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PubMed2006

Association between genetic variations of vascular endothelial growth factor receptor 2 and atopy in the Korean population.

BACKGROUND: Vascular endothelial growth factor (VEGF) has been suggested to be a key mediator in the development of atopy and T(H)2 inflammation. OBJECTIVE: We sought to evaluate the effects of variations in the gene coding VEGF receptor (VEGFR) 2 on intermediate phenotypes of asthma in the Korean population. METHODS: A cohort of 2055 children and adolescents responded to a questionnaire concerning asthma symptoms and risk factors and underwent methacholine bronchial challenge and skin tests. The VEGFR2 gene, including the promoter area, was sequenced on 24 healthy subjects to discover informative single nucleotide polymorphisms (SNPs; minor allele frequency >2%). After haplotype reconstruction, 4 tagging SNPs (IVS6+54A>G, +889G>A, +1416T>A, and IVS25-92G>A) were scored. These SNPs were also scored in 480 adult asthmatic patients to verify the above genetic association study. RESULTS: The prevalence of atopy was associated with a single SNP (+889G>A) of VEGFR2 with borderline significance (P = .048; relative risk, 1.13; 95% CI, 1.00-1.28). However, haplotype analysis showed that the atopy prevalence was strongly associated with a haplotype (AGAG) of VEGFR2 (P = .002; relative risk, 1.25; 95% CI, 1.09-1.42). As for airway hyperresponsiveness, neither individual SNPs nor haplotypes were found to be associated. Interestingly, the significant association was also found between atopy and the AGAG haplotype among adult asthmatic patients (P = .008; odds ratio, 1.66; 95% CI, 1.14-2.44). CONCLUSIONS: The present study demonstrated that genetic variations of VEGFR2 are significantly associated with atopy in the Korean population.

Adolescent↗
PubMed1999

Childhood environment and adult atopy: results from the European Community Respiratory Health Survey.

BACKGROUND: Previous literature has indicated that environmental exposures in childhood influence development of atopic sensitization. OBJECTIVE: We sought to study the association between childhood environment and adult atopy. METHODS: Thirteen thousand nine hundred thirty-two subjects aged 20 to 44 years from 36 areas in Europe, New Zealand, the United States, and Australia took part in the European Community Respiratory Health Survey, answering interviewer-led questionnaires and providing blood tests for measurement of specific IgE to grass, house dust mite, cat, and Cladosporium allergens. RESULTS: Atopy was negatively associated with family size (OR = 0. 93; 95% CI = 0.90-0.96 per 1 sib), partly attributable to an independent protective effect of a greater number of brothers (OR = 0.92; 95% CI = 0.89-0.95 per 1 brother). Accounting for total number of siblings, no further influence was detected for number of older or younger siblings. Bedroom sharing was associated with a lower prevalence of atopy, particularly to cat allergen. A protective effect of family size and bedroom sharing could only be detected in subjects reporting no parental allergy (family size, test for interaction P =.012). The presence of a dog in the home in childhood was negatively associated with adult atopy (OR = 0.85, 95% CI = 0. 78-0.92), an effect that remained after adjustment for parental allergy, sibling allergy, and adult pet ownership. CONCLUSION: Subjects from large families with brothers, shared bedrooms, and dogs in childhood were less often atopic as adults. Our findings are consistent with the hypothesis that infectious agents could inhibit development of atopy during childhood. However, in subjects with a strong genetic predisposition, environmental factors in childhood are possibly of less importance.

Adult↗
PubMed2003

Association between antenatal cytokine production and the development of atopy and asthma at age 6 years.

