Abstract
Background:
Anaphylaxis is a life-threatening condition with significant global health implications. Understanding its risk factors in children across diverse populations is crucial for effective prevention and management strategies.
Objective:
The aim is to identify risk factors for severe anaphylaxis in children, using data from a Southeast Asian population.
Methods:
A retrospective study was conducted at a tertiary care hospital, Thailand, from 2015 to 2023. Data from 335 pediatric patients with anaphylaxis, classified into severe and nonsevere groups, were analyzed. Risk factors were identified using multivariable logistic regression.
Results:
Severe anaphylaxis occurred in 24 patients (7.2%). Males (58%) and food allergens, particularly shellfish and wheat, were the predominant factors. Severe cases were associated with an age greater than 12 years (adjusted odds ratio [aOR]: 5.67, P < 0.05), cardiovascular manifestations (aOR: 129.94, P < 0.01), and an early onset of symptoms (aOR: 0.96, P < 0.05).
Conclusion:
Age >12 years, cardiovascular symptoms, and early symptom onset were significant risk factors for severe anaphylaxis in children. These findings highlight the need for heightened vigilance and tailored management strategies in older children and those with cardiovascular involvement. Future studies in diverse populations are needed to confirm the generalizability of these risk factors.
Keywords: Cardiovascular symptoms, food allergy, global health, pediatric allergy, severe anaphylaxis
1. Introduction
Anaphylaxis is a life-threatening allergic reaction that can occur rapidly after exposure to an allergen [1]. The incidence of anaphylaxis in children is approximately 21 to 25.1 per million [2, 3], highlighting the need for close monitoring and care. Episodes can occur immediately after exposure to allergens, depending on the trigger [4]. Managing severe anaphylaxis is crucial for the well-being of affected individuals.
According to the World Allergy Organization (WAO) severity grading system, anaphylaxis is classified into 5 grades, with the most severe involving respiratory failure or cardiovascular collapse. The incidence of severe anaphylaxis among children is approximately 0.1% to 0.5% [1]. Immediate recognition and intervention are critical in such cases, with the administration of an epinephrine injection being the most important treatment [5].
Previous studies have shown that triggers in children differ from those in adults [6]. In children, food allergens such as nuts, milk, eggs, and shellfish are the primary cause [7, 8]. In contrast, adults more commonly experience anaphylaxis due to medications (eg, non-steroidal anti-inflammatory drugs [NSAIDs] and antibiotics) and insect stings. Data collected in the United States from 1999 to 2009 indicated that the incidence of food-induced anaphylaxis in individuals under 18 years old treated in hospitals doubled during this period [2, 3], significantly surpassing the rates observed in adults [9]. A prospective multicenter observational study from Spanish pediatric emergency departments (EDs) included 453 children under 18 years old diagnosed with anaphylaxis. Of these, 61 episodes (13.5%, 95% confidence interval [CI]: 10.6–16.9) were classified as severe. Children with a history of asthma, rapid onset of symptoms, non-well-appearing presentation, tachycardia, or hypotension upon ED arrival were more likely to experience severe episodes [10].
The purpose of this study is to identify the risk factors associated with severe anaphylaxis that contribute to morbidity and mortality, thereby enabling close monitoring and improved care for at-risk patients. Furthermore, this research aims to enhance understanding of the symptoms and causes of anaphylaxis in pediatric patients.
