J Dermatol 1986;114:583-90. 2. Greaves M. Chronic urticaria. J Allergy Clin Immunol 2000;105:664-72. 3. Asero R, Lorini M, Tedeschi A, Miadonna A. In vivo and in vitro diagnostic methods in autoimmune chronic urticaria [abstract]. J Allergy Clin Immunol 2000;105:S268. 4. Hide M, Francis DM, Grattan CEH, Hakimi J, Kochan JP, Greaves MW. Autoantibodies against the high affinity IgE receptor as a cause of histamine release in chronic urticaria. N Engl J Med 1993;328:1599-604. 5. Leznoff A, Susman GL. Syndrome of idiopathic chronic urticaria and angioedema with thyroid autoimmunity: a study of 90 patients. J Allergy Clin Immunol 1989;84:66-71. 6. Rumbyrt JS, Katz JL, Schocker AL. Resolution of chronic urticaria in patients with thyroid autoimmunity. J Allergy Clin Immunol 1995;96:901-5. 7. Bar-Sela S, Reshef T, Mekori Y. IgE antithyroid microsomal antibodies in a patient with chronic urticaria. J Allergy Clin Immunol 1999;103:1216-7.
1/8/117792 doi:10.1067/mai.2001.117792
Manufacturing and labeling issues for commercial products: Relevance to food allergy To the Editor: Food allergy affects more than 6 million Americans1 who must avoid potentially life-threatening allergens that appear in commercial food products. For these individuals, successful avoidance requires clear and accurate food processing and labeling practices. In January 2001, the US Food and Drug Administration reported an investigation of food companies in which it was found that 25% of products contained undeclared allergenic ingredients, often from cross-contamination.2 Ingredient statements such as “May contain peanut” are presumably helpful, but they are in fact poorly correlated with actual risks for contamination3 and are therefore frustrating to consumers. There have been no reports to determine the impact of food labeling procedures (undeclared allergens, label terminology, etc) on food-allergic individuals and their families. We analyzed unsolicited calls from consumers to the Food Allergy and Anaphylaxis Network (FAAN) alerting FAAN of allergic reactions from incorrectly labeled commercial products or providing “Good Samaritan” notification of labeling issues. Over a period of 24 months, 319 calls were logged. Ninety-eight calls were eliminated from analysis for the following reasons: repeat calls for the same issue (32), no clear follow-up or investigation of the concern (48), lack of details (4), concern shown to be incorrect (14). This left 221 calls for further analysis. Seventy (32%) of the calls were associated with reactions due to ingestion of a product; the remainder were to pose questions or provide information concerning labeling changes/errors. The implicated food proteins included milk (84), peanut (60), nuts (31), egg (14), seeds (5), wheat (2), and mixed or other allergens (25).
TABLE I. Types of problems/label issues reported Percent (n = 206)
Cross-contaminated by unlabeled allergen Visible ingredient, not disclosed on label Allergen newly disclosed on label Completely wrong contents in package Outer package label different from individual package label inside Ambiguous terminology (“spices,” “natural flavors”) Reaction from milk in product labeled “Pareve” Label in English placed over a foreignlanguage label Different package sizes of same product have different ingredients
28 26 22 7 6 5 3 1.5 1.5
Eleven complaints pertained to products that are not ingested, such as cosmetics. Four products were from in-store supermarket bakeries. A variety of issues were reported in connection with the 206 remaining commercial food products, as delineated in Table I. Among episodes of cross-contamination, 65% were called to FAAN’s attention because of otherwise unexplained reactions to the product and 35% were based on consumer-initiated calls to the manufacturer. The potential for error was confirmed by the company in 88% of these incidents (eg, shared processing equipment). A large number of calls (22%) were made to alert FAAN that a new allergen had been added to a commercial product; this underscores the need for reading the label on every item purchased, even when the product is familiar. Because members of FAAN are provided with lists of words that signify common allergens (eg, casein and whey indicate cow’s milk protein, and natural flavors might indicate a food allergen), we suspect that problems caused by these ambiguous terms were underreported. In conclusion, current labeling and manufacturing procedures present an enormous variety of challenges for food-allergic individuals and their families. We suggest that simple language be used (eg, the term milk should be used in place of the term casein), that allergens be declared when they are present in spices or natural flavors, and that precautionary statements such as “May contain . . .” not be used unless it is clear that there are no viable methods of preventing contamination despite good manufacturing practices. Implementation of allergen prevention plans is needed for industry to reduce the introduction of unintended allergens and to ensure accurate labeling. Finally, continued patient education regarding careful label-reading is paramount. Aimee S. Altschul, MDa Debbie L. Scherrer, BAb Anne Muñoz-Furlong, BAb Scott H. Sicherer, MDa aDepartment of Pediatric Allergy, Jaffe Food Allergy Institute Mount Sinai School of Medicine New York, NY bThe Food Allergy and Anaphylaxis Network Fairfax, Va REFERENCES 1. Sampson HA. Food allergy. Part 1: immunopathogenesis and clinical disorders. J Allergy Clin Immunol 1999;103:717-28. 2. US Food and Drug Administration, Center for Food Safety and Applied Nutrition, Office of Scientific Analysis and Support. Food allergen partnership. January 2001. Available at: www.cfsan.fda.gov/~dms/alrgpart.html. Accessed April 18, 2001. 3. Niemann LM, Hlywka JJ, Hefle SL. Immunochemical analysis of retail foods labeled as “May contain peanut” or other similar declaration: implications for food allergic individuals [abstract]. J Allergy Clin Immunol 2000;105:S188.
1/8/117794 doi:10.1067/mai.2001.117794