Randomized Trial of Peanut Consumption in Infants at Risk for Peanut Allergy
Source: New England Journal of Medicine
The prevalence of peanut allergy among children in Western countries has doubled in the past 10 years, and peanut allergy is becoming apparent in Africa and Asia. We evaluated strategies of peanut consumption and avoidance to determine which strategy is most effective in preventing the development of peanut allergy in infants at high risk for the allergy.
We randomly assigned 640 infants with severe eczema, egg allergy, or both to consume or avoid peanuts until 60 months of age. Participants, who were at least 4 months but younger than 11 months of age at randomization, were assigned to separate study cohorts on the basis of preexisting sensitivity to peanut extract, which was determined with the use of a skin-prick test — one consisting of participants with no measurable wheal after testing and the other consisting of those with a wheal measuring 1 to 4 mm in diameter. The primary outcome, which was assessed independently in each cohort, was the proportion of participants with peanut allergy at 60 months of age.
Among the 530 infants in the intention-to-treat population who initially had negative results on the skin-prick test, the prevalence of peanut allergy at 60 months of age was 13.7% in the avoidance group and 1.9% in the consumption group (P<0.001). Among the 98 participants in the intention-to-treat population who initially had positive test results, the prevalence of peanut allergy was 35.3% in the avoidance group and 10.6% in the consumption group (P=0.004). There was no significant between-group difference in the incidence of serious adverse events. Increases in levels of peanut-specific IgG4 antibody occurred predominantly in the consumption group; a greater percentage of participants in the avoidance group had elevated titers of peanut-specific IgE antibody. A larger wheal on the skin-prick test and a lower ratio of peanut-specific IgG4:IgE were associated with peanut allergy.
The early introduction of peanuts significantly decreased the frequency of the development of peanut allergy among children at high risk for this allergy and modulated immune responses to peanuts. (Funded by the National Institute of Allergy and Infectious Diseases and others; ClinicalTrials.gov number, NCT00329784.)
OBJECTIVES: To examine the role of prenatal and postnatal second-hand tobacco smoke (SHS) exposure on asthma, rhinitis, and eczema development up to 16 years of age.
METHODS: A birth cohort of 4089 children was followed for 16 years. Information on parental smoking habits, lifestyle factors, and symptoms of allergic disease was gathered using repeated parental questionnaires. Generalized estimating equations assessed the overall and age-specific associations between SHS exposure and allergic disease at ages 1 to 16 years.
RESULTS: Exposure to SHS in utero was associated with an overall elevated risk of developing asthma up to 16 years (odds ratio [OR] = 1.45; 95% confidence interval [CI], 1.15–1.83) but not for rhinitis or eczema. After additional adjustment for parental smoking throughout childhood, excess overall risks for asthma remained statistically significant. Moreover, a dose-dependent pattern with SHS was observed. Exposure to SHS during infancy was associated with an overall elevated risk of asthma (OR = 1.23; 95% CI, 1.01–1.51), rhinitis (OR = 1.18; 95% CI, 1.01–1.39), and eczema (OR = 1.26; 95% CI, 1.09–1.45) up to 16 years. When age-specific associations were examined, the elevated risks related to SHS exposure in utero or during infancy were mostly confined to early childhood for asthma and rhinitis, whereas the excess risk of eczema appeared greatest at later ages.
CONCLUSIONS: Our findings indicate that early SHS exposure, in utero or during infancy, influences the development of allergic disease up to adolescence. Excess risks for asthma and rhinitis were seen primarily in early childhood, whereas those for eczema occurred at later ages.
Fatal injuries and nonfatal occupational injuries and illnesses involving insects, arachnids, and mites
Fatal injuries and nonfatal occupational injuries and illnesses involving insects, arachnids, and mites
Source: Bureau of Labor Statistics
Although not often associated with injuries and deaths at the workplace, insects, arachnids, and mites were involved in 83 fatal occupational injuries from 2003 to 2010. The majority of these workplace deaths were due to bee stings. Annual nonfatal work-related injury and illness case counts involving insects, arachnids, and mites that led to days away from work ranged from 4,930 to 6,870 between 2008 and 2010. Most of these nonfatal cases were due to stings or bites, some venomous and some nonvenomous.
This issue of Beyond the Numbers article examines fatal and nonfatal workplace injuries and illnesses related to insects, arachnids, and mites using data from two Bureau of Labor Statistics (BLS) sources: the Census of Fatal Occupational Injuries (CFOI) and the Survey of Occupational Injuries and Illnesses (SOII). CFOI data used here are from 2003 to 2010 and aggregated to support extended analysis. SOII data are from 2008 to 2010. BLS began publishing national SOII estimates for state and local government in 2008, so that period was chosen to keep the coverage of CFOI and SOII data in this study as comparable as possible. For this article, the term “insects” refers to the entire category, for short.
