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Coincidence of atopy and its profile (monosensitization/polysensitization) between sibling pairs.

BACKGROUND: Results of epidemiologic studies have shown that childhood atopy is probably a hereditary disorder. In the atopic population, some individuals are sensitized to only 1 class of allergens (monosensitized), whereas others are sensitized to more than 1 class of allergens (polysensitized). OBJECTIVE: To investigate whether atopy and its profile (monosensitization/polysensitization) tend to coincide in sibling pairs. METHODS: We evaluated sensitization to 5 classes of aeroallergens (house dust mites, animal danders, pollens, molds, and cockroach) using skin prick testing in 564 children with symptoms suggestive of allergic diseases (index children) and their paired siblings. RESULTS: The frequency of sibling atopy was highest (56.8%) for polysensitized index children (n=222), intermediate (45.4%) for monosensitized index children (n=196), and lowest (30.8%) for nonsensitized index children (n=146). The proportion of polysensitization among atopic siblings was significantly higher for polysensitized (47.6%) than for monosensitized (32.6%) index children. Polysensitized index children were found to more frequently have polysensitized siblings (27.0%) than were monosensitized index children (14.8%), with an odds ratio of 2.13 (95% confidence interval, 1.30-3.49), whereas the likelihood of having a monosensitized sibling was similar for monosensitized and polysensitized index children. CONCLUSION: These data suggest a coincidence of atopy and its profile in terms of monosensitization and polysensitization in sibling pairs, although the relative importance of genetic and environmental influences requires further study.

Allergens↗

Exposure to pets and atopy-related diseases in the first 4 years of life.

BACKGROUND: It is still unclear how early-life exposure to pets is related to children's risk of developing atopy-related diseases. We estimated associations between early-life exposure to pets and atopy-related diseases at 0-4 years of life in a cohort of Norwegian children. METHODS: A population-based cohort of 2531 children born in Oslo, Norway, was followed from birth to the age of 4 years. Information on early-life exposure to pets, a number of possible confounders, and atopy-related diseases was mainly collected by questionnaire. RESULTS: In logistic regression analysis adjusting for potential confounders, the odds ratio for being exposed to pets in early life (reference category: not exposed) was, for bronchial obstruction at 0-2 years of life, 1.2 (95% confidence interval 0.9, 1.8); for asthma at the age of 4 years, 0.7 (0.5, 1.1); for allergic rhinitis at the age of 4 years, 0.6 (0.4, 1.0); and for atopic eczema at 0-6 months of life, 0.7 (0.5, 0.9). CONCLUSIONS: The results indicate that early-life exposure to pets or lifestyle factors associated with exposure to pets reduce the risk of developing atopy-related diseases in early childhood. However, these findings might also be explained by selection for keeping pets.

Animals↗

A dual long-term effect of breastfeeding on atopy in relation to heredity in children at 4 years of age.

BACKGROUND: The long-term effect of early feeding on atopic sensitization is still unsolved. The aim of this study was to evaluate the long-term effect of breastfeeding on atopy in groups of 4-year-old children stratified by atopic heredity. METHODS: We collected four groups of 4-year-old children from a birth cohort: two groups with differing backgrounds of atopic heredity, all exclusively breast-fed for at least 3 months; and two groups with differing atopic heredity, but all fed with cow's milk-based formula during their first weeks. The data were collected with a questionnaire, skin prick testing, and measurement of serum total and allergen-specific IgE levels. RESULTS: Breastfeeding significantly decreased the risk of allergic rhino-conjunctivitis [odds ratio (OR) 0.41, 95% confidence interval (CI) 0.18-0.95] and sensitization to furred pets, as measured by skin prick results, in children with atopic heredity, whereas in children without atopic heredity, breastfeeding was related to an increased risk of symptomatic atopy (OR 2.57, 95% CI 1.16-5.70), and high serum IgE values. A significant interaction was found between heredity and breastfeeding. CONCLUSIONS: The long-term effect of breastfeeding was dual: in children with atopic heredity, breastfeeding protected against atopy, whereas in children without atopic heredity, it increased the risk of atopy.

Animals↗

The rise of atopy and links to infection.

