• Clinical and Experimental Pediatrics
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• v.64 no.8
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• pp.393-399
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• 2021

Food allergies and food-induced anaphylaxis are important health problems. Several cofactors modulating the onset of anaphylaxis have been identified. In the presence of cofactors, allergic reactions may be induced at lower doses of food allergens and/or become severe. Exercise and concomitant infections are well-documented cofactors of anaphylaxis in children. Other factors such as consumption of nonsteroidal anti-inflammatory drugs, alcohol ingestion, and stress have been reported. Cofactors reportedly play a role in approximately 30% of anaphylactic reactions in adults and 14%-18.3% in children. Food-dependent exercise-induced anaphylaxis (FDEIA) is the best-studied model of cofactor-induced anaphylaxis. Wheat-dependent exercise-induced anaphylaxis, the most common FDEIA condition, has been studied the most. The mechanisms of action of cofactors have not yet been fully identified. This review aims to educate clinicians on recent developments in the role of cofactors and highlight the importance of recognizing cofactors in food allergies and food-induced anaphylaxis.

• Clinical and Experimental Pediatrics
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• v.51 no.4
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• pp.351-354
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• 2008

Anaphylaxis is an acute systemic reaction caused by IgE-mediated immunological release of mediators from mast cells and basophils to allergenic triggers, such as food, insect venoms, and medications. An alternative definition was recently proposed as follows: anaphylaxis is a "condition caused by an IgE mediated reaction" that is "often life threatening and almost always unanticipated." The reaction can be severe enough to lead to the rapid onset of symptoms, including dizziness, upper airway occlusion, bronchial constriction, hypotension, urticaria, cardiovascular arrhythmias and possible cardiac arrest. The incidence or prevalence of anaphylaxis in Korean pediatrics has not known. Thus, Epidemiology of Anaphylaxis in Pediatrics based on the data from Korean Health Insurance Review and Assessment Service (KHIRA) from 2001 to 2007 and questionnaire to the member of Korean Academy of Pediatric Allergy and Respiratory Disease (KAPARD) who are working at the training hospitals was studied. The incidence of anaphylaxis under age 19 is 0.7-1.0 per 100,000 year-person. The causes of anaphylaxis based on data from KHIRA were unknown (61.7%), food (24.9%), medications (12.4%), and serum (1.0%).

• Journal of The Korean Society of Clinical Toxicology
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• v.15 no.1
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• pp.24-30
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• 2017

Purpose: This study was conducted to investigate the frequency and clinical characteristics of anaphylaxis patients who are registered inaccurately with other disease codes. Methods: Study subjects presenting at the emergency department (ED) were retrospectively collected using disease codes to search for anaphylaxis patients in a previous studies. The study group was divided into an accurate and inaccurate group according to whether disease codes were accurately registered as anaphylaxis codes. Results: Among 266 anaphylaxis patients, 144 patients (54%) received inaccurate codes. Cancer was the most common comorbidity, and the radio-contrast media was the most common cause of anaphylaxis in the accurate group. Cutaneous and respiratory symptoms manifested more frequently in the inaccurate group, while cardiovascular and neurological symptoms were more frequent in the accurate group. Blood pressure was lower, and shock and non-alert consciousness were more common in the accurate group. Administration of intravenous fluid and epinephrine use were more frequent in the accurate group. Anaphylaxis patients with a history of cancer, shock, and epinephrine use were more likely to be registered as anaphylaxis codes accurately, but patients with respiratory symptoms were more likely to be registered with other disease codes. Conclusion: In cases of anaphylaxis, the frequency of inaccurately registered disease codes was higher than that of accurately registered codes. Anaphylaxis patients who were not treated with epinephrine at the ED who did not have a history of cancer, but had respiratory symptoms were at increased risk of being registered with disease codes other than anaphylaxis codes.