BACKGROUND: Various lines of evidence suggest that antenatal factors are important in determining susceptibility to atopy and asthma. One possible mechanism is cytokines, production of which in the placenta is high throughout gestation and which protect placental integrity via control of local immunological homoeostasis. We investigated antenatal cytokine concentrations in a prospective birth cohort, intensively monitored for atopy and asthma outcomes at age 6 years. METHODS: Cryopreserved cord-blood serum samples from 407 children were assayed for interleukins 4, 5, 6, 10, 12, and 13, interferon gamma, and tumour necrosis factor alpha (TNFalpha). Associations between family, antenatal, and perinatal factors, cord-blood cytokine concentrations, and atopy or asthma outcomes were analysed by logistic regression. Causal effects of cytokines on outcomes were estimated by propensity scores based on family, antenatal, and perinatal factors. FINDINGS: Detectable cord-blood concentrations of interleukin 4 and interferon gamma were each associated with lower risk of physician-diagnosed asthma (adjusted odds ratios 0.60 [95% CI 0.37-0.99] and 0.60 [0.37-0.97] respectively), current asthma (0.59 [0.33-1.00] and 0.39 [0.22-0.71]), and current wheeze (0.55 [0.32-0.93] and 0.52 [0.31-0.90]) and atopy (sensitisation to some inhalant allergens) outcomes at 6 years. High concentrations of TNFalpha were associated with lower risk of atopy but not with asthma risk. These associations were broadly unaltered by propensity-score adjustment. Maternal smoking was associated with higher risk of both wheeze at 6 years and lower concentrations of interleukin 4 and interferon gamma in cord blood. INTERPRETATION: The mechanism underlying attenuated T-helper-1/T-helper-2 cytokine production in high-risk children also apparently operates in control of cytokine production in the fetoplacental unit. The finding that this mechanism is dysregulated by maternal smoking suggests it is a target for antenatal environmental factors relevant to asthma aetiology.

Asthma↗
PubMed2006

Effect of albendazole treatments on the prevalence of atopy in children living in communities endemic for geohelminth parasites: a cluster-randomised trial.

BACKGROUND: Epidemiological studies have shown inverse associations between geohelminth (intestinal helminth) infection and atopy, leading to the suggestion that geohelminths might protect against allergy. Periodic deworming of school children with anthelmintics is a widely implemented intervention and has raised concerns that such programmes could increase allergy. We investigated the effect of repeated anthelmintic treatments with albendazole over 12 months on the prevalence of atopy and clinical indices of allergy. METHODS: We did a cluster-randomised controlled trial in schoolchildren from 68 rural schools. Children were randomly assigned by school to either albendazole (34 schools, 1164 children) every 2 months for 12 months, or to no intervention (34 schools, 1209 children). The intervention schools received a total of seven albendazole treatments. The primary outcome was atopy at 12 months (allergen skin-test reactivity), and analysis was by intention-to-treat for whole-school analyses and per protocol for children. This study is registered as an International Standard Randomised Controlled Trial, number ISRCTN61195515. FINDINGS: Data for analysis were available for all schools and from 67.4% (784 of 1164) and 70.1% (848 of 1209) of children in albendazole and no-treatment groups, respectively. Albendazole treatment caused large reductions in geohelminth prevalence over the study period (adjusted odds ratio 0.13, 95% CI 0.09-0.19, p<0.001), but there was no evidence that treatment was associated with an increase in atopy prevalence (0.97, 0.68-1.39, p=0.862), or clinical allergy (wheeze, 1.07, 0.54-2.11, p=0.848) in the albendazole compared with the no-treatment group. INTERPRETATION: We saw no increase in the prevalence of atopy or clinical allergy associated with albendazole treatment. Deworming programmes for schoolchildren are unlikely to be accompanied by an increase in allergy.

Albendazole↗
PubMed1995

Linkage of high-affinity IgE receptor gene with bronchial hyperreactivity, even in absence of atopy.