Atopy is the state of allergy to common environmental antigens. Genetic and environmental factors promote the disorder. The impressive rise in prevalence, mainly centred on socio-economically developed communities around the world, emphasizes the potent action of environmental factors in moulding this immune disorder which is characterized by inadequately restrained Th-2 immune mechanisms and IgE production. Reversing the epidemiological trend depends on our identifying the major environmental inputs and acting against these. As yet, the nature of these environmental factors remains to be clarified. Candidate factors include changes in diet, chemical air pollution and microbial exposures in developed countries. This article limits its scope to changing microbial exposures as a potential mechanism. (a) It records epidemiological data that have associated atopic status with less natural exposure to pathogens, parasites and commensal micro-organisms, but with more exposure to certain antibiotics and public health immunizations in early life. (b) It records studies in mice that support the concept that certain microbial exposures can inhibit experimental allergy. (c) It considers potential immune mechanisms for such an action, including the possibility that certain natural infections promote immune regulatory processes that can restrain atopy. It is concluded that the hypothesis that changing patterns of microbial exposure may have promoted the rise in atopy is viable, and that exciting possibilities for reversing the rise of atopy may be derived from further studies.

Animals↗

Bronchial hyperresponsiveness and adult onset wheeze: the influence of atopy.

The commonly held belief that adult onset wheezing illness is primarily nonatopic in nature suggests that the role of atopy in the pathophysiology of bronchial hyperresponsiveness (BHR) in adult onset wheeze may be minimal. This study examined risk factors for BHR (BHR: provocative dose causing a 20% fall in forced expiratory volume in one second PD20 < or =16.38 micromol methacholine) among 82 subjects with adult onset wheeze and among 191 subjects who had never wheezed. Subjects were identified from a cohort of subjects aged 39-45 yrs who were known to have had no childhood wheeze and who were involved in a 30 yr follow-up survey. Risk factors for BHR were examined among all subjects with BHR and among subjects with BHR stratified according to whether or not they had ever wheezed. The prevalence of BHR was 40% (33/82) among the subjects with adult onset wheeze and 11% (21/191) among the subjects who had never wheezed. Lower baseline lung function (odds ratio (OR) = 0.94; 95% confidence interval (CI) = 0.92-0.97 per unit forced expiratory volume (FEV1)% predicted) and atopy (OR = 7.23; CI = 2.53-20.64 for all three measures of atopic compared to nonatopic) were associated with BHR, while smoking and family history showed no statistically significant relation to BHR. This pattern was also apparent in analyses stratified by symptom status. A family history of atopy increased the risk that BHR was accompanied by wheezing symptoms (OR = 4.75; CI = 1.53-14.72 for more than one affected relative compared to no affected relatives). These findings suggest that atopy is associated with bronchial hyperresponsiveness in adults known to have had no childhood wheeze. A familial factor reflecting genetic influences and/or shared environmental factors may influence whether bronchial hyperresponsiveness is associated with symptoms.

Adolescent↗

Atopy--a favourable prognostic factor for survival in Hodgkin's disease.

One hundred and forty-eight patients with Hodgkin's disease (HD) were stratified into 4 groups according to atopic status. Group 1 had a personal history of atopy and Group 2 a family history of atopy. In Groups 3 and 4 there was no history of atopy but high serum IgE levels (Group 3) and normal IgE levels (Group 4). Comparison of the survival of these groups by the logrank method showed a significant trend (P = less than 0.0001) where survival was ranked Group 1 greater than 2 greater than 3 greater than 4. Known prognostic factors in HD--age, sex, stage, symptoms and histology--had to be taken into account, since their distribution differed between the atopic groups. In Group I there was more stage IA and IIA disease and less "B" symptoms, in Group 3 more nodular sclerosis histology and more "B" symptoms and in Group 4 more lymphocyte-depleted histology and a higher mean age than expected from their distribution in the combined groups. Adjustment to allow for the variation in each of the other prognostic factors and for a combination of age, symptoms and histology still showed a significant trend of survival on the basis of atopic status. The increased survival of atopic patients suggests that atopic mechanisms or the genetic basis to atopy has a protective effect in HD either directly or by interaction with treatment.

Adult↗

Toll-like receptor 4 polymorphism and severity of atopy in asthmatics.