2. Materials and methods
This retrospective descriptive study investigated risk factors for severe anaphylaxis in Thai children aged 0 to 15 years treated at Songklanagarind Hospital. Medical records coded with International Classification of Diseases 10th Revision (ICD-10) diagnoses for anaphylaxis (code T78.0, T78.2, T80.5), adverse reaction to food/transfusion (code T78.1, T78.9, T80.9), allergy (code T78.4), and urticarial/angioneurotic edema (code T78.3) from both inpatient and outpatient departments at Songklanagarind Hospital were reviewed for children aged 0 to 15 years between January 2015 and December 2023. Demographic data, including triggers, clinical manifestations, investigations, and medications, were collected. Four hundred fifteen medical records were initially screened and 80 records were excluded because they did not meet the criteria for anaphylaxis diagnosis. Patients were categorized into 2 groups as nonsevere and severe anaphylaxis. The criteria for classification of hypotension, in alignment with the WAO classification [11], include evidence of end-organ dysfunction, decrease in systolic blood pressure (SBP) of ≥30% from baseline, or SBP < 70 mmHg + (2 × age in years) in children, or < 90 mmHg in adults.
Earlier onset was measured from the initial symptoms as recorded in the chief complaints, using a 30-minute threshold [12] as the reference point for onset time.
The sample size was calculated based on a 13.5% prevalence of severe anaphylaxis in children, as reported in a prospective observational study conducted across 7 Spanish pediatric EDs between May 2016 and April 2018. The required sample size was determined to be 265 children. However, data from 335 children were ultimately reviewed during the study period.
The study was approved by the Human Research Ethics Committee, Faculty of Medicine, Prince of Songkla University (REC 66-163-1-1).
2.1. Statistical analysis
All data were entered into Microsoft Excel, and statistical analyses were performed using the R program (R Foundation for Statistical Computing, Vienna, Austria). The characteristics of the children were described using numbers and percentages (for categorical variables) or means ± standard deviations (for continuous variables). The severity grading and types of triggers were also reported as numbers and percentages.
The t test was used to compare continuous variables, while the chi-square test or Fisher exact test was applied for categorical variables. Multivariate logistic regression was employed to determine the association between severe anaphylaxis and risk factors. A P value <0.05 was considered statistically significant.
3. Results
A thorough review of electronic medical records coded with ICD-10 diagnoses for anaphylaxis at Songklanagarind Hospital (in both inpatient and outpatient settings) revealed 335 patients of anaphylaxis in children aged 0 to 15 years during the period from January 2015 to December 2023. These cases were categorized into nonsevere and severe anaphylaxis groups based on the WAO definitions. Among these, 24 children (7.2%) were diagnosed with severe anaphylaxis. The majority of patients presented with grade III anaphylaxis (263 patients, 78.5%) (Fig. 1). Comprehensive data collection encompassed demographics, triggers, clinical manifestations, investigations, and treatments. As detailed in Table 1, 206 children (61.5%) were male, and the average age was 7.7 years (SD: 4.5). The highest incidence rate was observed among children aged 6 to 11 years. Most patients arrived at the hospital within 30 minutes of symptom onset. The average onset time was 35 minutes. Five patients in this population with severe anaphylaxis experienced refractory anaphylaxis that required more than 2 doses of adrenaline in the hospital. There were 2 cases of biphasic anaphylaxis reported, one from a wasp sting, with the biphasic reaction occurring 15 hours after the initial reaction and the other from a fire ant sting, but the time of the biphasic reaction was not recorded.
Figure 1.
Distribution of patients with anaphylaxis classified by severity grade according to the World Allergy Organization (WAO) criteria.
Table 1.
Characteristics of the anaphylactic patients, N = 335
| Characteristics | n (%) |
|---|---|
| Male | 206 (61.49) |
| Age, mean (SD), y | 7.73 (4.53) |
| 0–5 y | 123 (36.72) |
| 6–11 y | 139 (41.49) |
| 12–15 y | 73 (21.79) |
| Onset, mean (SD), min | 35.4 (37.83) |
| <30 min | 159 (47.46) |
| 30–60 min | 137 (40.9) |
| 60–120 min | 32 (9.55) |
| 120–180 min | 7 (2.09) |
| History of atopic disease | 196 (58.51) |
| Atopic dermatitis | 43 (12.84) |
| Allergic rhinitis | 104 (31.04) |
| Asthma | 51 (15.22) |
| History of food allergy | 86 (25.67) |
| History of drug allergy | 29 (8.66) |
3.1. Incidence, triggers of anaphylaxis
Food allergy emerged as the most prevalent cause of anaphylaxis, accounting for a substantial 206 cases (61.5%). This was followed by insect sting allergy, responsible for 29.3% of cases, and drug allergy, which caused 9.3% in Table 2. Among food-induced anaphylaxis, shellfish was the most common culprit (85 children, 25.4%), followed by wheat (50 children, 14.9%) and eggs (23 children, 6.9%). There were 4 cases (8% of wheat anaphylaxis) of wheat-dependent exercise-induced anaphylaxis. In cases of drug-induced anaphylaxis, antibiotics were the leading trigger (9 children, 2.7%), followed by NSAIDs.