See also: Workplace Safety & Health Topics – Insects and Scorpions (CDC)
Active or Passive Exposure to Tobacco Smoking and Allergic Rhinitis, Allergic Dermatitis, and Food Allergy in Adults and Children: A Systematic Review and Meta-Analysis
Allergic rhinitis, allergic dermatitis, and food allergy are extremely common diseases, especially among children, and are frequently associated to each other and to asthma. Smoking is a potential risk factor for these conditions, but so far, results from individual studies have been conflicting. The objective of this study was to examine the evidence for an association between active smoking (AS) or passive exposure to secondhand smoke and allergic conditions.
Methods and Findings
We retrieved studies published in any language up to June 30th, 2013 by systematically searching Medline, Embase, the five regional bibliographic databases of the World Health Organization, and ISI-Proceedings databases, by manually examining the references of the original articles and reviews retrieved, and by establishing personal contact with clinical researchers. We included cohort, case-control, and cross-sectional studies reporting odds ratio (OR) or relative risk (RR) estimates and confidence intervals of smoking and allergic conditions, first among the general population and then among children.
We retrieved 97 studies on allergic rhinitis, 91 on allergic dermatitis, and eight on food allergy published in 139 different articles. When all studies were analyzed together (showing random effects model results and pooled ORs expressed as RR), allergic rhinitis was not associated with active smoking (pooled RR, 1.02 [95% CI 0.92–1.15]), but was associated with passive smoking (pooled RR 1.10 [95% CI 1.06–1.15]). Allergic dermatitis was associated with both active (pooled RR, 1.21 [95% CI 1.14–1.29]) and passive smoking (pooled RR, 1.07 [95% CI 1.03–1.12]). In children and adolescent, allergic rhinitis was associated with active (pooled RR, 1.40 (95% CI 1.24–1.59) and passive smoking (pooled RR, 1.09 [95% CI 1.04–1.14]). Allergic dermatitis was associated with active (pooled RR, 1.36 [95% CI 1.17–1.46]) and passive smoking (pooled RR, 1.06 [95% CI 1.01–1.11]). Food allergy was associated with SHS (1.43 [1.12–1.83]) when cohort studies only were examined, but not when all studies were combined.
The findings are limited by the potential for confounding and bias given that most of the individual studies used a cross-sectional design. Furthermore, the studies showed a high degree of heterogeneity and the exposure and outcome measures were assessed by self-report, which may increase the potential for misclassification.
We observed very modest associations between smoking and some allergic diseases among adults. Among children and adolescents, both active and passive exposure to SHS were associated with a modest increased risk for allergic diseases, and passive smoking was associated with an increased risk for food allergy. Additional studies with detailed measurement of exposure and better case definition are needed to further explore the role of smoking in allergic diseases.
US prevalence of self-reported peanut, tree nut, and sesame allergy: 11-year follow-up
Source: Journal of Allergy and Clinical Immunology
Allergy to peanuts and tree nuts (TNs) is the leading cause of fatal allergic reactions in the United States, and the prevalence appears to be increasing.
We sought to determine the US prevalence of self-reported peanut, TN, and sesame allergy in 2008 and compare results with comparable surveys conducted in 1997 and 2002.
A nationwide, cross-sectional, random telephone survey for peanut and TN allergy was conducted with a previously used questionnaire, with additional questions about sesame.
A total of 5,300 households (13,534 subjects) were surveyed (participation rate, 42% vs 52% in 2002 and 67% in 1997). Peanut allergy, TN allergy, or both was reported by 1.4% of subjects (95% CI, 1.2% to 1.6%) compared with 1.2% in 2002 and 1.4% in 1997. For adults, the prevalence was 1.3% (95% CI, 1.1% to 1.6%), which was not significantly different from prior surveys. However, the prevalence of peanut or TN allergy for children younger than 18 years was 2.1% (95% CI, 1.6% to 2.7%) compared with 1.2% in 2002 (P = .007) and 0.6% in 1997 (P < .001). The prevalence of peanut allergy in children in 2008 was 1.4% (95% CI, 1.0% to 1.9%) compared with 0.8% in 2002 (P = not significant) and 0.4% in 1997 (P 3 million subjects) and appear to be increasingly reported among children over the past decade. Sesame allergy is reported much less commonly.
Prospective Study of Peripregnancy Consumption of Peanuts or Tree Nuts by Mothers and the Risk of Peanut or Tree Nut Allergy in Their Offspring
The etiology of the increasing childhood prevalence of peanut or tree nut (P/TN) allergy is unknown.
To examine the association between peripregnancy consumption of P/TN by mothers and the risk of P/TN allergy in their offspring.
