Atopy In Early Childhood Research Articles

The link between early childhood lower airway symptoms, airway hyperresponsiveness, and school-age lung function

BackgroundThe role of early airway hyperresponsiveness (AHR) in the lung function of school-age children is currently unclear. ObjectiveTo conduct a prospective follow-up study of lung function in schoolchildren with a history of lower airway symptoms and AHR to methacholine in early childhood and to compare the findings to schoolchildren with no previous or current lung diseases. We also explored symptoms and markers of type 2 inflammation. MethodsIn 2004 to 2011, data on atopic markers, lung function, and AHR to methacholine were obtained from 193 symptomatic children under 3 years old. In 2016 to 2018, a follow-up sample of 84 children (median age, 11 years; IQR, 11-12) underwent measurements of atopic parameters, lung function, and AHR to methacholine. Moreover, in 2017 to 2018, 40 controls (median age, 11 years; IQR, 9-12) participated in the study. ResultsSchoolchildren with early childhood lower airway symptoms and increased AHR had more frequent blood eosinophilia than their peers without increased AHR and lower prebronchodilator forced expiratory volume in 1 second (FEV1) and FEV1/forced vital capacity Z-scores than those without increased AHR and controls. Post-bronchodilator values were not significantly different between the two AHR groups. Atopy in early childhood (defined as atopic eczema and at least 1 positive skin prick test result) was associated with subsequent lung function and atopic markers, but not AHR. ConclusionIn symptomatic young children, increased AHR was associated with subsequent obstructive lung function, which appeared reversible by bronchodilation, and blood eosinophilia, indicative of type 2 inflammation.

Infant gut bacterial community composition and food-related manifestation of atopy in early childhood.

Background:Immunoglobulin E–mediated food allergy (IgE-FA) has emerged as a global public health concern. Immune dysregulation is an underlying mechanism for IgE-FA, caused by “dysbiosis” of the early intestinal microbiota. We investigated the association between infant gut bacterial composition and food-related atopy at age 3–5 years using a well-characterized birth cohort.Methods:The study definition of IgE-FA to egg, milk, or peanut was based on physician panel retrospective review of clinical and questionnaire data collected from birth through age 3–5 years. Using 16S rRNA sequencing, we profiled the bacterial gut microbiota present in stool specimens collected at 1 and 6 months of age.Results:Of 447 infants with data for analysis, 44 (9.8%) met physician panel review criteria for IgE-FA to ≥1 of the three allergens. Among children classified as IgE-FA at 3–5 years, infant stool samples showed significantly less diversity of the gut microbiota compared with the samples of children classified as no IgE-FA at age 3–5 years, especially for milk and peanut (all covariate-adjusted p’s for alpha metrics <.007). Testing of individual operational taxonomic units (OTUs) revealed 6-month deficiencies in 31 OTUs for IgE-FA compared with no IgE-FA, mostly in the orders Lactobacillales, Bacteroidales, and Clostridiales.Conclusions:Variations in gut microbial composition in infant stool were associated with a study definition of IgE-FA at 3–5 years of age. This included evidence of a lack of bacterial diversity, deficiencies in specific OTUs, and delayed microbial maturation. Results support dysbiosis in IgE-FA pathogenesis.

Dietary and Plasma Polyunsaturated Fatty Acids Are Inversely Associated with Asthma and Atopy in Early Childhood

Polyunsaturated fatty acids (PUFAs) influence immune function and risk of allergic disease. Prior evidence of the effect of PUFA intake on childhood asthma and allergy is inconclusive. To investigate associations of PUFA plasma levels and dietary intake with asthma and allergy at age 3 years in this ancillary study of the Vitamin D Antenatal Asthma Reduction Trial. Plasma PUFA levels were reported as relative abundances from mass spectrometry profiling, and dietary PUFA intake was derived from food frequency questionnaire responses. Associations between PUFA and outcomes, including asthma and/or recurrent wheeze, allergic sensitization, and total IgE at age 3 years, were evaluated in adjusted regression models. Additional regression models analyzed the combined effects of antenatal vitamin D and early childhood PUFA on outcomes. Total, omega-3, and omega-6 plasma PUFA relative abundances were significantly (P < .05) inversely associated with both asthma and/or recurrent wheeze and allergic sensitization. Likewise, dietary PUFA intake was inversely associated with asthma and/or recurrent wheeze (P < .05 for omega-6 PUFA only). For both dietary and plasma measures of total, omega-3, and omega-6 PUFAs, inverse associations with outcomes were strongest among subjects with both high umbilical cord blood 25-hydroxyvitamin D and high PUFA at age 3 years. PUFA dietary intake and plasma levels are inversely associated with asthma and/or recurrent wheeze and atopy at age 3 years. Antenatal vitamin D could modulate the effect of early childhood PUFA on risk of asthma and allergy.