Table 2.
Triggers of anaphylaxis
| Triggers | n (%) | Mean age (y) | Age group, n (%) | ||
|---|---|---|---|---|---|
| <6 y | 6–11 y | ≥12 y | |||
| Food | 206 (61.49) | ||||
| Cow milk | 21 (6.27) | 4.82 | 13 (61.9%) | 7 (33.33%) | 1 (4.76%) |
| Egg | 23 (6.87) | 1.81 | 22 (95.65%) | 1 (4.35%) | 0 (0.0%) |
| Shellfish | 85 (25.37) | 9.07 | 16 (18.82%) | 46 (54.12%) | 23 (27.06%) |
| Wheat | 50 (14.93) | 4.70 | 36 (72.0%) | 10 (20.0%) | 4 (8.0%) |
| Nuts | 5 (1.49) | 4.93 | 4 (80.0%) | 1 (20.0%) | 0 (0.0%) |
| Others* | 22 (6.57) | 10.00 | 4 (18.18%) | 9 (40.91%) | 9 (40.91%) |
| Insect | 98 (29.25) | ||||
| Fire ant | 32 (9.55) | 10.27 | 5 (15.62%) | 14 (43.75%) | 13 (40.62%) |
| Wasp | 21 (6.27) | 8.50 | 7 (33.33%) | 9 (42.86%) | 5 (23.81%) |
| Hornet | 20 (5.97) | 8.82 | 2 (10.0%) | 16 (80.0%) | 2 (10.0%) |
| Bee | 13 (3.88) | 7.66 | 5 (38.46%) | 6 (46.15%) | 2 (15.38%) |
| Others† | 12 (3.58) | 10.08 | 2 (16.67%) | 7 (58.33%) | 3 (25.0%) |
| Drug | 31 (9.25) | ||||
| Antibiotics | 9 (2.69) | 10.29 | 1 (11.11%) | 4 (44.44%) | 4 (44.44%) |
| Nonsteroidal anti-inflammatory drugs | 6 (1.79) | 9.44 | 1 (16.67%) | 3 (50.0%) | 2 (33.33%) |
| Chemotherapy | 4 (1.19) | 8.11 | 2 (50.0%) | 1 (25.0%) | 1 (25.0%) |
| Blood component | 4 (1.19) | 10.23 | 0 (0.0%) | 3 (75.0%) | 1 (25.0%) |
| Others‡ | 8 (2.39) | 8.73 | 3 (37.5%) | 2 (25.0%) | 3 (37.5%) |
Fried silkworm, fried beetle, fried ant eggs, fried insects, fried Buprestis beetle, beef, gelatin, monosodium glutamate, banana, coconut milk, pineapple, and Marian plum.
Dust mites and centipede.
N-Acetylcysteine, paracetamol, ammonium carbonate and glycyrrhiza mixture, bromhexine, oseltamivir, contrast, and cisatracurium.