Endotoxin exposure may have a protective effect against asthma and atopy. An Asp299Gly polymorphism in the Toll-like receptor 4 (TLR4) gene reduces responsiveness to endotoxin. This study determined the effect of TLR4 polymorphism on the risk and severity of asthma and atopy. In all, 336 UK Caucasian families with > or = 2 affected sibs (physician's diagnosis of asthma and current medication use) and 179 Caucasians without asthma or a family history of asthma were genotyped using ARMS-PCR. No association of the TLR4 polymorphism was found with the risk of developing asthma, either in parent-affected sibling trios, or in case-control analyses (P>0.05). In the first affected asthmatic siblings, the atopy severity score (based on size and number of positive skin-prick tests and specific IgE) was higher in those with the Asp/Gly or Gly/Gly genotypes (mean 1.8, s.d. 1.1, n=39) compared to those with the Asp/Asp genotype (mean 1.2, s.d. 1.0, n=279) (P=0.003, t-test). No associations were found with total IgE, FEV(1) % predicted, slope of FEV(1) response to methacholine or asthma severity score (P>0.05). This study confirms the previously observed lack of association of TLR4 polymorphisms with asthma. In contrast, the findings suggest that genetically determined hyporesponsiveness to endotoxin may increase atopy severity.

Amino Acid Substitution↗

Validation of a screening questionnaire for atopy with serum IgE tests in a population of pregnant Dutch women.

BACKGROUND: We have started a large birth cohort study in which pregnant women with and without atopy are differentially included. In view of the large number of subjects to be screened (12000), a simple questionnaire was developed for the assessment of atopy in pregnant women. OBJECTIVE: The objective of our study was to evaluate the efficacy of a questionnaire using serum IgE tests. METHODS: During a antenatal visit to the midwife clinic, 175 expecting mothers completed a questionnaire and from each subject blood was obtained in which total and specific IgE against house dust mite, cat, dog, birch and grass was determined. RESULTS: When atopy was defined as the presence of a positive test for IgE against at least one allergen, seven questions from the questionnaire had a sensitivity and specificity of 55.0% and 88.7%, respectively. With the use of the questionnaire it was possible to select about 50% of the subjects with specific IgE to one or more common inhalant allergens. The positive predictive value of the screening questions was 71.7%. Taking total IgE into account did not change these results. CONCLUSION: The screening questionnaire is an efficient tool for differential inclusion of subjects with and without atopy in epidemiological studies.

Allergens↗

Gaseous air pollution and atopy.

BACKGROUND: Photochemical air pollutants are commonly thought to be implicated in the gradual increase in the prevalence of atopy. However, no epidemiological data are available. METHODS: To clarify this issue, we performed a cross-sectional epidemiological survey in 2604 primary school children, 10 and 11 years old, living in seven communities among which some have the highest photochemical exposure in France. The mean levels of the main gaseous air pollutants (SO2, NO2 and O3) were measured during a 2-month period in 1993. The protocol included a standardized questionnaire, skin prick tests to common aeroallergens and in the atopic children, collection of a sample of mattress dust to measure group 1 mite allergens. Atopy was only defined on the basis of the skin prick tests. RESULTS: Percentage of positive skin tests and the number of positive skin tests were similar in the different communities looked at. The distribution of dust samples with a group 1 allergen level greater than 2 microg/g dust, was also similar. Logistic regression analysis including potential confounding factors, as well as the mean level of air pollutants, did not demonstrate any association between atopy and mean SO2, NO2 and O3 levels. CONCLUSION: The increase in photochemical air pollutants is unlikely to be a major determinant for the recent increase in the prevalence of atopy.

Air Pollutants↗

Family patterns of asthma, atopy and airway hyperresponsiveness: an epidemiological study.

BACKGROUND: The patterns of inheritance of asthma have largely been explored using data of symptom history collected by questionnaires which are subject to bias and which may therefore distort the measured relationship. OBJECTIVE: The purpose of this study was to examine family patterns of allergic disease using objective measurements of atopy and of airway hyperresponsiveness (AHR). METHODS: A large random sample of children aged 8-11 years was studied and 3 months later, their parents were also invited for study. Of the sample of 1655 children, both parents of 661 children were studied. In all subjects, respiratory illness history was measured by questionnaire, atopy by skin tests and AHR by responsiveness to histamine. RESULTS: The odds ratio for a child to have AHR if either parent had the same condition was approximately 2. 0, which was the same as the odds ratio for wheeze or diagnosed asthma in the presence of the same condition in either parent. The odds ratio for atopy was smaller (approximately 1.4, NS) but the risk of a nonatopic child having AHR if the parent had AHR was 3.0 (P = 0.01). The correlation between weal size in the child and parent was poor and the severity of AHR in the child was only modestly correlated with the severity of AHR in the parent (R = 0.51, P = 0.04). CONCLUSION: The use of objective measurements did not strengthen the association between atopic or asthmatic conditions in the parent and child, but did suggest that atopy and AHR are inherited independently.