Design, Setting, and Participants
Prospective cohort study. The 10 907 participants in the Growing Up Today Study 2, born between January 1, 1990, and December 31, 1994, are the offspring of women who previously reported their diet during, or shortly before or after, their pregnancy with this child as part of the ongoing Nurses’ Health Study II. In 2006, the offspring reported physician-diagnosed food allergy. Mothers were asked to confirm the diagnosis and to provide available medical records and allergy test results. Two board-certified pediatricians, including a board-certified allergist/immunologist, independently reviewed each potential case and assigned a confirmation code (eg, likely food allergy) to each case. Unadjusted and multivariable logistic regression analyses were used to evaluate associations between peripregnancy consumption of P/TN by mothers and incident P/TN allergy in their offspring.
Peripregnancy consumption of P/TN.
Main Outcomes and Measures
Physician-diagnosed P/TN allergy in offspring.
Among 8205 children, we identified 308 cases of food allergy (any food), including 140 cases of P/TN allergy. The incidence of P/TN allergy in the offspring was significantly lower among children of the 8059 nonallergic mothers who consumed more P/TN in their peripregnancy diet (≥5 times vs <1 time per month: odds ratio = 0.31; 95% CI, 0.13-0.75; Ptrend = .004). By contrast, a nonsignificant positive association was observed between maternal peripregnancy P/TN consumption and risk of P/TN allergy in the offspring of 146 P/TN-allergic mothers (Ptrend = .12). The interaction between maternal peripregnancy P/TN consumption and maternal P/TN allergy status was statistically significant (Pinteraction = .004).
Conclusions and Relevance
Among mothers without P/TN allergy, higher peripregnancy consumption of P/TN was associated with lower risk of P/TN allergy in their offspring. Our study supports the hypothesis that early allergen exposure increases tolerance and lowers risk of childhood food allergy.
Treatments for Seasonal Allergic Rhinitis
Source: Agency for Healthcare Research and Quality
This review compared the effectiveness and common adverse events of medication classes used to treat seasonal allergic rhinitis (SAR) in adolescents and adults, in pregnant women, and in children. We sought to compare the following classes of drugs: oral and nasal antihistamines and decongestants; intranasal corticosteroids, mast cell stabilizers (cromolyn), and anticholinergics (ipratropium); oral leukotriene receptor antagonists (montelukast); and nasal saline.
We identified English-language studies using a peer-reviewed search strategy. The following databases were
searched on July 18, 2012, with no date restrictions: MEDLINE® (PubMed® and Ovid), Embase® (Ovid), Cochrane Central Register of Controlled Trials (CENTRAL), Cochrane Database of Systematic Reviews, and DARE (Database of Abstracts of Reviews of Effects).
We consulted a Technical Expert Panel to identify the treatment comparisons most relevant to patients and providers. Subpopulations of interest were individuals with asthma or eye symptoms. Outcomes of interest were patient-reported symptom scores, quality of life, and adverse events. Inclusion was limited to studies that reported an outcome of interest and directly compared drugs of interest that were approved by the U.S. Food and Drug Administration (FDA). Two independent reviewers performed study selection and data abstraction. Disagreements were resolved by consensus or a third reviewer.
We identified 59 trials that addressed 13 of 22 treatment comparisons of interest for adolescents and adults, 0 of 17 comparisons of interest for pregnant women, and 1 of 21 comparisons of interest for children. Across all comparisons, 20 of 39 drugs FDA approved for the treatment of SAR were studied. For adolescents and adults with SAR, evidence was sufficient to form the following conclusions. For the treatment of nasal symptoms, montelukast (oral leukotriene receptor antagonist) and intranasal corticosteroid were similarly effective (high strength of evidence [SOE]). For the treatment of nasal symptoms and eye symptoms, intranasal corticosteroid, nasal antihistamine, and combination intranasal corticosteroid plus nasal antihistamine were similarly effective (high SOE), and montelukast and oral selective antihistamine were similarly effective (moderate SOE). For improved quality of life, montelukast and oral selective antihistamine were similarly effective (moderate SOE), and combination oral selective antihistamine plus intranasal corticosteroid was superior to oral selective antihistamine alone (low SOE). To avoid insomnia, oral selective antihistamine was superior to oral decongestant and to combination oral selective antihistamine plus oral decongestant (moderate SOE). In patients codiagnosed with SAR and asthma, montelukast was superior to oral selective antihistamine for reduced asthma rescue medication use (moderate SOE). In sensitivity analyses using a lower threshold for minimum clinical effectiveness, combination oral selective antihistamine plus oral decongestant was superior to oral selective antihistamine alone for the treatment of nasal symptoms in adolescents and adults with SAR (moderate SOE). In this population, we did not find evidence that any single treatment was both more effective and had lower risk of harms. Evidence for both effectiveness and harms was insufficient regarding the comparison between oral selective and oral nonselective antihistamine in children. All effectiveness and harms outcomes were limited by short trial durations.
Several effectiveness comparisons demonstrated similarity of treatments for selected outcomes. For most harms comparisons, the evidence was insufficient. Conclusions were limited by (1) lack of comparative evidence for all drugs within each class and (2) lack of evidence on the magnitude of symptom change that constitutes a minimal clinically important difference.