3.2. Clinical characteristics of anaphylaxis reactions
The clinical manifestations of anaphylaxis are illustrated in Table 3. Cutaneous symptoms, such as urticaria and angioedema, were the most frequently observed, occurring in 320 children (95.5%). Respiratory symptoms affected 79.1% of patients, with chest tightness reported by 46.8% and wheezing by 17.7%. Figure 2 shows the frequency of symptoms for each trigger of anaphylaxis. Cutaneous and respiratory symptoms were the 2 most common manifestations across all triggers. No patients in this study had pre-existing heart conditions, except one with Takayasu arteritis who had contrast-induced anaphylaxis.
Table 3.
Clinical manifestation of anaphylaxis
| Clinical manifestation | n (%) | Age group (n = 335) | ||
|---|---|---|---|---|
| <6 y (n = 123) | 6–11 y (n = 139) | ≥12 y (n = 73) | ||
| Cutaneous symptom | 320 (95.52) | 115 (93.50%) | 134 (96.40%) | 71 (97.26%) |
| Angioedema | 146 (43.58) | |||
| Urticaria | 132 (39.4) | |||
| Erythema | 36 (10.75) | |||
| Pruritus | 6 (1.79) | |||
| Respiratory symptom | 265 (79.1) | 88 (71.54%) | 118 (84.89%) | 59 (80.82%) |
| Wheezing | 59 (17.72) | |||
| Chest tightness | 156 (46.85) | |||
| Cough | 15 (4.5) | |||
| Secretion | 11 (3.3) | |||
| Sneezing | 2 (0.6) | |||
| Rhinorrhea | 15 (4.5) | |||
| Nasal congestion | 5 (1.49)) | |||
| Stridor | 2 (0.6) | |||
| Respiratory failure | 0 (0) | |||
| Cardiovascular symptom | 33 (9.85) | 7 (5.69%) | 16 (11.51%) | 10 (13.70%) |
| Dizziness | 6 (1.79) | |||
| Hypotension | 20 (5.97) | |||
| Syncope | 4 (1.19) | |||
| Shock/cardiovascular collapse | 3 (0.9) | |||
| Gastrointestinal symptom | 105 (31.34) | 45 (36.59%) | 38 (27.34%) | 22 (30.14%) |
| Abdominal pain | 16 (4.78) | |||
| Nausea/vomiting | 67 (20) | |||
| Diarrhea | 22 (6.57) | |||
Figure 2.
Comparison of frequency of symptoms in each trigger of anaphylaxis.
3.3. Management of anaphylaxis
The treatment patterns, shown in Table 4, revealed that all patients received intramuscular adrenaline injections. No adrenaline use community before the hospital visit.
Table 4.
Treatment and investigation of anaphylaxis
| Variables | n (%) |
|---|---|
| Treatment | |
| Adrenaline | 335 (100) |
| Adrenaline ≥ 2 doses | 5 (1.5) |
| First generation H1-antihistamine | 112 (33.4) |
| Second generation H1-antihistamine | 98 (29.3) |
| Prednisolone | 29 (8.7) |
| Hydrocortisone | 64 (19.1) |
| Nebulized salbutamol | 33 (9.9) |
| Investigation | |
| Serum specific IgE | 204 (60.9) |
| Skin prick test | 149 (44.4) |
| Oral food challenge test/drug provocation test | 42 (12.5) |
3.4. Diagnostic evaluations of anaphylaxis
Diagnostic evaluations were performed in a significant proportion of cases. Among the 335 patients, 204 (60.9%) underwent additional testing, including skin prick tests (149 cases, 44.4%), specific IgE assays (204 cases, 60.9%), and oral food challenge or drug provocation tests (42 cases, 12.5%).
3.5. Predictors of severe anaphylaxis
Risk factor analysis, presented in Table 5, yielded compelling insights. Univariate analysis, shown in Table 6, identified several factors associated with severe anaphylaxis, including: age ≥ 12 years (odds ratio [OR]: 4.72; 95% CI: 1.42–15.66), insect stings as a trigger (OR: 2.62; 95% CI: 1.13–6.05), cardiovascular manifestations (OR: 114.62; 95% CI: 34.22–383.84), and early onset of symptoms (OR: 0.98; 95% CI: 0.95–1).
