Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “atopy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1998

Atopy in cough sensitivity to capsaicin and bronchial responsiveness in young females.

We have shown previously that female sex is a determinant of cough sensitivity to inhaled capsaicin, but the relationship between atopy and the cough sensitivity has not been examined. The capsaicin cough threshold, defined as the lowest concentration of capsaicin causing five or more coughs, nonspecific bronchial responsiveness, defined as the provocative concentration of methacholine causing a 20% fall in the forced expiratory volume in one second (PC20), total immunoglobulin E (IgE) and specific IgEs to eight common aeroallergens (house dust 1, 2 and 6, Dermatophagoides pteronyssinus and D. farinae, Japanese cedar, ragweed and orchard grass) in the serum were measured in 71 nonsmoking, healthy young women aged 20.6+/-0.1 yrs (mean+/-EM). A structured interviewer-led questionnaire on allergic diseases revealed that one and six subjects had mild current and past asthma, respectively. These seven subjects were excluded from the data analysis. PC20 was significantly lower in 42 subjects showing a positive specific IgE than in 22 subjects showing a negative specific IgE to any of the eight allergens (p<0.05), while the capsaicin cough threshold was not significantly different between the subgroups. PC20 was significantly lower in subjects with positive specific IgE to Dermatophagoides and house dust, but not to the three kinds of pollen examined. It was confirmed that atopy indicated by specific immunoglobulin E to mite-related antigens, but not to pollen antigens, is associated with nonspecific bronchial responsiveness, and it is suggested that atopy is not a determinant of airway cough sensitivity in healthy, nonasthmatic subjects.

Adult↗
PubMed2004

Interaction of atopy and smoking on respiratory effects of occupational dust exposure: a general population-based study.

BACKGROUND: For individual exposures, effect modification by atopy or smoking has been reported on the occurrence of occupational airway disease. It is unclear if effect modification can be studied in a general population by an aggregated exposure measure. Assess relationship between airway obstruction and occupational exposure using a job-exposure-matrix (JEM) classifying jobs into 3 broad types of exposure, and test for effect modification by atopy, and smoking. METHODS: Data from 1,906 subjects were analyzed, all participants of the European Community Respiratory Health Survey. Job titles were categorized by an a priori constructed job exposure matrix into three classes of exposure to respectively organic dust, mineral dust, and gases/ fumes. Relationships were assessed for 'current wheeze', bronchial hyperresponsiveness (BHR), 'current asthma' (wheeze+BHR), and 'chronic bronchitis' (morning phlegm or morning cough), and lung function. RESULTS: Subjects with organic dust exposure in their work environment more frequently had 'current asthma' (OR 1.48, 95% C.I. 0.95;2.30), and a lower FEV1 (-59 mL, 95% C.I. -114;-4). The relationship was only present in asthmatic workers, and their risk was four-fold greater than in subjects with either atopy or exposure alone. Mineral dust exposure was associated with 'chronic bronchitis' (OR 2.22, 95% C.I. 1.16;4.23) and a lower FEV1/FVC ratio (-1.1%, 95% C.I. -1.8;-0.3). We observed an excess risk in smokers, greater than the separate effects of smoking or mineral dust exposure together. CONCLUSION: Occupational exposure to organic dust is associated with an increased risk of asthma, particularly in atopics. Chronic bronchitis occurs more frequently among individuals exposed to mineral dust, and smoking doubles this risk.

Adult↗
PubMed2000

Mimicking microbial 'education' of the immune system: a strategy to revert the epidemic trend of atopy and allergic asthma?

Deficient microbial stimulation of the immune system, caused by hygiene, may underly the atopy and allergic asthma epidemic we are currently experiencing. Consistent with this 'hygiene hypothesis', research on immunotherapy of allergic diseases also centres on bacteria-derived molecules (eg DNA immunostimulatory sequences) as adjuvants for allergen-specific type 1 immune responses. If we understood how certain microbes physiologically 'educate' our immune system to interact safely with environmental nonmicrobial antigens, we might be able to learn to mimic their beneficial actions. Programmed 'immunoeducation' would consist of safe administration, by the correct route, dose and timing, of those microbial stimuli that are necessary to 'train' the developing mucosal immune system and to maintain an appropriate homeostatic equilibrium between its components. Overall, this would result in a prevention of atopy that is not limited to certain specific allergens. Although such a strategy is far beyond our present potential, it may in principle revert the epidemic trend of atopy and allergic asthma without jeopardizing the fight against infectious diseases.