Adult↗

Selective development of a strong Th2 cytokine profile in high-risk children who develop atopy: risk factors and regulatory role of IFN-gamma, IL-4 and IL-10.

BACKGROUND: The immunological processes in early life and their relation to allergic sensitization leading to a Th2 cytokine profile are still not well understood. OBJECTIVE: To analyse the environmental and genetic risk factors and immunological responses at birth in relation to the development of atopic disease at 12 months of age in a longitudinal study of high-risk children. METHODS: High-risk children were followed from birth till 12 months of age. Mononuclear cells obtained at birth and 6 and 12 months thereafter were analysed for their proliferative and cytokine responses after polyclonal and allergen-specific stimulation. RESULTS: At 12 months of age 25% children had developed an atopic disease. Two atopic parents, parental smoking and atopic dermatitis of at least one of the parents were significant risk factors. In cord blood of newborns who developed atopy, an increased percentage of CD4+CD45RO+ cells and an increased polyclonal-stimulated proliferation were observed. Furthermore, an impaired allergen-induced, but not polyclonal-stimulated IFN-gamma production was found, suggesting a regulatory defect. At 6 and 12 months of age, a strong Th2 profile (characterized by increased levels of IL-4, IL-5, and IL-13) after both polyclonal and, to a lesser extent, allergen-specific stimulation was found in the children developing atopy. Allergen-induced IL-10 production at 12 months of age was only observed in the non-atopic children. CONCLUSION: Our data indicate that the first 6 months of life represent a critical time window for the initiation of immunological changes resulting in the development of atopy. The selective development of a Th2 cytokine profile in high-risk children who develop atopy is due to increased production of Th2 cytokines, possibly caused by impaired allergen-induced IFN-gamma production in the neonatal period. Furthermore, the decreased allergen-induced IL-10 levels observed in the atopic children at 12 months of age may result in a lack of down-regulation of the inflammatory process.

Allergens↗

Crete: does farming explain urban and rural differences in atopy?

BACKGROUND: Urban-rural differences in the prevalence of atopy and associated allergic diseases have been reported in several non-European countries. Within Europe, where such variations are less striking, a farm childhood has been postulated to be protective. OBJECTIVE: We aimed to compare the prevalence of atopy in urban and rural children living in Crete and to examine the role of early exposure to a farming environment in explaining any measured differences. METHODS: A cross-sectional survey of children attending secondary schools in Iraklion, the capital city, and five villages 100 km to the south. Atopy was determined by the responses to skin prick tests with seven common aeroallergens. RESULTS: Nine-hundred and ninety-seven children participated in the survey. 19.6% of those living in Iraklion, but only 9.6% of those from the villages, had a positive response to one or more skin prick tests. Among urban children there were significant gradients in the prevalence of atopy across several categories of animal contact and consumption of farm (unpasteurized) milk products--before the age of 5 years. These differences, however, were not apparent among the rural children.

Adolescent↗

Low prevalence of atopy in young Danish farmers and farming students born and raised on a farm.

BACKGROUND: Recent studies have shown that in several countries atopic sensitization to common allergens (common atopy) and atopic symptoms are markedly less prevalent in children living on a farm, compared with non-farm children living in the same rural areas. Living conditions on farms may, however, vary largely between different countries. It is also not yet known whether the "protective" effect of a farm environment can also be found in adults. MATERIALS AND METHODS: Common atopy and respiratory health were assessed by skin prick tests (SPT), questionnaire and measurement of bronchial hyper-responsiveness (BHR) in the Sund Stald (SUS) study, a cohort study on respiratory health in Danish farming students and conscripts from the same rural areas as controls. Results of SPT were confirmed by IgE serology in all SPT+ subjects and a subset of SPT- subjects. Prevalences of common atopy, respiratory symptoms and bronchial hyper- responsiveness were compared for farmers and controls, and for those who had or had not lived on a farm in early childhood. RESULTS: In multiple logistic regression analyses adjusting for ever smoking and a familial history of allergy, both being a farmer (ORs 0.62-0.75) and having had a farm childhood (ORs 0.55-0.75) appeared to contribute independently to a lower risk of sensitization to common allergens as assessed by SPT and IgE serology. A farm childhood was also inversely associated with high total IgE (OR 0.68), presence of respiratory symptoms (ORs 0.69-0.79) and BHR (OR 0.61) in these analyses. Direction and strength of the association between being a farmer and respiratory symptoms or BHR varied widely (ORs 0.69-1.28). CONCLUSION: The "anti-atopy" protective effect of a farm childhood could be confirmed in Danish farming students: prevalences of positive SPT, specific and total IgE, allergic symptoms and BHR were lower in those being born or raised on a farm. Past exposure to the farm environment in early childhood may therefore also contribute to a lower risk of atopic sensitization and disease at a later age.