Table 5.
Risk factor between nonsevere and severe anaphylaxis
| Variables | Nonsevere anaphylaxis, n (%) | Severe anaphylaxis, n (%) | P value |
|---|---|---|---|
| Total number of patient | 311 | 24 | - |
| Male | 192 (61.74) | 14 (58.33) | 0.9105 |
| Age, mean (SD), y | 7.8 (3.76–11.36) | 10.52 (7.22–13.98) | 0.0233 |
| Onset, mean (IQR), min | 30 (10–60) | 15 (8.75–30) | 0.0565 |
| Any atopic disease | 185 (59.49) | 11 (45.83) | 0.2744 |
| Trigger by food | 197 (63.34) | 9 (37.5) | 0.0221 |
| Trigger by drug | 28 (9) | 3 (12.5) | 0.4759 |
| Trigger by insect | 86 (27.65) | 12 (50) | 0.037 |
| Cutaneous manifestation | 299 (96.14) | 21 (87.5) | 0.0831 |
| Respiratory manifestation | 250 (80.39) | 15 (62.5) | 0.0694 |
| Cardiovascular manifestation | 13 (4.18) | 20 (83.33) | <0.001 |
| Gastrointestinal manifestation | 97 (31.19) | 8 (33.33) | 1 |
IQR, interquartile range.
Table 6.
Univariate analysis to identify risk factor for severe anaphylaxis
| Risk factors | OR (95% CI) | P value |
|---|---|---|
| Age ≥ 12 y | 4.72 (1.42–15.66) | 0.011 |
| Cardiovascular manifestation | 114.62 (34.22–383.84) | <0.001 |
| Trigger by insect | 2.62 (1.13–6.05) | 0.026 |
| Trigger by food | 0.35 (0.15–0.82) | 0.014 |
| Early onset | 0.98 (0.95–1) | 0.033 |
CI, confidence interval; OR, odds ratio.
Multivariate logistic regression, presented in Table 7, reinforced the significance of these risk factors. Specifically, age ≥ 12 years (OR: 5.67; 95% CI: 1.04–30.78), cardiovascular manifestations (OR: 129.94; 95% CI: 34.38–491.1), and early symptom onset (OR: 0.96; 95% CI: 0.93–1).
Table 7.
Multivariable analysis to identify risk factor for severe anaphylaxis
| Risk factors | Adjusted OR (95% CI) | P value |
|---|---|---|
| Age ≥ 12 y | 5.67 (1.04–30.78) | 0.044 |
| Cardiovascular manifestation | 129.94 (34.38–491.1) | <0.001 |
| Early onset | 0.96 (0.93–1) | 0.047 |
CI, confidence interval; OR, odds ratio.
Among the predictors assessed, older age and earlier onset were significantly associated with an increased risk of severe anaphylaxis. To further investigate the predictive ability of these factors, along with the presence of cardiovascular manifestations, we conducted a receiver operating characteristic (ROC) curve analysis. The ROC curve analysis, incorporating these 3 predictors, demonstrated a high level of discrimination, with an area under the curve of 0.954, as shown in Figure 3.
Figure 3.
ROC curve analysis of severe anaphylaxis to older age, early onset, and cardiovascular manifestation. ROC, receiver operating characteristic.
4. Discussion
Anaphylaxis is a life-threatening allergic reaction that can develop rapidly and unpredictably in children [1], often requiring urgent medical attention. The severity and speed of its onset make it one of the most critical conditions for healthcare providers to manage. Our study highlights key risk factors for severe anaphylaxis in children, including the presence of cardiovascular manifestations, age (≥12 years), and the early onset of symptoms. These findings are significant, as they help identify children at higher risk for severe outcomes and could guide clinicians in making timely and informed decisions about treatment and monitoring.