Asthma is a manifestation of bronchial hyperreactivity (BHR) and forms part of the spectrum of atopic disease. Some pedigree studies of atopy have suggested linkage with the high-affinity IgE receptor (Fc epsilon RI beta) gene on chromosome 11q13, but others find no linkage. The molecular genetics of asthma and BHR have not been studied in the general population. We examined the genetic linkage of the Fc epsilon RI beta gene with clinical asthma and the underlying phenotypes of BHR (to methacholine) and atopy (defined by skinprick testing) in 123 affected sibling-pairs recruited from the general population. We found evidence of significant linkage of a highly polymorphic microsatellite marker in the fifth intron of the Fc epsilon RI beta gene to a diagnosis of asthma (18.0% excess of shared alleles, p = 0.002) and to BHR (21.7% excess of shared alleles, p = 0.001). Significant linkage was also observed in siblings sharing BHR when those with atopy were excluded (32.8% excess of shared alleles, p = 0.004). Atopy in the absence of BHR did not show significant linkage to the Fc epsilon RI beta gene (7.2% excess of shared alleles, p = 0.124). These findings suggest that mutations in the Fc epsilon RI beta gene or a closely linked gene influence the BHR underlying asthma, even in the absence of atopy.

Adult↗
PubMed1997

Prevalence of wheeze and asthma and relation to atopy in urban and rural Ethiopia.

BACKGROUND: Asthma and allergy in developing countries may be associated with adoption of an urbanised "western" lifestyle. We compared the rates of asthma symptoms and atopy in urban populations in Jimma, southwest Ethiopia, at an early stage of economic development with those among the population of remote, rural, subsistence areas, and assessed the potential role of environmental aetiological factors leading to the differences. METHODS: Information on wheeze of 12 months' duration, diagnosed asthma, and cough for 3 months of the year was gathered by questionnaire in random household samples of 9844 people from urban Jimma and of 3032 from rural areas. Atopy was defined by allergen skin-test response to Dermatophagoides pteronyssinus and mixed threshings measured in a one-in-four subsample of those aged 5 years and older from both groups. FINDINGS: All respiratory symptoms were rare in children and were significantly less common overall in the rural than in urban group (wheeze odds ratio 0.31 [95% CI 0.22-0.43], p < 0.0001). Asthma was reported by 351 (3.6%) of the urban group, with a median reported duration of 8.5 years (IQR 4-17 years) that was unrelated to age. Atopy was a strong risk factor for asthma in urban Jimma. In the rural areas, skin sensitivity to mixed threshings was only slightly less common than in urban Jimma (0.67 [0.40-1.12], p = 0.13), whereas sensitivity to D pteronyssinus was significantly more common (3.24 [2.40-4.38], p < 0.0001), and since none of the 119 atopic individuals in the rural area reported wheeze or asthma, atopy was possibly associated with a reduction in the risk of disease among this group. Wheeze or D pteronyssinus sensitivity were positively associated with housing style, bedding materials, and use of malathion insecticide, but no single factor accounted for the urban-rural differences. INTERPRETATION: Wheeze and asthma are especially rare in rural subsistence areas, and atopy may be associated with a reduced prevalence of these symptoms in this environment. In urban Jimma, self-reported asthma seemed to emerge as a clinical problem about 10 years before our study began, which is consistent with an effect of new environmental exposures. The factor or factors leading to the increase in asthma and allergy have not been identified, although exposures related to general changes in the domestic environment are likely to be involved.

Adolescent↗
PubMed2003

Sex differences in asthma, atopy, and airway hyperresponsiveness in a university population.