Asthma↗
PubMed1995

Postnatal maternal smoking increases the prevalence of asthma but not of bronchial hyperresponsiveness or atopy in their children.

We have compared the prevalence of asthma, bronchial hyperresponsiveness (BHR), and atopy in relation to parental smoking in children aged 7 to 13 years. Information on the presence of asthma was obtained from a questionnaire, BHR was assessed by a methacholine challenge test, and atopy was defined as a positive response to a skin prick test. A complete history of the parents' smoking habits during their children's life, including prenatal smoking habits, was recorded. The prevalence of maternal smoking increased from 37.9% during pregnancy to 45.3% at the cross-sectional survey. None of the outcomes was significantly related to paternal smoking, whereas postnatal maternal smoking was positively associated with asthma (odds ratio [OR] = 2.8; 95% confidence interval [CI], 1.3 to 6.1). A negative association between prenatal maternal smoking and atopy was found (OR = 0.6; 95% CI, 0.3 to 0.9). We found no significant association between BHR and parental smoking. Our results indicate that postnatal maternal smoking increases the prevalence of asthma in the offspring without inducing BHR.

Adolescent↗
PubMed1996

Prevalence of allergic bronchopulmonary aspergillosis and atopy in adult patients with cystic fibrosis.

BACKGROUND: Underestimation of allergic bronchopulmonary aspergillosis (ABPA) prevalence in the cystic fibrosis (CF) population is suspected due to nonuniform diagnostic criteria, nonspecific signs and symptoms, assessment during asymptomatic intervals, and physician nonaggressiveness in making the diagnosis. OBJECTIVE: To define the prevalence of ABPA in adult patients with CF, as the increased duration of bronchiectasis may increase the probability of Aspergillus fumigatus (Af) colonization. We also sought to determine whether atopy increases the prevalence of ABPA in adults with CF. METHODS: We examined a cross-sectional population of adult patients with CF at the University of Washington for 1 year. RESULTS: Information was collected on 53 of 65 (82%) patients. Fifteen of 51 (29%) had an immediate skin test reaction to Af, and 30 of 51 (59%) had at least one positive skin test. Increased total serum IgE (>450 IU/mL) was present in 0 of 53; increased IgE-Af and IgG-Af were found in 12 of 53 (23%) and 9 of 53 (17%), respectively; 24 of 53 (45%) had Af-precipitins. Peripheral blood eosinophilia was present in one patient. Eight of 49 (16%) patients' sputum cultures grew Af. ABPA-CB (ABPA-central bronchiectasis) was present in one patient and ABPA-S (ABPA-seropositive) in no patients. Atopy was present in 20 of 51 (39%). CONCLUSION: There was a low prevalence of ABPA in the adult CF population despite frequent immunologic responses to Af. The prevalence of ABPA was too small to determine an association with atopy.

Adult↗
PubMed1999

Allergic bronchopulmonary aspergillosis in cystic fibrosis: role of atopy and response to itraconazole.

STUDY OBJECTIVES: (1) To determine the relationship between IgE levels and the prevalence of allergic bronchopulmonary aspergillosis (ABPA) in cystic fibrosis (CF) patients, (2) to establish the usefulness of assessing atopy as an identifying risk factor for ABPA, (3) to evaluate the clinical course of patients receiving and not receiving itraconazole as reflected in oral steroid dose requirements and number of acute episodes of ABPA, and (4) to determine the role of acute episodes of ABPA in pulmonary exacerbations of CF. DESIGN: Retrospective review of online clinical database and medical records. SETTING: CF clinic and inpatient services of Lucile Salter Packard Children's Hospital at Stanford. PATIENTS: One hundred seventy-two patients with CF for whom serial serum total IgE levels were measured over a 5-year study period, 1992 to 1996. INTERVENTIONS: We reviewed records of patients followed up at the CF Center at Stanford who had serum total IgE measured between January 1, 1992, and December 31, 1996. Total IgE and Aspergillus fumigatus (Af) specific IgE antibodies were measured by commercial fluorometric solid-phase immunoassay. Precipitating antibodies to Af were measured by double immunodiffusion. Patients who were diagnosed as having ABPA were treated with itraconazole unless significant liver dysfunction was present. Oral steroid dosing requirements and acute episodes of ABPA for days with vs days without itraconazole were compared. MEASUREMENTS AND RESULTS: Serum total IgE was elevated (> 1 SD > geometric mean for age) in 51% of patients tested. IgE > 500 IU/mL, chosen as a screening cutoff for evaluating possible ABPA, was present in 19% of patients at some time during the study period. Atopy (defined as > or = 1 IU/mL IgE antibody to > or = 1 allergen) was present in 61% of 104 patients tested for specific allergen sensitization. ABPA was diagnosed in 16 patients (9%). ABPA occurred in 22% of atopic CF patients but only in 2% of nonatopic patients (p = 0.001). Six percent of pulmonary exacerbations requiring hospitalization were associated with acute episodes of ABPA. Over the study period, itraconazole use was associated with a reduced average daily oral steroid dose of 47% (p = 0.05) and a reduction in the number of acute ABPA episodes by 55% (p < 0.001). CONCLUSIONS: Screening for atopy may be a cost-effective way to select CF patients for periodic monitoring with total serum IgE levels, since there is an increased risk of ABPA developing in atopic CF patients. Itraconazole treatment of ABPA is safe and associated with fewer acute episodes of ABPA despite reduction in average daily oral steroid dose.