The natural history of peanut sensitization and allergy in a birth cohort

Information on the natural history of peanut-induced allergic sensitization (PAS) and clinical peanut allergy (PA) remains limited. Most previous studies selected children who were given a diagnosis of PA, which does not provide the population perspective and probably ignores those with low levels of sensitization.1,2 There are no population-based studies on the natural history of PAS or PA. To provide a population perspective, we used the Isle of Wight birth cohort (n = 1456) and determined the natural history of PAS and PA, focusing on incidence, persistence, and remission.

Is atopy in early childhood a risk factor for ADHD and ASD? A longitudinal study

ObjectivePrevious studies have found a temporal concordance in the increased prevalence of atopic diathesis/atopic diseases, attention-deficit hyperactivity disorder (ADHD), and autistic spectrum disorder (ASD) worldwide. But, the temporal association among these 3 distinct diseases is unknown. Method14,812 atopic subjects diagnosed with any atopic disease (asthma, atopic dermatitis, allergic rhinitis, or allergic conjunctivitis) before the age of 3 (atopic cohort) and 6944 non-atopic subjects with no lifetime atopic disease (non-atopic cohort), born between 1997 and 2000, were enrolled and followed to December 31, 2010 to identify the development of ADHD and ASD. ResultsThe presence of any atopic disease in early childhood increased the risk of developing ADHD (hazard ratio [HR]: 1.97) and ASD (HR: 3.40) in later life. Greater numbers of atopic comorbidities (4 comorbidities: ADHD: HR: 2.53; ASD: HR: 4.29) were significantly related to a greater risk of developing ADHD and ASD. DiscussionAtopic diathesis in early childhood elevated the risk of developing ADHD and ASD in later life, with the dose-dependent relationship of more atopic comorbidities with a greater likelihood of ADHD and ASD.

Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze

Severe viral respiratory illnesses and atopy are risk factors for childhood wheezing and asthma. The aim of this study was to explore associations between severe respiratory infections and atopy in early childhood with wheeze and asthma persisting into later childhood. 147 children at high atopic risk were followed from birth to age 10 yrs. Data on all respiratory infections occurring in infancy were collected prospectively and viral aetiology ascertained. Atopy was measured by skin prick tests at 6 months, and 2 and 5 yrs. History of wheeze and doctor-diagnosed eczema and asthma was collected regularly until 10 yrs of age. At 10 yrs, 60% of the cohort was atopic, 25.9% had current eczema, 18.4% current asthma and 20.4% persistent wheeze. 35.8% experienced at least one lower respiratory infection (LRI) associated with fever and/or wheeze in first year of life. Children who had wheezy or, in particular, febrile LRI in infancy and were atopic by 2 yrs, were significantly more likely to have persistent wheeze (RR 3.51, 95% CI 1.83-6.70; p<0.001) and current asthma (RR 4.92, 95% CI 2.59-9.36; p<0.001) at 10 yrs. Severe viral respiratory infections in infancy and early atopy are risk factors for persistent wheeze and asthma. The strongest marker of the asthmatogenic potential of early life infections was concurrent fever. The occurrence of fever during respiratory illnesses is an important marker of risk for wheeze and asthma later in childhood, suggesting it should be measured in prospective studies of asthma aetiology.

Chromosome 17q21 Gene Variants Are Associated With Asthma and Exacerbations But Not Atopy in Early Childhood

Bisgaard H, Bonnelykke K, Sleiman PMA, et al. Am J Respir Crit Care Med . 2009;179(3):179–185 PURPOSE OF THE STUDY. To determine the association between the 17q12–q21 locus and various clinical characteristics of asthma and atopic sensitization during childhood. STUDY POPULATION. The Copenhagen Prospective Study on Asthma in Childhood (COPSAC) included a birth cohort of 411 children born to mothers with a history of asthma. Three hundred seventy-six …

The Association of Early Life Exposure to Antibiotics and the Development of Asthma, Eczema and Atopy in a Birth Cohort: Confounding or Causality?