BACKGROUND: A male predominance in atopy, a preadolescent male predominance in asthma, and a female predominance in airway hyperresponsiveness (AHR) have been previously documented, mostly in separate populations. OBJECTIVE: We examined gender differences in a single population of 500 randomly selected university students from a previous publication which addressed sensitivity and specificity of histamine bronchoprovocation (Cockcroft et al. J Allergy Clin Immunol. 1992;89:23-30). METHODS: In these 500 subjects (age 21.8 +/- 1.5 years) we assessed gender differences in asthma, atopy, and AHR. We compared our findings with those in the literature from a PUBMED search using the keywords gender, asthma, atopy, AHR, and bronchial reactivity. RESULTS: A diagnosis of asthma made by another physician was seen in 31, a male-to-female ratio of 2.9:1 (P = 0.004). Our definition of asthma increased the total to 52 and reduced the male-to-female ratio to 1.2:1. Atopy was seen in 190, male-to-female ratio of 1.5:1 (P = 0.001). Borderline to mild AHR had a female predominance with a male-to-female ratio of 1:1.5 (P = 0.02), whereas moderate AHR had a marked predominance with a male-to-female ratio of 7:1 (P = 0.03). CONCLUSIONS: In our population, the associations among gender and asthma, atopy, and AHR were similar to those seen in the literature with the exception of males having more severe AHR. This may be the one factor contributing to the higher prevalence of asthma (including previous doctor-diagnosed asthma in our population) in boys and young men.

Adult↗
PubMed2000

Atopy in Danish children and adolescents: results from a longitudinal population study.

BACKGROUND AND OBJECTIVE: Atopy is an objectively measurable trait related to the presence of rhinitis and asthma, but our knowledge about its longitudinal predictors is limited. Data from a 6-year follow-up study of a population sample of children and adolescents (n = 408), aged 7 to 17 years at enrollment, were analyzed to investigate the prevalence and predictors of atopy. METHODS: Case history, including allergic diseases and smoking habits, was obtained by interview and questionnaire. Skin prick test reactivity to common allergens, total serum IgE, airway responsiveness, and pulmonary function were measured using standard techniques. RESULTS: The point prevalence of atopy increased from the first to the second survey, 26% and 44%, respectively; 23% of the participants had a positive skin prick test only at the second survey. Sensitization to house dust mite (HDM) (P < .001), grass (P < .001), dog (P < .001), cat (P < .001), and birch (P = .02) increased significantly in both males and females. No gender differences in the prevalence of positive reactions were found at the first survey, whereas atopy to grass (P = .01) and HDM (P = .02) were more prevalent in males than in females at the second survey. Confining the analysis to participants who were found to be non-atopic at the first survey showed that exposure to maternal smoking (OR 2, CI 1.3 to 3.1; P = .002), increased serum IgE (OR 1.7, CI 1.2 to 2.3; P = .001), new asthma (OR 1.6, CI 1.2 to 2.7; P = .03), and new rhinitis (OR 2.1, CI 1.2 to 3.6; P = .01), but not active smoking, were associated with an increased risk for the presence of a positive skin prick test at the second survey. CONCLUSIONS: This longitudinal population study showed an increase in the point prevalence of atopy in Danish children and adolescents; and, furthermore, that exposure to maternal smoking during childhood, increased serum IgE, and new symptoms of asthma or rhinitis were associated with an increased risk for developing sensitization to common aeroallergens in late adolescence.

Adolescent↗
PubMed2002

Atopy and house dust mite sensitization as risk factors for asthma in children.

BACKGROUND: Recent evidence suggests that asthma is not invariably related to atopy. The aim of this study was to evaluate the frequency of atopy, asthma and sensitization to eight common allergens in a large group of children with allergic symptoms. METHODS: 1426 children referred to our Paediatric Asthma and Allergy Center because of allergic symptoms were examined. Bronchial asthma, allergic rhino-conjunctivitis, food allergy and atopic dermatitis were diagnosed with standardized methods. Atopy was diagnosed if at least one skin test was positive. RESULTS: Of the 1426 children examined, 629 (44%) were atopic and 769 (56%) were non-atopic. Asthma was diagnosed in the same proportion (i.e., 64%) of atopic and non-atopic children. However, after division into age groups, non-atopic asthma was significantly more prevalent (chi2 = 8.46) in children between 0 and 3 years old (group 1). On the other hand, atopy was significantly associated with asthma only in group 3 (odds ratio 1.85). Furthermore, a significant association with asthma symptoms was found for house dust mite (HDM) in group 3 (odds ratio 4.8). CONCLUSIONS: Asthma is related to atopy in pre-selected children only from the age of 7 years. House dust mite sensitization seems to be an important determinant of asthma in these "older" children.