Acute Disease↗
PubMed2003

Evidence for the transmissibility of atopy: hypothesis.

The etiology of atopy is unknown. Its family distribution suggests transmissibility. Populations moving from countries with a low incidence to those with a high incidence increase to the higher rate. African and New Guinea village groups developed asthma with return of individuals who have acquired atopy in the city. Protection (and possibly immunity) develops with early exposure to child care or to affected older siblings. T helper (Th) type 2 clones driving specific allergies remain active even without further allergen exposure. Other IgE responses remain normal. Once boosted to completeness, the patterns of skin test results remain quite stable, possibly by the localization of abnormality maintained by immunity. An example of a virus causing the immortality of Th2 cells is herpes simplex virus type 1. It infects mouse or human Th2 cells and, although it does not multiply, causes immortality by increasing FAS-mediated apoptosis of T cells directed against the infected cells. Human T-cell leukemia virus 1 and probably others use similar ploys. Abnormal levels of FAS receptors and resistance to FAS apoptosis in nasal polyp lymphocytes and abnormal Th2 clones of atopy are interesting in this regard. The localizing role of a staphylococcal superantigen in atopic dermatitis, and possibly in autoimmunity in nonatopic eczema and intrinsic asthma, encourage the consideration of roles for microorganisms in localization and etiology. The epidemiology and characteristics of atopic disease support the plausibility of a viral hypothesis.

Humans↗
PubMed2001

Relation of two different subtypes of croup before age three to wheezing, atopy, and pulmonary function during childhood: a prospective study.

OBJECTIVE: Some retrospective evidence suggests that children with a history of croup may be at increased risk of subsequently developing asthma, atopy, and diminished pulmonary function. The objective of this study was to determine the long-term outcome of croup (as diagnosed by a physician) in early life. METHODS: Lower respiratory illnesses (LRIs) in the first 3 years of life were assessed in 884 children who were enrolled in a large longitudinal study of airway diseases at birth. Pulmonary function tests, markers of atopy, and wheezing episodes were studied at different ages between birth and 13 years. RESULTS: Ten percent of children had croup with wheeze (Croup/Wheeze), 5% had croup without wheeze (Croup/No Wheeze), 36% had another LRI (Other LRI), and 48% had no LRI. Respiratory syncytial virus was more frequently isolated in children with Croup/Wheeze and Other LRI than in those with Croup/No Wheeze. There was no association between croup in early life and markers of atopy measured during the school years. Only children with Croup/Wheeze and with Other LRI had a significant risk of subsequent persistent wheeze later in life. Significantly lower levels of indices of intrapulmonary airway function were observed at ages <1 (before any LRI), 6, and 11 years in children with Croup/Wheeze and Other LRI compared with children with No LRI. Conversely, inspiratory resistance before any LRI episode was significantly higher in infants who later developed Croup/No Wheeze than in the other 3 groups. CONCLUSIONS: We distinguish 2 manifestations of croup with and without wheezing. Children who present with croup may or may not be at increased risk of subsequent recurrent lower airway obstruction, depending on the initial lower airway involvement, and preillness and postillness abnormalities in lung function associated with this condition.

Asthma↗
PubMed2003

Indoor and outdoor environmental exposures, parental atopy, and physician-diagnosed asthma in Taiwanese schoolchildren.