Wickens K, Ingham T, Epton M, et al; New Zealand Asthma and Allergy Cohort Study Group. Clin Exp Allergy . 2008;38(8):1318–1324 PURPOSE OF THE STUDY. The goal was to examine the association between antibiotic exposure in infancy and the development of asthma, eczema, and atopy in early childhood. A secondary goal was to determine whether the association is secondary to confounding chest infections in infancy. STUDY POPULATION. Expectant mothers were recruited from a random sample of midwives in 2 major New Zealand cities between 1997 and 2001; full details on the nonresponding mothers are incomplete. METHODS. This was a birth cohort study that collected reported antibiotic exposure before 3 months and before 15 months, along with outcomes (wheeze, asthma, eczema, rash, and inhaler use) at 15 months ( N = 1011) and 4 …

Chromosome 17q21 Gene Variants Are Associated with Asthma and Exacerbations but Not Atopy in Early Childhood

An asthma predisposition locus on chromosome 17q12-q21 has recently been replicated in different ethnic groups. To characterize the asthma and atopy phenotypes in early childhood that associate with the 17q12-21 locus. The single nucleotide polymorphism (SNP), rs7216389, was genotyped in 376 of 411 children from the Copenhagen Prospective Study on Asthma in Childhood (COPSAC) birth cohort born to mothers with asthma together with 305 mothers and 224 fathers. Nineteen additional SNPs in the region were genotyped in the children. Investigator-diagnosed clinical endpoints were based on diary cards and clinic visits every 6 months and at acute symptoms from birth. Lung function, bronchial responsiveness, and sensitization were tested longitudinally from early infancy. rs7216389 was significantly associated with the development of wheeze (hazard ratio 1.64 [1.05-2.59], P value = 0.03), asthma (hazard ratio, 1.88 [1.15-3.07], P = 0.01), and acute severe exacerbations (hazard ratio 2.66 [1.58-4.48], P value = 0.0002). The effect on wheeze and asthma was observed for early onset but not late onset of disease. The increased risk of exacerbations persisted from 1 to 6 years of age (incidence ratio 2.48 [1.42-4.32], P value = 0.001), and increased bronchial responsiveness was present in infancy and at 4 years of age, but not at 6 years. In contrast, rs7216389 conferred no risk of eczema, rhinitis, or allergic sensitization. Variation at the chromosome 17q12-q21 locus was associated with approximately twofold increased risk of recurrent wheeze, asthma, asthma exacerbations, and bronchial hyperresponsiveness from early infancy to school age but without conferring risk of eczema, rhinitis, or allergic sensitization. These longitudinal clinical data show this locus to be an important genetic determinant of nonatopic asthma in children.

Effects of dog ownership in early childhood on immune development and atopic diseases

Exposure to pets in childhood has been associated with a reduced risk of wheezing and atopy. Our objective was to determine whether the effects of pet exposure on immune development and atopy in early childhood can be explained by alterations in exposure to innate immune stimuli in settled dust. Two hundred and seventy-five children at increased risk of developing allergic diseases were evaluated to age 3 years for pet ownership, blood cell cytokine responses, and atopy. Can f 1, Fel d 1, endotoxin, ergosterol, and muramic acid were measured in settled dust from 101 homes. Dog exposure at birth was associated with decreased atopic dermatitis (AD) (12% vs. 27%; P=0.004) and wheezing (19% vs. 36%; P=0.005) in year 3. The rates of AD (23%) and wheezing (42%) in year 3 were relatively high in children who acquired dogs after birth. The prevalence of dog sensitization (10-12%) did not vary according to dog exposure. Can f 1 levels in bedroom dust were positively associated with IL-10 (r=0.26; P=0.01), IL-5 (r=0.34, P<0.001), and IL-13 (r=0.28; P=0.004) responses at age 1, and IL-5 (r=0.24; P=0.022) and IL-13 (r=0.25; P=0.015) responses at age 3. In contrast, endotoxin was associated with IFN-gamma (r=0.31; P=0.002) and IL-13 (r=0.27; P=0.01) responses at age 3 but not at age 1, and similar relationships were present for muramic acid. Adjustment for levels of innate immune stimuli in house dust did not significantly affect the relationships between Can f 1 and cytokine responses. Exposure to dogs in infancy, and especially around the time of birth, is associated with changes in immune development and reductions in wheezing and atopy. These findings are not explained by exposure to endotoxin, ergosterol, or muramic acid.

The association of early life exposure to antibiotics and the development of asthma, eczema and atopy in a birth cohort: confounding or causality?

