BackgroundWe have noticed changes in paediatric anaphylaxis triggers locally in Singapore.ObjectiveWe aimed to describe the demographic characteristics, clinical features, causative agents and management of children presenting with anaphylaxis.MethodsThis is a retrospective study of Singaporean children presenting with anaphylaxis between January 2005 and December 2009 to a tertiary paediatric hospital.ResultsOne hundred and eight cases of anaphylaxis in 98 children were included. Food was the commonest trigger (63%), followed by drugs (30%), whilst 7% were idiopathic. Peanut was the top food trigger (19%), followed by egg (12%), shellfish (10%) and bird's nest (10%). Ibuprofen was the commonest cause of drug induced anaphylaxis (50%), followed by paracetamol (15%) and other nonsteroidal anti-inflammatory drugs (NSAIDs, 12%). The median age of presentation for all anaphylaxis cases was 7.9 years old (interquartile range 3.6 to 10.8 years), but food triggers occurred significantly earlier compared to drugs (median 4.9 years vs. 10.5 years, p < 0.05). Mucocutaneous (91%) and respiratory features (88%) were the principal presenting symptoms. Drug anaphylaxis was more likely to result in hypotension compared to food anaphylaxis (21.9% vs. 2.7%, Fisher's exact probability < 0.01). There were 4 reported cases (3.6%) of biphasic reaction occurring within 24 h of anaphylaxis.ConclusionFood anaphylaxis patterns have changed over time in our study cohort of Singaporean children. Peanuts allergy, almost absent a decade ago, is currently the top food trigger, whilst seafood and bird's nest continue to be an important cause of food anaphylaxis locally. NSAIDs and paracetamol hypersensitivity are unique causes of drug induced anaphylaxis locally.

ABSTRACT. Objective. Nonsteroidal antiinflammatory drugs (NSAIDs), mainly ibuprofen, are used extensively among children as analgesic and antipyretic agents. Our initial survey in the Kendang Kerbau Children's Hospital in Singapore showed NSAIDs to be the second most common adverse drug reaction-causing medications among children of Asian descent. We attempted to characterize the clinical and epidemiologic profile of NSAID reactions in this group of patients.Methods. A retrospective case series from a hospitalbased pediatric drug allergy clinic was studied. A diagnosis of NSAID hypersensitivity was made with a modified oral provocation test. Atopy was evaluated clinically and tested with a standard panel of skin-prick tests. We excluded from analysis patients with any unprovoked episodes of urticaria and/or angioedema, patients <1 year of age, and patients who refused a diagnostic challenge test.Results. Between March 1, 2003, and February 28, 2004, 24 patients, including 14 male patients (58%) and 18 Chinese patients (75%), with a mean age of 7.4 years (range: 1.4 -14.4 years), were diagnosed as having crossreactive NSAID hypersensitivity. A family history consistent with NSAID hypersensitivity was elicited for 17% of patients. None of the patients reported any episodes of angioedema/urticaria unrelated to NSAIDs. The median cumulative reaction-eliciting dose was 7.1 mg/kg. Facial angioedema developed for all patients (100%) and generalized urticaria for 38% of challenged patients, irrespective of age. There was no circulatory compromise, but respiratory symptoms of tachypnea, wheezing, and/or cough were documented for 42% of patients. A cross-reactive hypersensitivity response to acetaminophen was documented for 46% of our patients through their history and for 25% through diagnostic challenge. Compared with patients with suspected adverse drug reactions to antibiotics, patients in the NSAID group were older (7.4 vs 4.8 years) and more likely to have a diagnosis of asthma (odds ratio: 7.5; 95% confidence interval: 3.1-19).Conclusions. Early presentations of facial angioedema and urticaria are key features of dose-and potency-dependent, cross-reactive reactions to NSAIDs in a subpopulation of young, Asian, atopic children. Significant overlap with acetaminophen hypersensitivity, especially among very young patients, for whom the use of a cyclooxygenase-2-specific medication may not be feasible, severely limits options for medical antipyretic treatment. A spirin and other nonsteroidal antiinflammatory drugs (NSAIDs) are a widely used group of medications whose mechanism of action involves inhibition of prostaglandin production through blockade of the cyclooxygenase (COX) enzymes known as COX-1 and COX-2. This blockade also results in the shunting of arachidonic acid metabolism toward the 5-lipoxygenase pathway, resulting in increased production and release of cysteinyl leukotrienes.Acetaminophen, the most ubiquitously used antipyretic medication for children worldwide, is an "old" medication whose mechanism of a...

Evidence is accumulating that the establishment of the gut microbiome in early life influences the development of atopic eczema. In this longitudinal study, we used integrated multi-omics analyses to infer functional mechanisms by which the microbiome modulates atopic eczema risk. We measured the functionality of the gut microbiome and metabolome of 63 infants between ages 3 weeks and 12 months with well-defined eczema cases and controls in a sub-cohort from the Growing Up in Singapore Toward healthy Outcomes (GUSTO) mother-offspring cohort. At 3 weeks, the microbiome and metabolome of allergen-sensitized atopic eczema infants were characterized by an enrichment of Escherichia coli and Klebsiella pneumoniae , associated with increased stool D-glucose concentration and increased gene expression of associated virulence factors. A delayed colonization by beneficial Bacteroides fragilis and subsequent delayed accumulation of butyrate and propionate producers after 3 months was also observed. Here, we describe an aberrant developmental trajectory of the gut microbiome and stool metabolome in allergen sensitized atopic eczema infants. The infographic describes an impaired developmental trajectory of the gut microbiome and metabolome in allergen-sensitized atopic eczema (AE) infants and infer its contribution in modulating allergy risk in the Singaporean mother-offspring GUSTO cohort. The key microbial signature of AE is characterized by (1) an enrichment of Escherichia coli and Klebsiella pneumoniae which are associated with accumulation of pre-glycolysis intermediates (D-glucose) via the trehalose metabolic pathway, increased gene expression of associated virulence factors (invasin, adhesin, flagellin and lipopolysaccharides) by utilizing ATP from oxidative phosphorylation and delayed production of butyrate and propionate, (2) depletion of Bacteroides fragilis which resulted in lower expression of immunostimulatory bacterial cell envelope structure and folate (vitamin B9) biosynthesis pathway, and (3) accompanied depletion of bacterial groups with the ability to derive butyrate and propionate through direct or indirect pathways which collectively resulted in reduced glycolysis, butyrate and propionate biosynthesis.

Food allergy rates in Singapore are low despite delayed introduction of allergenic foods. Early introduction of allergenic foods may thus not be necessary in populations in which overall food allergy prevalence is low, and thus infant feeding recommendations should be carefully tailored to individual populations.

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