Changes in Australian food anaphylaxis admission rates following introduction of updated allergy prevention guidelines.

BACKGROUND: Food anaphylaxis admission rates have increased steadily in recent decades. Global food allergy prevention guidelines recommending early introduction of allergenic foods were introduced in 2015-2016. Australian guidelines to not delay the introduction of allergenic foods were introduced in 2007-2008. OBJECTIVE: Our aim was to examine whether introduction of Australian guidelines (2007-2008) and global allergy prevention guidelines (2015-2016) were associated with reductions in food anaphylaxis admission rates. METHODS: We compared food anaphylaxis admission rates across 3 periods: 1998-1999 to 2006-2007, 2007-2008 to 2014-2015, and 2015-2016 to 2018-2019. RESULTS: Annual food anaphylaxis admission rates increased 9-fold between 1998-1999 and 2018-2019, from 2.0 per 105 population to 18.2 per 105 population; the highest absolute rates were in those younger than 1 year. When year-on-year rates of change were examined across the 3 time periods, the annual rate of increase slowed after 2007-2008 in those aged 1 to 4 years (17.6%, 6.2%, and 3.9% per year, respectively) and those aged 5 to 9 years (22%, 13.9%, and -2.4%, respectively), and after 2015-2016, in those aged 10 to 14 years (17.5%, 18.0%, and 10.8%, respectively). By contrast, the year-on-year rate of increase accelerated in those younger than 1 year (5.2%, 8.0%, and 18.0%, respectively) and in all age groups older than 15 years. CONCLUSIONS: Although food anaphylaxis continues to increase overall, there is preliminary evidence indicating a slowing in the year-on-year rate of increase among those aged 1 to 4, 5 to 9, and 10 to 14 years, coinciding with introduction of updated infant feeding and allergy prevention guidelines in 2007-2008 and 2015-2016. Changes to the guidelines may have contributed to an attenuated rate of increase in food anaphylaxis in these age groups, as well as to increased rates in those younger than 1 year.

ASCIA guidelines for prevention of anaphylaxis in schools, pre-schools and childcare: 2015 update.

The aim of these guidelines is to assist staff in school and childcare settings to plan and implement appropriate risk minimisation strategies, taking into consideration the needs of the allergic child, the likely effectiveness of measures and the practicality of implementation. Although these guidelines include risk minimisation strategies for allergic reactions to insect stings or bites, latex and medication, the major focus relates to food allergy. This is due to the higher relative prevalence of food allergy in childhood (compared with other allergic triggers) and the higher likelihood of accidental exposure in these settings. Care of the allergic child in the school, pre-school or childcare settings requires accurate information obtained from parents and carers, staff training in the recognition and management of acute allergic reactions, planning for unexpected reactions (including in those not previously identified as being at risk), age appropriate education of children with severe allergies and their peers, and implementation of practical strategies to reduce the risk of accidental exposure to known allergic triggers. Strategy development also needs to take into account local or regional established legislative or procedural guidelines and the possibility that the first episode of anaphylaxis may occur outside the home. Food bans are not recommended as the primary risk minimisation strategy due to difficulties in implementation and lack of proven effectiveness.

Time trends in Australian hospital anaphylaxis admissions in 1998-1999 to 2011-2012.

BACKGROUND: Studies from the United Kingdom, the United States, and Australia have reported increased childhood food allergy and anaphylaxis prevalence in the 15 years after 1990. OBJECTIVE: We sought to examine whether childhood food allergy/anaphylaxis prevalence has increased further since 2004-2005. METHODS: We examined hospital anaphylaxis admission rates between 2005-2006 and 2011-2012 and compared findings with those from 1998-1999 to 2004-2005. RESULTS: Overall population food-related anaphylaxis admission rates (per 10(5) population per year) increased from 5.6 in 2005-2006 to 8.2 in 2011-2012 (a 1.5-fold increase over 7 years). The highest rates occurred in children aged 0 to 4 years (21.7 in 2005-2006 and 30.3 in 2011-2012, a 1.4-fold increase), but the greatest proportionate increase occurred in those aged 5 to 14 years (5.8-12.1/10(5) population/y, respectively, a 2.1-fold increase) compared with those aged 15 to 29 years and 30 years or older (a 1.5- and 1.3-fold increase, respectively). Not only did absolute food-related anaphylaxis admissions increase, but the modeled year-on-year rate of increase in overall food-related anaphylaxis admissions also increased over time from an additional 0.35 per 10(5) population/y in 1998-1999 (all ages) to 0.49 in 2004-2005 and 0.63 in 2011-2012 (P < .001). CONCLUSIONS: Food-related anaphylaxis has increased further in all age groups since 2004-2005. Although the major burden falls on those aged 0 to 4 years, there is preliminary evidence for a recent acceleration in incidence rates in those aged 5 to 14 years. This contrasts with the previous decade in which the greatest proportionate increase was in those aged 0 to 4 years. These findings suggest a possible increasing burden of disease among adolescents and adults who carry the highest risk for fatal anaphylaxis.