In general, studies reporting positive associations between antibiotic exposure and respiratory and allergic disease have been unable to determine the nature of this association. To examine the association between antibiotic exposure in infancy and the development of asthma, eczema and atopy in early childhood. In a birth cohort study, we collected reported antibiotic exposure before 3 months and before 15 months along with outcomes (wheeze, asthma, eczema, rash, inhaler use) at 15 months (n=1011) and 4 years (n=986). Atopy was measured using skin prick tests at 15 months. We found significant univariate associations of antibiotic exposure before 3 months with asthma developing between birth and 15 months [OR 2.32 (95% CI 1.45-3.69)]. After adjustment for chest infections, this association reduced (OR=1.58, 95% CI 0.96-2.60) becoming marginally significant (P=0.07). A marginally significant association of antibiotics with atopy (OR=1.44, 95% CI 0.96-2.14) in the univariate analysis also reduced after adjustment for chest infections (OR=1.36, 95% CI 0.91-2.05). There was no effect of antibiotic exposure before 15 months on asthma developing after 15 months and present between 3 and 4 years (OR=1.35 95% CI 0.85-2.14). Antibiotic exposure before 3 months was not associated with eczema and rash developing between birth and 15 months but exposure before 15 months was related to eczema [OR 1.83 (95% CI 1.10-3.05)] and rash [OR 1.61 (95% CI 1.02-2.53)] developing after 15 months and remaining present at 4 years. These effects reduced in the multivariate analysis. Our findings suggest that the effect of antibiotics on respiratory disease may be due to confounding by chest infections at an early age when asthma may be indistinguishable from infection.

Sex-related differences in immune development and the expression of atopy in early childhood

Sex and age are known to influence the clinical expression of asthma and allergic diseases. We sought to evaluate whether immune response profiles also vary by sex and age. We performed a prospective birth cohort study (Childhood Origins of Asthma) designed to evaluate interactions among age, sex, immune responses, and virus infections on the development of asthma and allergic diseases. Two hundred eighty-nine subjects were enrolled at birth, and 275 maintained prospective follow-up for 3 years. Cytokine response profiles at birth, 1, and 3 years of age; rates of wheezing, atopic dermatitis, and viral illnesses; and biomarkers of atopy, including total and specific IgE levels and peripheral eosinophil counts, were evaluated. PHA-induced IFN-gamma responses were higher in boys at 1 year of age (median, 35 vs 19 pg/mL; P < .001) and at 3 years of age (median, 282 vs 181 pg/mL; P = .07). Among children who wheezed during the third year of life, boys had increased IFN-gamma, IL-5, and IL-13 responses at age 3 years (P < .001, P = .008, and P = .01, respectively). Boys also demonstrated increased rates of sensitization (P = .05 at year 1), total IgE levels (P = .03 at year 1 and P = .006 at year 3), and peripheral eosinophil counts (2.62 vs 1.85; P = .05 at year 3). Sex-specific differences in immune responses develop during early childhood; some of these differences developmentally proceed, whereas others occur in parallel to the clinical expression of various atopic phenotypes. The differential expression of atopic diseases between boys and girls in early childhood is accompanied by sex-specific differences in immune response profiles.

Time-dependent Effects of Dog Exposure and Genotype at Immune-Related Genes on Wheezing and Atopy in Early Childhood

Immune-Related Genes on Wheezing and Atopy in Early Childhood J. Bufford1, Z. Li2, C. Reardon3, K. A. Roberg3, C. Tisler3, E. Anderson3, D. DaSilva3, I. Ostrovnaja4, S. Hoffjan5, D. Nicolae4, R. Gangnon2, C. Ober5, R. F. Lemanske, Jr.6, J. E. Gern3; 1Medicine, University of Wisconsin-Madison, Madison, WI, 2Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, WI, 3Pediatrics, University of Wisconsin-Madison, Madison, WI, 4Department of Statistics, University of Chicago, Chicago, IL, 5Department of Human Genetics, University of Chicago, Chicago, IL, 6Pediatrics and Medicine, University of Wisconsin-Madison, Madison, WI. RATIONALE: Dog exposure is associated with reduced atopy and increased IL-10 and IL-13 responses in early childhood. Whether these influences depend on the age of the child is unknown. METHODS: 275 children in the Childhood Origins of ASThma study were evaluated to age 3 for pet ownership, and blood was obtained for PHA-induced cytokine responses and RAST. Dog exposure was categorized into groups: never (D0, n=165), at birth but not age 3 (DB, n=21), at age 3 but not at birth (D3, n=13), or continuous (DB+3, n=76). All statistical comparisons were relative to nonexposed children (D0). 208 children were genotyped at selected immunoregulatory genes. RESULTS: Rates of wheezing in the third year of life (D0 35%; DB 15%, p=0.07; D3 42%, p=0.65; DB+3 20%, p=0.02) and rates of atopic dermatitis (AD) in the first 3 years (D0 37%; DB 14%, p=0.042; D3 46%, p=0.49; DB+3 14%, p=0.0004) were related to the timing of dog exposure. Notably, the prevalence of dog sensitization did not vary among these groups (D0 12%, DB 11%, D3 10%, DB+3 11%). There were interactions between dog exposure at birth and genotype on risk for wheezing at year 3 (IL10_-854C/T [p=0.006], -571C/A [p=0.002]; IL4RA Q551R [p=0.043], 676C/T [p=0.023], 7339A/G [p=0.024]) and for AD (IL4RA 150V [p=0.025], 676C/T [p=0.014], 7339A/G [p=0.016]; IL4_-589C/T [p=0.023]). CONCLUSIONS: The protective effects of dog exposure against subsequent AD and wheezing are age dependent and appear to be greatest in the newborn period. Furthermore, these effects may be modified by genotype at the IL10 and Th2 loci. Funding: NIH grants M01 RR03186, R01 HL61879 and P01 HL70831