Adult↗

Sibling effect on atopy in children of patients with asthma.

BACKGROUND: Multiple population studies have shown the presence of a sibling effect on atopic disease. However, it is unclear if the sibling effect is also of importance in subjects who are genetically at high risk for the development of atopy. OBJECTIVE: To study the presence of a sibling effect on markers of atopy (serum total IgE, specific IgE, skin tests) and asthma (bronchial hyper-responsiveness to histamine) in families ascertained through a parent with asthma. METHODS: First-degree offspring in 200 asthma families were studied (n = 541). Mixed effects regression models were used to account for the dependence of the observations within a family, and to adjust for possible confounding variables. RESULTS: Multiple regression analysis showed that having older siblings was inversely related to atopy, defined as >/= 2, >/= 3, >/= 4, or >/= 5 skin tests (P = 0.07-0.009). In addition, family size (number of siblings) had a significant protective effect on the presence of specific IgE to common aeroallergens (P = 0.03). Exposure to cigarette smoke in the first 3 years of life significantly increased the risk of having specific IgE to common aeroallergens (P = 0.04). No sibling effect was detected for serum total IgE or bronchial hyper-responsiveness to histamine. CONCLUSIONS: This study shows a protective sibling effect on the presence and severity of atopy but not on bronchial hyper-responsiveness in children who are genetically at risk. The identification of the sibling effect in high-risk families stresses the need to understand the basis of this effect, in order to design future prevention programmes.

Adolescent↗

Common polymorphisms in the CTLA-4 and CD28 genes at 2q33 are not associated with asthma or atopy.

Recently, genetic linkage of the chromosomal region 2q33 with asthma has been shown. The genes coding for CD28 and CTLA-4 have been localized to this chromosomal region. CD28 and CTLA-4 have been shown to be involved as an important costimulatory signal in the regulation of allergic inflammation and TH2 cytokine production, and thus both genes are good candidate genes for asthma and atopy. Two common polymorphisms in the CTLA-4 gene and one polymorphism in the CD28 gene found by single-strand conformation polymorphisms (SSCP) analysis and direct genomic sequencing were tested for association with asthma and atopy phenotypes in a population of 260 largely atopic children and young adults. No association was found between any of the three polymorphisms and asthma or atopy phenotypes. The newly described common CD28 polymorphism is situated in the third intron of the gene. We conclude that neither gene is likely to exert a major influence on the development of asthma or atopy in our population. However, it might prove useful to test for association of these polymorphisms with asthma in populations recruited through asthmatic but not necessarily atopic individuals.

Abatacept↗

Positive atopy patch test reaction to Malassezia furfur in atopic dermatitis correlates with a T helper 2-like peripheral blood mononuclear cells response.

The yeast Malassezia furfur belongs to the normal cutaneous flora, but is also a triggering allergen that can contribute to atopic dermatitis. To illuminate the effect of circulating allergen-specific T cells in atopic dermatitis, the peripheral mononuclear cell response was correlated with the in vivo skin prick test and atopy patch test reactivity to M. furfur. None of 16 healthy controls showed any positive in vivo reaction. The 40 atopic dermatitis patients, of whom 18 had serum IgE reactivity to M. furfur, were subdivided according to their in vivo reaction to M. furfur extract into three groups: skin prick test positive/atopy patch test positive (n = 12), skin prick test positive/atopy patch test negative (n = 12), and skin prick test negative/atopy patch test negative (n = 16). The skin prick test positive/atopy patch test positive and the skin prick test positive/atopy patch test negative groups had a significantly higher peripheral mononuclear cell stimulation index than the healthy controls. Interestingly, the stimulation index values in the skin prick test positive/atopy patch test positive group were significantly higher than in the skin prick test positive/atopy patch test negative group. In the M. furfur skin prick test positive atopic dermatitis patients (n = 24) a correlation was found between stimulation index and the M. furfur atopy patch test reactions, but not between stimulation index and M. furfur-specific serum IgE levels. Skin prick test positive and/or atopy patch test positive reactions to the recombinant M. furfur allergens rMal f 1, rMal f 5, and rMal f 6 were observed in 7, 14, and 16 of the 40 atopic dermatitis patients, respectively. Further, there was a correlation between production of the T helper 2-related cytokines interleukins 4, 5, and 13 and stimulation index to M. furfur extract, but not between the T helper 1-related interferon-gamma and stimulation index to M. furfur extract. Our data strongly suggest a relationship between circulating specific T cells with a T helper 2-like cytokine profile and positive atopy patch test reactions.