OBJECTIVE: Parental atopy and environmental exposures are recognized risk factors for childhood asthma. However, the relative contributions of specific risk factors and the overall contributions of indoor and outdoor exposures remain unexplored. This study was undertaken to identify risk factors, estimate the population attributable risk of each exposure, and compare the data for boys versus girls for physician-diagnosed asthma in Taiwanese schoolchildren. METHODS: During a February to June 2001 cross-sectional national survey, 35 036 6- to 15-year-old schoolchildren were chosen from 22 elementary and 22 middle schools located within 1-km catchment areas of 22 air-monitoring stations in Taiwan. The main outcome measure was physician-diagnosed asthma, as reported by the parents. We investigated hereditary and indoor and outdoor environmental factors for childhood asthma by questionnaire. The adjusted prevalences of questionnaire-determined outdoor indicators were also compared with air-monitoring data. RESULTS: Outdoor air pollutants were associated with parent-reported perceived ambient air pollution. Physician-diagnosed asthma was reported for 8.1% of the boys (1330 of 16 441) and 5.6% of the girls (894 of 16 056). The risk of physician-diagnosed asthma was significantly associated with parental atopy and perceived ambient air pollution in both sexes. The presence of visible cockroaches (odds ratio [OR]: 1.30; 95% confidence interval [CI]: 1.07-1.59), mold on walls at home (OR: 1.20; 95% CI: 1.01-1.41), and water damage (OR: 1.33; 95% CI: 1.02-1.70) were also associated with asthma in girls; however, only visible mold on walls at home was related to asthma in boys. Mutually adjusted analytical models produced statistically significant associations between any indoor factor and asthma in girls (OR: 1.24; 95% CI: 1.00-1.56) but not in boys (OR: 1.04; 95% CI: 0.87-1.25). For all hereditary and environmental factors, the total population attributable risk was 44.31% in boys and 60.61% in girls. CONCLUSIONS: Parental atopy contributed more to childhood asthma than indoor or outdoor environmental factors. Girls may be more susceptible to indoor factors than boys.

Adolescent↗
PubMed2006

Recurrent wheeze in early childhood and asthma among children at risk for atopy.

OBJECTIVES: Little is known about the natural history of wheezing disorders among children at risk for atopy. We examined the relation between early wheeze and asthma at 7 years of age among children with parental history of asthma or allergies followed from birth. METHODS: Information on wheeze was collected bimonthly from birth to age 24 months and every 6 months thereafter. Recurrent early wheeze was defined as > or =2 reports of wheezing in the first 3 years of life. Frequent early wheeze was defined as > or =2 reports of wheezing per year in the first 3 years of life. At 7 years of age, asthma was defined as physician-diagnosed asthma and wheezing in the previous year. RESULTS: Of the 440 participating children, 223 (50.7%) had > or =1 report of wheeze before 3 years old, 111 (26.0%) had recurrent early wheeze, and 12 (2.7%) had frequent early wheeze. Whereas only 31 (13.9%) of 223 children with > or =1 report of wheeze developed asthma at 7 years of age, 24 (21.6%) of 111 children with recurrent early wheeze developed asthma at 7 years of age. Among the 12 children with frequent early wheeze, 6 (50%) had asthma at 7 years of age. After adjustment for other covariates, recurrent early wheeze in children at risk for atopy was associated with a fourfold increase in the odds of asthma at 7 years of age, and frequent early wheeze was associated with an approximately 12-fold increase in the odds of asthma at 7 years of age. Most (94%) of the children without frequent early wheeze did not develop asthma at 7 years of age. CONCLUSIONS: The absence of recurrent early wheeze indicates a very low risk of asthma at school age among children with parental history of asthma or allergies. Early identification of children who will develop asthma at school age is difficult, even in children at risk for atopy. However, children with parental history of asthma or allergies who have frequent early wheeze, in particular, are at greatly increased risk of asthma and merit close clinical follow-up.

Asthma↗
PubMedDate not supplied

The presence of atopy does not determine the type of cellular infiltrate in nasal polyps.

BACKGROUND AND OBJECTIVES: Any relationship between atopy and nasal polyposis remains to be further studied to determine the contribution of atopy to the pathogenesis of nasal polyps. MATERIALS AND METHOD: We have compared the inflammatory cellular infiltrate in nasal polyp tissue taken during resection from 10 atopic and 11 non-atopic subjects. We have used immunohistochemistry to enumerate the individual inflammatory cell types using monoclonal antibodies against tryptase (AA1) to identify mast cells, the secreted forms of eosinophil cationic protein (EG2) to identify activated eosinophils, neutrophil elastase (NE+) to demonstrate neutrophils, and T cell surface markers (CD3) to identify pan T cells. RESULT: The number of AA1+ and NE+ cells tended to be higher in atopics, but no statistical significance was found (p = 0.06, p = 0.12). Eosinophil numbers (EG2) were abundant in both groups and found to be not different between them (p = 0.65). Some subjects had CD3+ cells with no significant difference between atopic and non-atopic subjects (p = 0.21). Significant correlation was found between NE+ and AA1+ or EG2 cells (r = 0.59, r = 0.63, p < 0.05, respectively). CONCLUSION: These results suggest that the presence of atopy does not determine either the type of extent of cellular infiltration of nasal polyps.