The Potential Role of Allergen-Specific Sublingual Immunotherapy in Atopic Dermatitis

Atopic dermatitis is a chronic inflammatory skin disease associated with increasing prevalence, morbidity, and cost in developed Western countries. Frequently associated with respiratory allergy during adulthood, atopic dermatitis often represents the first phenotypic appearance of atopy in early childhood when the allergic 'march' starts and progressively moves toward food allergy, asthma, and rhinitis. At present, a consistent body of evidence supports the view that atopic dermatitis may represent the skin compartmentalization of a systemic allergic inflammation. Lymphocytes infiltrating early lesional skin express a T helper (Th) 2 pattern of cytokine secretion (increased levels of interleukin [IL]-4 and/or IL-13 and decreased levels of interferon-gamma) as well as the typical Th2-type chemokine receptor CCR4, specific to the thymus and activation-regulated chemokines. Keratinocytes from patients with atopic dermatitis produce thymic stromal lymphopoietin, a novel cytokine that supports the early lymphocyte development in mouse models, and activates dendritic cells involved in the pathogenesis of allergic diseases in humans. Increased levels of circulating hemopoietic precursor cells have been reported in atopic dermatitis, as in allergic asthma and rhinitis. Furthermore, the recognition of CD34+ hemopoietic precursor cells, and evidence for cellular differentiation/maturational events occurring within atopic dermatitis skin lesion infiltrates, are consistent with the recent reinterpretation of the Th2/Th1 paradigm, where Th2 cells appear to belong to the early stages and Th1 to the ultimate stages of a linear, rather than divergent, pattern of lymphoid differentiation. This more detailed understanding of the immunologic derangements contributing to the atopic dermatitis pathogenesis has led to growing interest in allergen-specific immunotherapy for the disease. Due to the complexity intrinsic to atopic dermatitis and the lack of consensus-based guidelines for standardized outcome measure, only eight studies are available in the literature for a qualitative evaluation of this treatment approach. Two of these studies were double blind and placebo controlled, and six were cohort studies. Immunotherapy was found to be effective in one controlled study and five observational reports. Uncertain results were provided by one low-powered, controlled study, and negative outcomes were raised by a unique study performed with oral immunotherapy, which is not an effective route of mucosal allergen administration. Thus, more efficacy studies are required before immunotherapy could be recommended for the routine treatment of atopic dermatitis. Allergen-specific sublingual immunotherapy, given its excellent safety profile and ability to interfere with the systemic aspects of allergic inflammation, appears a good potential candidate for the pathogenetic treatment of the disease.

Transient suppression of atopy in early childhood is associated with high vaccination coverage.