• Archives of Pharmacal Research
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• v.17 no.3
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• pp.154-160
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• 1994

The antigenicity of the aqueous extract of red ginseng (ARG) was evaluated using the following assay procedures : 1. active systemic anaphylaxis (ASA) in guinea pigs, 2 active cutaneous anaphylaxis (ACA) in guinea pigs, 3 passive cutaneous anaphylaxis (PCA) in guinea pigs, 2.active cutaneous anaphylaxis (ACA) in guinea pigs, 3. passive cutanepous anaphylaxis (PCA) in guina pigs with serum for guina pigs sensitized with ARG and 4. passive hemagglutination (PHA) with serum from guinea pigs sensitized with ARG. 1. ASA : No anaphylaxis reaction was observed in any of the sensitized guinea pigs by elictitation with ARG. 2. ACA : No skin reaction was observed in sensitized guinea pigs after intrademal injection of ARG. 3. PCA in guinea pigs : PCA titer of sera from all the sensitized animals was less than 10 in eliciation with ARG. 4. PHA reaction : When eythrocytes coated with challenge antigen were added to sensitized sera, the hemagglutination titer was less than 1. These results suggest that ARG has no antigenicity under the conditions used. And the dose levels of ARG employed in the present experiment were confirmed not to suppress immune reactions.

• Journal of Food Hygiene and Safety
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• v.6 no.3
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• pp.179-183
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• 1991

Antigenicity tests-ASA(Active Systemic Anaphylaxis), PSA(Passive Systemic Anaphylaxis), PCA(Passive Cutaneous Anaphylaxis)- of Bovine Somatotrophine(BST, Lucky Ltd.) were performed according to the established regulations of National Institude of Safety Research. The results were as follows: 1. No specific clinical signs related anaphylaxis were observed. Therefore, it was considered that BST has no antigenicity in guinea pigs and rabbits. 2. No blue spots were observed on the back of guinea pig in the peA test; BST-related IgE was not produced.

• IMMUNE NETWORK
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• v.7 no.3
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• pp.141-148
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• 2007

Background: Anti-IgE mAb which binds circulating but not receptor-bound IgE has been shown to be effective in treatment for asthma and other allergic diseases. However, the mechanisms by which anti-IgE mAb influences the pathophysiological responses are remained to be illustrated. This study was undertaken to examine the therapeutic efficacy of non-anaphylactogenic anti-mouse IgE mAb using murine models of IgE-induced systemic fatal anaphylaxis. Methods: Active systemic anaphylaxis was induced by either penicillin V(Pen V) or OVA and passive systemic anaphylaxis was induced by either anaphylactogenic anti-mouse IgE or a mixture of anti-chicken gamma globulin (CGG) IgG1 mAb and CGG. The binding of the Fc portion of anti-IgE to CHO-stable cell line expressing mouse Fc ${\gamma}$ RIIb was examined using flow cytometry. Fc fragments of anti-IgE mAb were prepared using papain digestion. The expression of phosphatases in lungs were assessed by Western blotting and immunohistochemistry. Results: Anti-IgE mAb prevented IgE- and IgG-induced active and passive systemic fatal reactions. In both types of anaphylaxis, anti-IgE mAb suppressed antigen-specific IgE responses, but not those of IgG. Anti-IgE mAb neither prevented anaphylaxis nor suppressed the IgE response in Fc ${\gamma}$ RIIb-deficient mice. The Fc portion of anti-IgE mAb was bound to murine Fc ${\gamma}$ RIIb gene-transfected CHO cells and inhibited systemic anaphylaxis. Anti-IgE mAb blocked the anaphylaxis-induced downregulation of Fc ${\gamma}$ RIIb-associated phosphatases such as src homology 2 domain-containing inositol 5-phosphatase (SHIP) and phosphatase and tensin homologue deleted on chromosome ten (PTEN). Conclusion: Anti-IgE mAb prevented anaphylaxis by delivering nonspecific inhibitory signals through the inhibitory IgG receptor, Fc ${\gamma}$ RIIb, rather than targeting IgE.