Age Factors↗
PubMed2000

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.

Child↗
PubMed2005

Vitamin C in breast milk may reduce the risk of atopy in the infant.

OBJECTIVE: To assess the effects of maternal dietary and supplement intake of vitamins C and E on breast milk antioxidant composition (vitamin C, alpha-tocopherol and beta-carotene) and their protective potential against the development of atopy in the infant. DESIGN, SUBJECTS AND METHODS: Mothers with atopic disease were recruited at the end of gestation and maternal sensitization was assessed by skin-prick testing. The 4-day food records of the mothers and breast milk samples were collected at the infants' age of 1 month. Infants' atopy was defined by the presence of atopic dermatitis during the first year of life and a positive skin-prick test reaction at 12 months of age (n=34). RESULTS: Maternal intake of vitamin C in diet but not as supplement was shown to determine the concentration of vitamin C in breast milk. A higher concentration of vitamin C in breast milk was associated with a reduced risk of atopy in the infant (OR=0.30; 95% CI 0.09-0.94; P=0.038), whereas alpha-tocopherol had no consistent relationship with atopy. The group at risk of suboptimal vitamin C supply from breast milk was identified as infants whose mothers suffer from food hypersensitivity. CONCLUSION: A maternal diet rich in natural sources of vitamin C during breastfeeding could reduce the risk of atopy in high-risk infants.

Adult↗
PubMed2000

The -403 G-->A promoter polymorphism in the RANTES gene is associated with atopy and asthma.

Asthma is a complex inflammatory condition often associated with bronchial hyperreactivity and atopy. Genetic and environmental factors are implicated and several candidate genes have been implicated. Of these, the chemokine RANTES is responsible for the recruitment of inflammatory cells such as eosinophils and T-lymphocytes. We have recently identified a polymorphism within the RANTES promoter (-403 G-->A) and have examined its role, using a PCR-RFLP assay, in the development of atopy and asthma in 201 Caucasian subjects. Atopic status was determined using skin prick testing and serum IgE levels. Severity of airway dysfunction was assessed using spirometric measurement (FEV1) and methacholine challenge (PC20). The -403 A allele was associated with an increased susceptibility to both atopy and asthma. Thus, the proportion of subjects carrying this allele was higher in each of atopic non-asthmatics, non-atopic asthmatics and atopic asthmatics compared with non-atopic, non-asthmatic controls. In particular, this allele was associated with skin test positivity but not IgE level. Homozygosity for the -403 A allele conferred a 6.5-fold increased risk of moderate/severe airway obstruction (FEV1 < or = 80% predicted), a marker for established asthma. Our data, whilst preliminary, indicate that the association of RANTES genotype with both atopy and asthma reflect independent effects, suggesting different mechanisms for the role of this chemokine in atopy and development of airway obstruction.

Adenine↗
PubMed2003

Maternal atopy and the number of offspring: is there an association?

We investigated the association between maternal atopy and the number of offspring. In a population- and pregnancy-based survey (part of the European Studies on Infertility and Subfecundity), we obtained information on the number of offspring, adverse pregnancy outcomes, age at pregnancy, and waiting time to pregnancy. The German portion of these surveys also included information on physician-diagnosis of asthma, atopic eczema, or hay fever. The odds ratio (OR) adjusted for age showed that the number of children was reduced among women with atopy (OR = 0.75, 95% CI: 0.57-0.98 in the pregnancy-based sample; OR = 0.79, 95% CI: 0.63-0.99 in the population-based sample). We did not identify other signs of reduced reproductive ability in atopic women. The results provide support for two assumptions: (i) either a lower number of offspring in atopic mothers combined with an increased risk of atopy in offspring of atopic mothers may explain the protective effect of a higher number of siblings on atopy in offspring; or (ii) successive pregnancies may decrease the atopic response of the mother and thus the risk of developing atopy in subsequent offspring.