Analysis of Variance↗
PubMed2000

Puzzling associations between childhood infections and the later occurrence of asthma and atopy.

The current unfavourable trends in asthma and atopy prevalences have raised great concern and have challenged investigators to accelerate search for new risk factors for atopic diseases. The lack or scarcity of intense, systemic infections in early life has been postulated to increase susceptibility of becoming sensitized to otherwise harmless allergens in later life. This hygiene hypothesis is considered one of the most plausible explanations for the current trends in atopic diseases to date. There are data to suggest that measles, hepatitis A, and Mycobacterium tuberculosis infection in early life may prevent the subsequent development of atopic diseases. The hypothesis is based on the concept that certain viral and bacterial infections, which induce a strongly polarized T helper (Th)-1 type response and a long-lasting memory immunity, are in early life able to reverse or prevent the biased Th1/Th2 balance in individuals prone to atopy and asthma. Evidence for the ability of mycobacterial infections to alter the Th1/Th2 balance has also been obtained from murine models. In humans, the critical time period during which immunomodulation with long-lasting effects is considered most successful is within the first two years of life. Possibly also nonpathogenic residents of the intestinal mucosa are involved in the proper maturation of the immune system. The use of antibiotics has been shown to be positively associated with the development of asthma and atopy. The mechanisms underlying these associations remain largely unknown.

Anti-Bacterial Agents↗
PubMed2004

The effect of passive smoking on asthma symptoms,atopy,and airway hyperresponsiveness in schoolchildren.

Passive smoking is a major cause of respiratory morbidity, and is associated with increased bronchial responsiveness in children. To evaluate the effect of smoking by a parent on asthma symptoms, atopy, and airway hyperresponsiveness (AHR), we conducted a cross-sectional survey of 503 schoolchildren that involved questionnaires, spirometry, allergy testing, and a bronchial challenge test. If the PC20 methacholine was less than 16 mg/mL, the subject was considered to have AHR. The prevalence of a parent who smoked was 68.7%. The prevalence of AHR was 45.0%. The sensitization rate to common inhalant allergens was 32.6%. Nasal symptoms such as rhinorrhea, sneezing, nasal itching, and nasal obstruction were present in 42.7%. Asthma symptoms such as cough and wheezing were present in 55.4%. The asthma symptoms were significantly more prevalent in children who had a parent who smoked than in those whose parents did not. The nasal symptoms, atopy, and AHR did not differ according to whether a parent smoked. In a multiple logistic regression model, the asthma symptoms and atopy were independently associated with AHR, when adjusted for confounding variables. Passive smoking contributed to asthma symptoms in schoolchildren and was not an independent risk factor of airway hyperresponsiveness in an epidemiological survey.

Adult↗
PubMed2005

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

Asthma is commonly described as an atopic disease in childhood, but some cases of this disorder do not fit this description. The aim of this study was to evaluate the frequency of atopy, asthma, and sensitization to house dust mites in children with allergic symptoms. This study was performed at the Severance Hospital of Yonsei University with patients who visited the allergy clinic for evaluation of nonspecific upper respiratory symptoms, typical symptoms of asthma, or a general health workup. The patients were divided into three age groups: 0-3 years (group 1), 4-7 years (group 2), and 8-12 years (group 3). Of the 1,244 children examined, 844 (67.8%) were atopic and 400 (32.2%) were non-atopic. The frequency of atopy and asthma increased with age. Asthma was diagnosed in the same proportion (64%) of atopic and non-atopic children. As risk factors for asthma symptoms, the positive values of house dust mite (HDM) sensitivity were significantly increased in groups 1, 2, and 3 to 53.5%, 68.9%, and 80.2%, respectively. A significant difference between the percentage of asthmatics sensitized to HDM and that of asthmatics not sensitized to HDM was found only in group 3. In conclusion, asthma is related to atopy with increasing age, and house dust mite sensitization seems to be an important determinant of asthma in older children in Korea.