• Korean Journal of Pharmacognosy
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• v.25 no.1
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• pp.35-40
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• 1994

Aqueous extreact of fresh ginseng (AFG) was examined for the antigenicity in Hartley guinea pigs in comparision with ovalbumin (OVA). When guinea pigs were sensitized with AFG emulsified with complete Freund's adjuvant (CFA), these animals showed negative reactions in active systemic anaphylaxis (ASA), active cutaneous anaphylaxis (ACA) and passive cutaneous anaphylaxis (PCA) tests and passive hemagglutination (PHA) reaction. On the contrary, when guinea pigs were sensitized with OVA emulsified with CFA as positive controls, these animals disclosed positive reactions in ASA, ACA and PCA tests and PHA reaction. From these results, AFG was considered not to possess antigenic properties in guinea pigs. In addition, the dose levels of AFG empolyed in the present experiment were confirmed not to suppress immune reactions.

• Journal of Korean Medicine Rehabilitation
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• v.25 no.4
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• pp.175-182
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• 2015

The purpose of this study was to report an anaphylaxis after treated with Bee-venom acupuncture. Anaphylaxis is a clinical syndrome characterized by the acute system reaction of multiple organ systems to an IgE-mediated immunologic mediator release in previously sensitized individuals. We investigated the patients who had injected with Bee-venom in our clinic from March 2, 2014 to May 30, 2015. and two patients of anaphylaxis treated by Bee-Venom acupuncture were observed. One case of anaphylaxis was expressed clinically hypotension drowsy mentality, dyspnea, vomiting and so on. The other case was expressed itching sensation, urticaria, breathlessness, abdominal pain and so on. Based on this case, Bee venom-induced anaphylaxis can occur although preceding reactions are local or mild systemic ones. So, Korean medical doctor using Bee-Venom acupuncture must be prepare the system consider a countermeasure by anaphylaxis.

• Archives of Pharmacal Research
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• v.23 no.4
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• pp.401-406
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• 2000

We investigated the effect of aqueous extract of Gleditsia sinensis thorns (Leguminosae) (GSAE) on the mast cell-dependent anaphylaxis. GSAE (0.005 to 1 ${g}/kg$) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in rats. GSAE (0.1 and 1 ${g}/kg$) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. When GSAE was pretreated at the same concentrations with systemic anaphylaxis, the plasma histamine levels were reduced in a dose-dependent manner. GSAE (0.001 to 1 ${m}g/ml$) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cyclic AMP in RPMC, When GSAE (1 ${m}g/ml$) was added, transiently and significantly increased about fourfold compared with that of basal cells. Moreover, GSAE (0.01 and 0.1 ${m}g/ml$) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-$\alpha$ production from RPMC. These results suggest a possible use of GSAE in managing mast cell-dependent anaphylaxis.

• Journal of Life Science
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• v.18 no.4
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• pp.494-502
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• 2008

The anaphylaxis shock reaction on the whole cells of H. pylori exhibited a symptom of slight illness for the first and second medication of causing antigen at an antigen concentration of WC (H) $60\;{\mu}g/100\;{\mu}l$ for WC (H) and no anaphylaxis shock symptom was observed at an antigen concentration of $20\;{\mu}g/100\;{\mu}l$ for WC (L). In the case of anaphylaxis shock reaction on the crude urease, no symptom was observed at an antigen concentration of $20\;{\mu}g/100\;{\mu}l$ for both urease (L) and urease (H). In the heterologous passive cutaneous anaphylaxis (PCA) test using a guinea pig-rat, no positive reaction was detected in all the medication groups of WC (H), WC (L), urease (H) and urease (L). In the skin sensitization test, it was observed that the best antigen concentration not causing skin disorder at each of $80\;{\mu}g/100\;{\mu}l$, $40\;{\mu}g/100\;{\mu}l$, $20\;{\mu}g/100\;{\mu}l$, and $20\;{\mu}g/100\;{\mu}l$ was $40\;{\mu}g/100\;{\mu}l$.