Adult↗
PubMed2001

Linkage to atopy on chromosome 19 in north-eastern Italian families with allergic asthma.

BACKGROUND: Allergic asthma is a multifactorial disease for which there is a widely assessed, although poorly understood, genetic involvement. Genome-wide screens reported evidence for linkage of allergic asthma-related phenotypes to several chromosomal locations. Markers on chromosome 19 have been linked to allergic asthma phenotypes in different populations in independent studies. OBJECTIVE: The aim of this study was to perform a genetic linkage analysis on chromosome 19 to search for DNA markers linked to phenotypes related to allergic asthma. METHODS: Using non-parametric multipoint linkage analysis on a total of 22 random DNA markers in 2 stages, a sample of 111 families (542 subjects) from north-eastern Italy, recruited through an asthmatic allergic proband, was investigated. Phenotypes examined were: clinical asthma, total serum elevated IgE, skin prick test positivity, bronchial hyper-responsiveness, and atopy defined as skin prick test positivity and/or elevated IgE. Simulation studies were performed to confirm the significance of the results. RESULTS: A novel linkage of atopy and skin prick test positivity to marker D19S601 (19q13.3) was found. Modest evidence for linkage of atopy, skin prick test positivity, and IgE was also found to marker D19S591 (19p13.3). Simulation analysis for atopy gave an NPL-Z > 3.326 in 2 replicates out of 1000 (P = 0.002) for D19S601, and an NPL-Z > 2.56 in 16 replicates out of 1000 (P = 0.016) for D19S591. CONCLUSIONS: On chromosome 19, suggestive linkage of atopy and skin prick test positivity with marker D19S601 (19q13.3) and modest evidence of linkage of marker D19S591 (19p13.3) to the atopic phenotypes investigated were found. These results suggest that these regions may contain susceptibility loci associated to atopic phenotypes.

Adult↗
PubMed2003

Early endotoxin exposure and atopy development in infants: results of a birth cohort study.

BACKGROUND: Exposure to endotoxin in childhood is currently discussed to protect from the development of allergic diseases. OBJECTIVE: To study the effect of early endotoxin exposure on incidence of atopic sensitization, atopic dermatitis and wheezing until the age of 2 years in infants with different risk status in terms of parental atopy. METHODS: Data of 1942 infants of an ongoing birth cohort study were analysed by logistic regression. Endotoxin was measured in settled dust of the mothers' mattresses at infants' age of 3 months. Data on allergic symptoms and physicians' diagnoses were gathered by questionnaire. Sensitization to common food and inhalant allergens was assessed by specific serum IgE. RESULTS: High endotoxin levels increased the risk of repeated wheeze [adjusted odds ratio (OR) for 4th exposure quartile (Q4) 1.52, 95% confidence interval (CI) 1.08-2.14], but were associated with neither sensitization to food allergens nor atopic dermatitis. Stratification by parental atopy showed that there was an association of endotoxin exposure with incidence of repeated wheeze as well as with sensitization to inhalant allergens (P for trend = 0.008 and 0.044, respectively) only in infants with parental atopy, with the highest risk in the 4th exposure quartile (repeated wheeze: ORQ4 1.77, 95% CI 1.14-2.73; sensitization to inhalant allergens: ORQ4 1.69, 95% CI 0.70-4.11). CONCLUSION: Early endotoxin exposure in terms of mattress dust endotoxin levels seemed to increase the risk of atopic reactions to inhalant allergens at the age of 2 years, especially in infants at risk due to parental atopy. Our data disagree with an early protective effect of endotoxin on atopy development until the age of 2 years.

Bedding and Linens↗
PubMed2001

Prematurity at birth reduces the long-term risk of atopy.