Previous research, such as a retrospective study from Korea, has also identified various risk factors for severe anaphylaxis. These factors include respiratory manifestations, a history of asthma, food allergies, and being aged ≥2 years [6]. In our cohort, cardiovascular symptoms emerged as a particularly strong predictor of severe anaphylaxis. This suggests that children with signs of cardiovascular compromise, such as hypotension or tachycardia, may be at an increased risk for more severe reactions. The association of cardiovascular symptoms with severe anaphylaxis may be expected, as the presence of such symptoms corresponds with grade V in the WAO 2024 classification. Thus, this may not represent a true risk factor, but rather a defining characteristic of severe anaphylaxis. The authors should consider discussing treatment response in these cases for a more nuanced analysis. In addition, we found that older children (aged ≥12 years) were more likely to experience severe anaphylaxis, which contrasts with some studies suggesting that younger children are more vulnerable. It is possible that older children and teens doing outdoor work, sports, and outdoor play (like gardening, biking, or helping with family businesses) are more exposed and increase the risk, especially in grassy or wooded areas.
Cardiovascular reactivity or symptom recognition between older and younger children might provide insight into the observed age effect. During adolescence, the immune response becomes more robust and complex, potentially leading to more intense hypersensitivity reactions. Hormonal changes, particularly increased levels of sex hormones like estrogen and testosterone, can modulate immune function and mast cell activity, potentially heightening the severity of allergic responses [13]. Additionally, older children may have had repeated allergen exposures, increasing the likelihood of sensitization and more severe reactions.
Although cardiovascular involvement is part of the clinical definition of severe anaphylaxis, we included it in the multivariable model a priori due to its strong clinical relevance and potential role as a confounder. As one of the most critical determinants of anaphylactic severity, it may influence the associations between other predictors and severe outcomes. Its inclusion allowed for more appropriate adjustment and improved model stability. We acknowledge the possibility of circularity and have addressed this as a limitation in the interpretation of our findings.
In conclusion, our study emphasizes the importance of early recognition of severe anaphylaxis and the need for prompt intervention. Healthcare providers should be vigilant in assessing children at risk for severe reactions, especially those with cardiovascular symptoms, older age, or rapid symptom onset. By identifying these risk factors, clinicians can ensure timely treatment and improve outcomes for children experiencing anaphylaxis.
4.1. Limitation
One limitation of this model is the inclusion of the variable related to the cardiovascular system, which is part of the clinical definition of severe anaphylaxis. This may introduce a circular relationship. However, we decided to include this variable from the beginning due to its important role both clinically and as a potential confounder that could affect the relationship of other variables. Including the cardiovascular system improves the accuracy of the estimation of other covariates, although it may attenuate the effects of variables that are related to severity through cardiovascular mechanisms.
Conflicts of interest
The authors declare no conflicts of interest.
Author contributions
TK conceptualized and designed the study, collected the data, interpreted the results, and drafted the manuscript. PS performed the statistical analysis. VK and PR contributed to data interpretation. BS assisted in data collection. AY conceptualized and designed the study, interpreted the results, and drafted the manuscript. All authors reviewed the manuscript for important intellectual content and approved the final version.
Footnotes
Ethical approval was obtained from the Institutional Review Board and Ethics Committee of Songklanagarind Hospital, Prince of Songkla University (REC 66-163-1-1).