To analyze prevalences of allergic sensitization and atopic disease in relation to vaccination coverage. A German atopy risk-enhanced birth cohort of 1314 neonates who were born in 1990 in 5 German cities was studied. A total of 943 children participated in the follow-up visit at 5 years of age. Atopic symptoms and diagnoses (derived from structured interviews), total serum immunoglobulin E, and specific immunoglobulin E against 9 common allergens (CAP Radio-Allergo-Sorbent Test Fluoro-Enzyme Immunoassay) were evaluated. Children were grouped into dose percentiles according to cumulative doses of any vaccine given up to 5 years of age (<10%, 0-11 doses; 10%-50%, 12-14 doses; 51%-90%, 15-20 doses; >90%, 21-27 doses). The cumulative vaccine dose was inversely related to atopic dermatitis prevalences at 6 months (13.8%, 5.2%, 5.1%, and 4.5%), 2 years (16.9%, 10.9%, 7.4%, and 3.7%), 3 years (27.6%, 16.4%, 13.5%, and 4.5%), and 5 years (28.3%, 16.0%, 9.3%, and 11.9%). Asthma followed a similar pattern at age 3 (22.4%, 8.6%, 6.7%, and 6.3%), age 4 (20.0%, 8.6%, 8.9%, and 8.1%), and age 5 (20.8%, 12.6%, 10.3%, and 5.5%). Allergic sensitization rates were inversely related to the cumulative vaccine dose at age 2 (37.5%, 29.1%, 23.8%, and 12.9%). Children with a higher vaccination coverage seemed to be transiently better protected against development of atopy in the first years of life.

Soluble CD30 and CD23 in cord blood are not related to atopy in early childhood.

Atopic disease, including atopic dermatitis (AD), is associated with a T-helper 2 (Th2)-dependent immune response. The cytokine receptor CD30 appears to be preferentially expressed on, and its soluble form (sCD30) released by, Th2 cells. Therefore, sCD30 may be a potential marker for atopic disorders. The aim of this study was to test the hypothesis that the sCD30 level in cord blood could be used to predict the development of atopy or AD in early childhood. In a case-control study, levels of sCD30, as well as soluble low-affinity immunoglobulin E (IgE) receptor (sCD23), interleukin-4 (IL-4) and IgE, were measured in cord blood in 35 children who subsequently developed allergic sensitization and AD before the age of three, and the results were compared to those of 35 matched children without a history of atopy. There was no difference in cord blood levels of sCD30 between controls (32.5 U/ml; 19.7-80.1) and children with subsequent atopy and AD (32.2 U/ml; 22-75.9) (median; quartiles). The concentration of sCD30 showed no relation to the levels of total IgE, sCD23 or IL-4. Levels of sCD23 were similar in children with subsequent atopy (60.2 U/ml; 44.5-76.8) and controls (55.2 U/ml; 38.3-72.5), whereas IL-4 was detectable in 10 of the atopic children and in only two of the controls (p <0.05). In conclusion, cord blood levels of sCD30 or sCD23 do not seem to be related to the subsequent development of atopy or AD at the age of three.

The prevalence of and risk factors for atopy in early childhood: A whole population birth cohort study

Objectives: A birth cohort was followed-up to age 4 years to record the development of allergic disorders and to study the influence of genetic and environmental factors. Methods: Information on family history and environmental factors was obtained at birth, and serum cord IgE was measured. At age 4 years, 1218 children were reviewed. Results: By age 4 years, 27% of the children had symptoms of allergic disease. Period prevalence of asthma increased from 8.7% in infancy to 14.9% at 4 years. Family history of atopy was the single most important risk factor for atopy in children. Sibling atopy was a stronger predictor of clinical disease than maternal or paternal atopy, whereas paternal atopy, male sex, and high cord IgE were significant for the development of allergen sensitization. Children of asthmatic mothers were three times more likely to have asthma (odds ratio [OR]: 3.0, 95% confidence interval [CI]: 1.6-5.8) and rhinitis (OR: 2.9, CI: 1.1-7.4). Formula feeding before 3 months of age predisposed to asthma at age 4 years (OR: 1.8, CI: 1.2-2.6). The effect of maternal smoking on childhood wheeze seen at 1 and 2 years was lost by age 4, except for a subgroup with negative skin test responses (nonatopic asthma). Less than half (46%) of the infantile wheezers were still wheezing at 4 years of age. Conclusion: Family history of atopy remains the most important risk factor for atopy in children, but other markers can be identified with a potential for intervention at an early age.

Eczema and atopy in early childhood: low IgA plasma cell counts in the jejunal mucosa.

Twenty-one children aged between 2 and 54 months, 14 with eczema and 7 with allergies in first-degree relatives, were referred for diagnostic jejunal mucosal biopsy for a variety of symptoms. A partial villous atrophy was found in 19 of the 21 biopsies obtained; the other 2 were normal. We report a highly significant (P less than 0.0001) lower IgA cell count in biopsies with partial villous atrophy compared with the results of our previous study of IgA and IgM plasma cells in the mucosal biopsies in children without eczema or a history of atopy matched for age and histological appearances. The IgM cell count was also lower.