Adult↗

[Cow milk-specific humoral and cellular immune response in infants with high risk of atopy under feeding a whey hydrolysate infant formula].

BACKGROUND: Hypoallergenic infant formulas (HAF) were developed for atopy prevention in infants with high risk of atopy if these cannot be breastfed. HAF mount an antigen-specific immune response in infants. The aim of the study was to analyse the immune response in infants fed with a new infant formula based on a whey hydrolysate (HAF) and to compare it with that of exclusively breastfed controls. PATIENTS AND METHODS: Plasma concentrations of cow milk-specific IgE were analysed in 94 infants with high risk of atopy, 44 were exclusively breastfed, 50 were fed with HAF. In addition, cow milk-specific IgG antibodies (26 breastfed, 30 fed with HAF) as well as proliferation of periph-eral blood mononuclear cells to bovine beta-lactoglobulin (BLG) (41 breastfed, 47 fed with HAF) were tested. Specific IgE and IgG antibodies were determined using enzymoimmunometric assay (Alastat). Cellular proliferation was measured using tritiated thymidine incorporation assay after 6 day stimulation with BLG. RESULTS: Elevated IgE to cow milk antibodies (> 0.35 kU/L) were detected in two infants from the breastfed group and in one from the HAF-fed group. The plasma concentrations of milk specific IgG antibodies in HAF-fed infants were insignificantly higher than those in breastfed ones. No significant difference was found in bovine BLG-specific cell proliferation between both groups. CONCLUSION: Concerning the properties investigated like antigenicity, allergenicity and immunogenicity, the extensively hydrolysed whey based hypoallergenic formula does not significantly differ from mother milk in 6 month-old infants with an increased atopy risk.

Age Factors↗

There is no evidence of an inverse relationship between TH2-mediated atopy and TH1-mediated autoimmune disorders: Lack of support for the hygiene hypothesis.

BACKGROUND: The findings of an inverse relationship between T(H)1- and T(H)2-mediated disorders would provide strong empiric support to the hygiene hypothesis. OBJECTIVE: We sought to investigate the relationship between T(H)2-mediated atopic allergy and T(H)1-mediated autoimmune conditions in a nationally representative population. METHODS: We used logistic regression to analyze adult data from the Third National Health and Nutrition Examination Survey. Data on allergic and autoimmune disease history were available for 20,050 subjects, and data on atopy were available for a subsample of 7304 subjects. Atopy was defined by one or more positive skin prick test responses (wheal of > or =3 mm) to 10 common aeroallergens. Allergic disease was defined by patient reports of physician-diagnosed asthma, hay fever, or both. T(H)1-mediated autoimmune disease was defined by patient reports of physician-diagnosed type 1 diabetes mellitus, thyroid disorders, and/or rheumatoid arthritis. RESULTS: Adjusted for age and sex and taking into account the complex survey design, there was no relationship between atopy and a history of autoimmune disorders (adjusted odds ratio, 1.01; 95% CI, 0.61-1.67; P =.97). In contrast, physician diagnosis of allergic disorders was associated with a significant increased risk of physician-diagnosed autoimmune disorders (adjusted odds ratio, 1.67; 95% CI, 1.35-2.07; P <.001). CONCLUSION: We found no evidence of an inverse relationship between atopy and patient reports of physician-diagnosed common autoimmune disorders in the adult American population. Contrary to our initial hypothesis, reports of physician-diagnosed common allergic disorders are positively associated with reports of physician-diagnosed autoimmune disorders, with this possibly being caused by ascertainment bias. These findings suggest that the T(H)1/T(H)2 paradigm might be an oversimplification.

Adolescent↗