Neonatal vitamin D status and childhood peanut allergy: a pilot study.

BACKGROUND: Although a number of factors have been proposed to explain the increase in food allergy during the last decade, the possibility that vitamin D status may play a pathogenic role has received recent attention. OBJECTIVE: To determine whether lower levels of neonatal 25-hydroxyvitamin D (25[OH]D) would be observed in children with peanut allergy compared with in population controls. METHODS: The concentration of 25(OH)D was measured from neonatal dried blood samples by liquid chromatography tandem mass spectrometry. Levels were compared between children with IgE-mediated peanut allergy younger than 72 months assessed during 2008-2011 in a specialist referral clinic in the Australian Capital Territory and population births matched by sex, birth date, and birth location. Odds ratios were calculated for the matched pairs across quintiles of 25(OH)D. RESULTS: Neonatal 25(OH)D levels ranged from 8 to 180 nmol/L (median, 66 nmol/L; interquartile range, 46-93 nmol/L); only 4 children (3%) had levels less than 25 nmol/L, and 24 (20.9%) had levels greater than 100 nmol/L. No significant association was found between socioeconomic or clinical factors and 25(OH)D levels. Compared with the reference group (50-74.9 nmol/L), levels of 75 to 99.9 nmol/L were associated with lower risk of peanut allergy (P = .02). No further reduction was found at levels of 100 nmol/L or higher, and the risk of peanut allergy at levels less than 50 nmol/L was not significantly different from the reference group. CONCLUSION: The relationship between neonatal 25(OH)D level and childhood peanut allergy was nonlinear, with slightly higher levels (75-99.9 nmol/L) associated with lower risk than those in the reference group (50-74.9 nmol/L). Vitamin D status may be one of many potential factors contributing to childhood peanut allergy pathogenesis.

Relationship between red meat allergy and sensitization to gelatin and galactose-α-1,3-galactose.

BACKGROUND: We have observed patients clinically allergic to red meat and meat-derived gelatin. OBJECTIVE: We describe a prospective evaluation of the clinical significance of gelatin sensitization, the predictive value of a positive test result, and an examination of the relationship between allergic reactions to red meat and sensitization to gelatin and galactose-α-1,3-galactose (α-Gal). METHODS: Adult patients evaluated in the 1997-2011 period for suspected allergy/anaphylaxis to medication, insect venom, or food were skin tested with gelatin colloid. In vitro (ImmunoCAP) testing was undertaken where possible. RESULTS: Positive gelatin test results were observed in 40 of 1335 subjects: 30 of 40 patients with red meat allergy (12 also clinically allergic to gelatin), 2 of 2 patients with gelatin colloid-induced anaphylaxis, 4 of 172 patients with idiopathic anaphylaxis (all responded to intravenous gelatin challenge of 0.02-0.4 g), and 4 of 368 patients with drug allergy. Test results were negative in all patients with venom allergy (n = 241), nonmeat food allergy (n = 222), and miscellaneous disorders (n = 290). ImmunoCAP results were positive to α-Gal in 20 of 24 patients with meat allergy and in 20 of 22 patients with positive gelatin skin test results. The results of gelatin skin testing and anti-α-Gal IgE measurements were strongly correlated (r = 0.46, P < .01). α-Gal was detected in bovine gelatin colloids at concentrations of approximately 0.44 to 0.52 µg/g gelatin by means of inhibition RIA. CONCLUSION: Most patients allergic to red meat were sensitized to gelatin, and a subset was clinically allergic to both. The detection of α-Gal in gelatin and correlation between the results of α-Gal and gelatin testing raise the possibility that α-Gal IgE might be the target of reactivity to gelatin. The pathogenic relationship between tick bites and sensitization to red meat, α-Gal, and gelatin (with or without clinical reactivity) remains uncertain.

Latitude, sunlight, vitamin D, and childhood food allergy/anaphylaxis.

Vitamin D is widely known for its role in bone metabolism, but this sterol hormone also has important immunomodulatory properties. Vitamin D is produced by the conversion of D3 in the skin following UVB exposure, or after ingestion of D2 or D3. At the extremes of latitude, there is insufficient UVB intensity in the autumn and winter months for adequate synthesis of vitamin D to occur. Growing evidence implicates vitamin D deficiency in early life in the pathogenesis of nonskeletal disorders (e. g., type 1 diabetes and multiple sclerosis) and, more recently, atopic disorders. Several studies have reported higher rates of food allergy/anaphylaxis or proxy measures at higher absolute latitudes. Although causality remains to be determined, these studies suggest a possible role for sunlight and/or vitamin D in the pathogenesis of food allergy/anaphylaxis.

Season of birth and childhood food allergy in Australia.