BACKGROUND: Antigen exposure in early life has long-lasting effects on atopic sensitization. Thus the predisposition to atopy of children born preterm can be assumed to differ from that of children born at term. OBJECTIVE: The aim of this study was to evaluate the association between premature birth and atopy. METHODS: At an outpatient clinic, we examined 2 groups of 10-year-old children, 72 who were born preterm (birth weight < 1500 g) and 65 who were born at term (birth weight > 2500 g). The atopy data were collected with a questionnaire, by performing skin prick testing, and by measuring the serum total IgE level, 3 allergen-specific IgE levels, the eosinophil cationic protein level, and the blood eosinophil level. The data on perinatal and neonatal events affecting the preterm children were collected from the hospital records. RESULTS: By the age of 10 years, the children born preterm had significantly less atopy than the children born at term: 15% versus 31% of children in the 2 groups were defined as having had obvious atopy (P = .03, odds ratio 0.41, 95% CI 0.18-0.93). The mean value of total IgE level was significantly higher in the term group, 74 kU/L versus 41 kU/L (P = .02). By skin prick testing, the children born at term had positive reactions 2 to 3 times more often; 37% versus 17% of children in the groups had at least 1 positive reaction (P = .007). CONCLUSION: Our data show that prematurity at birth is linked with a decreased long-term risk of atopic sensitization.

Female↗
PubMed2002

Pets, parental atopy, and asthma in adults.

BACKGROUND: Studies of exposure to pets and the risk of asthma have provided conflicting results. OBJECTIVE: We conducted a population-based incident case-control study to assess the relationship of current and previous pet keeping with the risk of adult-onset asthma. We also investigated whether genetic propensity as a result of parental atopy modifies these relations. METHODS: From the source population of 441,000 inhabitants of a geographically defined area in South Finland, we systematically recruited, during a 2.5-year period, all new cases of asthma in 21- to 63-year-old adults and randomly selected control subjects. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma and a control series of 932 control subjects. Information on current and past exposure to hairy pets was collected by using a self-administered questionnaire. RESULTS: In logistic regression analysis the risk of asthma was lower among subjects with pets during the past 12 months (adjusted odds ratio [OR], 0.74; 95% confidence interval [CI], 0.57-0.96) but higher among subjects with pets more than 12 months previously (adjusted OR, 1.39; 95% CI, 1.05-1.84). Parental atopy increased the risk of asthma (OR, 1.88; 95% CI, 1.47-2.41), but there was no interaction between parental atopy and pet exposure. CONCLUSIONS: The present results are consistent with the hypothesis that both keeping furry pets and parental atopy increase the risk of asthma development in adulthood. Parental atopy does not modify the effects of pet exposure. The negative association between current pets and the risk of asthma is consistent with selective avoidance of these pets by symptomatic individuals.

Adult↗
PubMed2003

Atopy patch tests in young adult patients with atopic dermatitis and controls: dose-response relationship, objective reading, reproducibility and clinical interpretation.

The clinical interpretation and reproducibility of atopy patch tests was studied in 23 selected young adult patients with atopic dermatitis and 25 healthy controls using standard inhalant allergens. Non-invasive measurements were used for objective assessment of test reactions and the participants were retested after 6 weeks. Ten of 19 (53%) evaluable patients with atopic dermatitis had at least one positive atopy patch test. However, there was no clear clinical relevance of the atopy patch test results when related to patient history and distribution of dermatitis. Reproducible and dose-dependent results were obtained with Dermatophagoides pteronyssinus, grass and cat with a reproducibility rate of 0.69 to 0.81 in patients and 0.60-0.96 in controls. A unique finding was a significant positive correlation between a positive atopy patch test, allergen dose and increase in transepidermal water loss and erythema, while measurement of capacitance did not distinguish between positive and negative reactions. The results of the present study do not support the routine use of atopy patch tests in the evaluation of adult patients with atopic dermatitis.

Adolescent↗