Animals↗
PubMed1999

Incidence rate of adult-onset asthma in relation to age, sex, atopy and smoking: a Swedish population-based study of 15813 adults.

SETTING: Our knowledge about asthma incidence in an adult population is limited. The aim of the present investigation was to estimate the incidence rate of adult-onset asthma in relation to age, sex, atopy and smoking in a random population sample. METHODS: A random sample of 20000 subjects 20 to 50 years of age was investigated using a short respiratory questionnaire. It was answered by 15813 persons. Adult-onset asthma was defined as a positive response to 'physician-diagnosed' asthma from 16 years of age. Subjects were also asked to report the year of asthma diagnosis, and also, when relevant, the year of smoke-start and smoke-stop. Incidence rates of adult-onset asthma and incidence rate ratios (IRR) were calculated. RESULTS: The incidence rate of adult-onset asthma among females was 1.3 cases/1000 person-years compared with 1.0/1000 person-years for males (IRR 1.3, 95% confidence interval [CI] 1.0-1.6). The incidence rate was high (3.0/1000 person-years) among females aged 16-20 years. There was a strong association between the incidence rate of adult-onset asthma and hay fever, atopic dermatitis and family history of atopy. Compared with never-smokers, the IRR for female smokers was 1.6 (95% CI 1.1-2.2), while for male smokers it was unity. Both male and female ex-smokers had moderately increased rate ratios, of 1.5 and 1.1, respectively. CONCLUSIONS: In this retrospective study, reported atopic symptoms and family history of atopy were strongly associated with incidence of adult-onset asthma. Tobacco smoking may be associated with an increased incidence rate of adult-onset asthma, especially among women.

Adolescent↗
PubMed1976

Immunoglobulin E, atopy, and nickel allergy.

Statements in the literature as to whether a relation exists between atopy and nickel allergy are contradictory. I have attempted to make the diagnosis of the two states more stringent by using immunoglobulin E (IgE) determinations and serial dilution tests with nickel sulfate. The IgE determinations proved to be of less value in cases of pure eczema, and nonspecific (?) increases were sometimes observed. The incidence of family atopy was higher in other reports, but the clinical significance of this was unclear. Serial dilution tests gave important information, and a warning is issued against uncritical acceptance of a test reaction with 5.0% nickel sulfate in a patient with suspected atopy.

Dermatitis, Atopic↗
PubMed1999

Association of a lymphotoxin alpha gene polymorphism and atopy in Italian families.

Tumour necrosis factor (TNF) is a proinflammatory cytokine that increases human airway tissue responsiveness and is considered a candidate gene for asthma. Two common polymorphisms (LTalphaNcoI and TNFalpha-308) in the TNF gene complex were studied in 600 subjects from 131 Italian families with atopic asthmatic children. Skin prick test (SPT), total IgE levels, atopy (defined as increased IgE levels or SPT positivity or both), bronchial hyperresponsiveness, and clinical asthma were investigated. The observed distribution of the identical by descent alleles at the LTalphaNcoI locus was different from expected for SPT and atopy (p=0.015). The LTalphaNcoI genotype distribution for increased IgE levels was different between males and females (p=0.0011), and an association of the 2.2 genotype with increased IgE levels was observed in females (p=0.0032). The results indicate that the LTalpha gene, or a closely linked locus, is associated with atopy, and suggest a sex difference in the effect of the gene.

Alleles↗
PubMed1999

Linkage and association studies of atopy and the chromosome 11q13 region.

The clinical syndrome atopy is largely determined by genetic factors. In 1989, the first linkage of markers within and flanking the chromosomal region 11q13 and atopy was reported. In the following years, the gene coding for the beta chain of the high affinity IgE receptor was localised to this region and two polymorphisms in this gene have been shown to be associated with the atopic phenotype. We investigated two independent populations (population based and outpatient department) with different degrees of clinical symptoms. Using highly polymorphic markers we could find no evidence for linkage or allelic association of this particular genomic region to the atopic phenotype defined by enhanced IgE responsiveness (p>0.05). Neither did we succeed in finding either of the two polymorphisms described, nor could we identify any other polymorphisms within the gene. However, we found weak evidence for linkage in asthmatic sib pairs regarding maternal alleles (p=0.03). We conclude from our data that in our populations the gene for the beta chain of the high affinity IgE receptor is of minor importance for enhanced IgE responsiveness, and that it might influence atopy with clinical signs like asthma through maternally derived alleles.

Adolescent↗