BACKGROUND: Recent studies suggest a possible role for low ultraviolet radiation exposure and low vitamin D status as a risk factor for food allergy. We hypothesized that children born in autumn/winter months (less sun exposure) might have higher food allergy rates than those born in spring/summer. METHODS: We compared IgE-mediated food allergy rates by season of birth in 835 children aged 0-4 yr assessed 1995-2009 in a specialist referral clinic, using population births as controls. To address potential concerns about generalizability, we also examined national prescriptions for adrenaline autoinjectors (2007) and infant hypoallergenic formula (2006-2007). RESULTS: Although live births in the general ACT population showed no seasonal pattern (50% autumn/winter vs. 50% spring/summer), autumn/winter births were more common than spring/summer births among food allergy patients (57% vs. 43%; p < 0.001). The same seasonal pattern was observed with peanut (60% vs. 40%; p < 0.001) and egg (58% vs. 42%; p = 0.003). Regional UVR intensity was correlated with relative rate of overall food allergy (ß, -1.83; p = 0.05) and peanut allergy (ß, -3.27; p = 0.01). National data showed that autumn/winter births also were more common among children prescribed EpiPens (54% vs. 46%; p < 0.001) and infant hypoallergenic formula (54% vs. 46%; p < 0.001). CONCLUSIONS: The significantly higher rates of food allergy in children born autumn/winter (compared to spring/summer), the relationship between relative food allergy rates and monthly UVR, combined with national adrenaline autoinjector and infant hypoallergenic formula prescription data, suggest that ultraviolet light exposure/vitamin D status may be one of many potential factors contributing to childhood food allergy pathogenesis.

Characteristics of childhood peanut allergy in the Australian Capital Territory, 1995 to 2007.

BACKGROUND: It is unknown whether clinical features of peanut allergy have changed in the past decade alongside possible increasing prevalence. OBJECTIVE: The clinical features of peanut allergy over 13 years were examined with regard to age of onset, sex distribution, severity, and incidence. METHODS: Retrospective study of 778 patients (age 4 months to 66 years) diagnosed with peanut allergy at a community-based specialist allergy practice in the Australian Capital Territory. RESULTS: Most peanut allergy (90%) developed by age 72 months. In this group, there were no significant time-dependent changes in sex distribution, reaction severity, or age of first reaction (mean/median 12/15.1 months). Later age of first reaction was associated with an increased risk of anaphylaxis in the overall population (P < .01) and in those with onset by 72 months, in whom risk increased by 22.7% (CI, 3.3-45.7) for every additional year of age (P < .02). Asthma was associated with increased risk of anaphylaxis (odds ratio, 1.9; P < .001). In children with peanut allergy, 22% experienced anaphylaxis with first exposure and 30% with anaphylaxis had preceding milder reactions. The estimated minimum incidences of peanut allergy and sensitization by age 72 months for children born in the Australian Capital Territory in 2004 were 1.15% and 1.53%, respectively (by end December 2007), compared with 0.73% and 0.84% for those born in 2001. CONCLUSION: Although most characteristics of peanut allergy have changed little over the period of the last 13 years (onset age, sex, comorbidity, severity), later onset was associated with greater risk of anaphylaxis. Our data are consistent with a rise in incidence.

Regional variation in epinephrine autoinjector prescriptions in Australia: more evidence for the vitamin D-anaphylaxis hypothesis.

BACKGROUND: There is little information on the regional distribution of anaphylaxis in Australia. OBJECTIVE: To examine the influence of latitude (a marker of sunlight/vitamin D status) as a contributor to anaphylaxis in Australia, with a focus on children from birth to the age of 4 years. METHODS: Epinephrine autoinjector (EpiPen) prescriptions (2006-2007) in 59 statistical divisions and anaphylaxis hospital admission rates (2002-2007) in 10 regions were used as surrogate markers of anaphylaxis. RESULTS: EpiPen prescription rates (per 100,000 population per year) were higher in children from birth to the age of 4 years (mean, 951) than in the overall population (mean, 324). In an unadjusted model of children from birth to the age of 4 years, decreasing absolute latitude was associated with a decrease in EpiPen prescription rates, such that rates were higher in southern compared with northern regions of Australia (beta, -44.4; 95% confidence interval, -57.0 to -31.8; P < .001). Adjusting for age, sex, ethnicity, indexes of affluence, education, or access to medical care (general, specialist allergy, or pediatric) did not attenuate the finding (beta, -51.9; 95% confidence interval, -71.0 to -32.9; P < .001). Although statistical power was limited, anaphylaxis admission rates (most prominent in children aged 0-4 years) showed a similar south-north gradient, such that admission rates were higher in southern compared with northern regions of Australia. CONCLUSIONS: EpiPen prescription rates and anaphylaxis admissions are more common in southern regions of Australia. These data provide additional support for a possible role of vitamin D in the pathogenesis of anaphylaxis.