References
- 1.Sampson HA, Muñoz-Furlong A, Campbell RL, Adkinson NF, Jr, Bock SA, Branum A, Brown SGA, Camargo CA, Cydulka R, Galli SJ, Gidudu J, Gruchalla RS, Harlor AD, Hepner DL, Lewis LM, Lieberman PL, Metcalfe DD, O’Connor R, Muraro A, Rudman A, Schmitt C, Scherrer D, Simons FER, Thomas S, Wood JP, Decker WW. Second symposium on the definition and management of anaphylaxis: summary report--Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network Symposium. J Allergy Clin Immunol. 2006;117:391-397. [DOI] [PubMed] [Google Scholar]
- 2.Ma L, Danoff TM, Borish L. Case fatality and population mortality associated with anaphylaxis in the United States. J Allergy Clin Immunol. 2014;133:1075-1083. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Rudders SA, Arias SA, Camargo CA, Jr. Trends in hospitalizations for food-induced anaphylaxis in US children, 2000-2009. J Allergy Clin Immunol. 2014;134:960-962. [DOI] [PubMed] [Google Scholar]
- 4.Jiang N, Xu W, Xiang L. Age-related differences in characteristics of anaphylaxis in Chinese children from infancy to adolescence. World Allergy Organ J. 2021;14:100605. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Lee S-Y, Ahn K, Kim J, Jang GC, Min TK, Yang H-J, Pyun BY, Kwon JW, Sohn MH, Kim KW, Kim KE, Yu J, Hong SJ, Kwon JH, Kim SW, Song TW, Kim WK, Kim HY, Jeon YH, Lee YJ, Lee HR, Kim HY, Ahn Y, Yum HY, Suh DI, Kim HH, Kim JT, Kim JH, Park YM, Lee S; Korean Academy of Pediatric Allergy and Respiratory Diseases Food Allergy and Atopic Dermatitis Study Group. A multicenter retrospective case study of anaphylaxis triggers by age in Korean children. Allergy Asthma Immunol Res. 2016;8:535-540. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Lane RD, Bolte RG. Pediatric anaphylaxis. Pediatr Emerg Care. 2007;23:49-56; quiz 57. [DOI] [PubMed] [Google Scholar]
- 7.Neugut AI, Ghatak AT, Miller RL. Anaphylaxis in the United States: an investigation into its epidemiology. Arch Intern Med. 2001;161:15-21. [DOI] [PubMed] [Google Scholar]
- 8.Simons FE, Ardusso LR, Bilò MB, El-Gamal YM, Ledford DK, Ring J, Sanchez-Borges M, Senna GE, Sheikh A, Thong BY; World Allergy Organization. World Allergy Organization guidelines for the assessment and management of anaphylaxis. World Allergy Organ J. 2011;4:13-37. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Olabarri M, Vazquez P, Gonzalez-Posada A, Sanz N, Gonzalez-Peris S, Diez N, Vinuesa A, Martinez-Indart L, Benito J, Mintegi S. Risk factors for severe anaphylaxis in children. J Pediatr. 2020;225:193-197.e5. [DOI] [PubMed] [Google Scholar]
- 10.Lieberman P. Use of epinephrine in the treatment of anaphylaxis. Curr Opin Allergy Clin Immunol. 2003;3:313-318. [DOI] [PubMed] [Google Scholar]
- 11.Turner PJ, Ansotegui IJ, Campbell DE, Cardona V, Carr S, Custovic A, Durham S, Ebisawa M, Geller M, Gonzalez-Estrada A, Greenberger PA, Hossny E, Irani C, Leung ASY, Levin ME, Muraro A, Oppenheimer JJ, Ortega Martell JA, Pouessel G, Rial MJ, Senna G, Tanno LK, Wallace DV, Worm M, Morais-Almeida M; WAO Anaphylaxis Committee and WAO Allergen Immunotherapy Committee. Updated grading system for systemic allergic reactions: joint statement of the World Allergy Organization Anaphylaxis Committee and Allergen Immunotherapy Committee. World Allergy Organ J. 2024;17:100876. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Lertnawapan R, Maek-a-nantawat W. Anaphylaxis and biphasic phase in Thailand: 4-year observation. Allergol Int. 2011;60:283-289. [DOI] [PubMed] [Google Scholar]
- 13.Gutiérrez-Brito JA, Lomelí-Nieto J, Muñoz-Valle JF, Oregon-Romero E, Corona-Angeles JA, Hernández-Bello J. Sex hormones and allergies: exploring the gender differences in immune responses. Front Allergy. 2024;5:1483919. [DOI] [PMC free article] [PubMed] [Google Scholar]