Allergen-specific IgE Levels Research Articles

Allergic sensitization and microbial load – a comparison between Finland and Russian Karelia

Epidemiological data have indicated that some infections are associated with a low risk of allergic diseases, thus supporting the idea (hygiene hypothesis) that the microbial load is an important environmental factor conferring protection against the development of allergies. We set out to test the hygiene hypothesis in a unique epidemiological setting in two socio-economically and culturally markedly different, although genetically related, populations living in geographically adjacent areas. The study cohorts included 266 schoolchildren from the Karelian Republic in Russia and 266 schoolchildren from Finland. The levels of total IgE and allergen-specific IgE for birch, cat and egg albumen were measured. Microbial antibodies were analysed against enteroviruses (coxsackievirus B4), hepatitis A virus, Helicobacter pylori and Toxoplasma gondii. Although total IgE level was higher in Russian Karelian children compared to their Finnish peers, the prevalence of allergen-specific IgE was lower among Russian Karelian children. The prevalence of microbial antibodies was, in turn, significantly more frequent in the Karelian children, reflecting the conspicuous difference in socio-economic background factors. Microbial infections were associated with lower risk of allergic sensitization in Russian Karelian children, enterovirus showing the strongest protective effect in a multivariate model. The present findings support the idea that exposure to certain infections, particularly in childhood, may protect from the development of atopy. Enterovirus infections represent a new candidate to the list of markers of such a protective environment. However, possible causal relationship needs to be confirmed in further studies.

Addressing issues of asthma in inner-city children

For children living in the inner city, asthma tends to be more frequent and severe. Although the causes for this heightened severity of asthma are not clearly established, environmental allergens likely play a major role. To characterize, understand, and treat children with asthma living in the inner city better, the National Institutes of Allergy and Infectious Diseases of the National Institutes of Health established an Inner City Asthma Program in 1991. Over the past 15 years, 3 separate inner-city asthma research networks have been formed and funded by this institute. The work from these programs has led to important observations including evidence that environmental allergens, particularly cockroach, are important for sensitization and severity of asthma of the affected children. Furthermore, reductions in the allergen load can lead to improved asthma control. The most recent program, the Inner City Asthma Consortium, was formed in 2002 with a goal to develop immune-based therapy for children with asthma in the inner city and to determine mechanisms of these therapies as well as immunopathogenesis of asthma in these high-risk children. This article reviews these programs and how they have begun the effort to understand and treat children with asthma who live in inner cities better and what their findings mean in relationship to unique features of asthma in inner city children.

The Relationship between Skin Test Responses and Nasal Responses to Mouse Allergen

RATIONALE: Mouse allergy is assessed using skin testing and serum levels of mouse allergen-specific IgE (m-IgE). However, it is unknown whether a positive skin test or m-IgE accurately identifies those with mouse allergy.

Test prowokacji nosowej z alergenem, alergiczne testy skórne oraz poziom alergenowo swoistych IgE w surowicy u dzieci chorych na astmę oskrzelową

The important element in the asthma diagnosis is a confirmation of trigger's asthma symptoms allergens. The aim of this study was to evaluate diagnostic value of an allergic skin prick test and serum allergen-specific IgE level with reference to nasal allergen provocation test (NPT) results in asthmatic children. Study was performed in 80 asthmatic children in 3-14 yrs aged. 118 NPTs accompanied by assessments of nasal airflow by rhinospirography, were done. In all subjects, allergic skin prick tests with mites and grasses or trees pollen allergens and serum allergen specific IgE levels with the allergen used in NPT were done. Concordance between SPT and TPN results was shown in 59% cases, most often in group with pollen than mites provocation. SPT's sensitivity and specificity in relation to TPN result was 71% and 53%, respectively. Concordance between asIgE level and TPN results was shown in 76% cases. asIgE results sensitivity and specificity in relation to TPN result was 71% and 82%, respectively. The usefulness of skin prick test results in allergologic diagnosis of asthma is lesser than serum allergen specific IgE determination, especially in patients with house dust mites allergens hypersensitivity. Nasal provocation test (NPT) with suspected allergen should be performed in asthmatic children with a negative or doubtful skin prick test or serum allergen specific IgE level results.

Molecular determinants of allergen-induced effector cell degranulation

Allergen-induced effector cell degranulation is a key event in allergic inflammation and leads to early-phase symptoms, such as allergic rhinitis, conjunctivitis, urticaria, or bronchial asthma. We sought to study molecular determinants of effector cell degranulation using a monoclonal IgE antibody specific for a peptide epitope of one of the most important respiratory allergens, the major grass pollen allergen Phl p 1, as a model system. A hybridoma cell line producing a monoclonal IgE antibody against a Phl p 1-derived peptide, P1, was established by means of immunization of mice and used to sensitize rat basophil leukemia cells, which were exposed to P1 monomer, P1 dimer, and P1 polymer. It is demonstrated that the number of IgE epitopes on an allergen molecule and the concentration of allergen-specific IgE antibodies determine the extent of degranulation. The P1 monomer did not cause mediator release and prevented degranulation induced by polymeric P1. Our results suggest that the number of IgE epitopes on an allergen molecule determines its allergenic activity and explains why increases of allergen-specific IgE levels make patients more sensitive to allergens. Allergen-derived monomeric structures isolated by means of combinatorial chemistry might be used to develop new therapeutic strategies for allergy. Our study reveals molecular factors that determine the immediate allergenic activity of allergens and hence influence clinical sensitivity to these allergens.

Early-life supplementation of vitamins A and D, in water-soluble form or in peanut oil, and allergic diseases during childhood

Early vitamin supplementation is given routinely to infants in many countries, but it is unclear whether this affects the risk of allergic diseases. We sought to study the association between early-life supplementation of vitamins A and D in water-soluble form or in peanut oil and allergic diseases up to 4 years of age. A prospective birth cohort of 4089 newborn infants was followed for 4 years using parental questionnaires repeatedly to collect information on exposure and health. At 4 years, the response rate was 90%, and allergen-specific IgE levels to food and airborne allergens were measured in 2614 of the participating children. Vitamins A and D were given to 98% of the children in infancy, and vitamins based in peanut oil dominated (90%). Children supplemented with vitamins A and D in water-soluble form during the first year of life had an almost 2-fold increased risk of asthma (adjusted odds ratio [OD], 2.18; 95% CI, 1.45-3.28), food hypersensitivity (adjusted OR, 1.89; 95% CI, 1.33-2.65), and sensitization to common food and airborne allergens (adjusted OR, 1.88; 95% CI, 1.34-2.64) at age 4 years compared with those receiving vitamins in peanut oil. No increased risk of IgE antibodies to peanut was seen in children receiving vitamins in peanut oil. Supplementation of vitamins A and D in water-soluble form seems to increase the risk of allergic disease up to the age of 4 years compared with supplementation with the same vitamins given in peanut oil. Vitamins A and D in oil does not seem to increase the risk of allergic disease during childhood.

GlutathioneS-Transferases M1 and P1 Prevent Aggravation of Allergic Responses by Secondhand Smoke

Secondhand tobacco smoke (SHS) and traffic-related air pollutants are associated with asthma and allergy. Diesel exhaust particles (DEPs) and SHS can interact with allergens in exacerbating allergic airway diseases through generation of reactive oxygen species. Glutathione S-transferases (GSTs) metabolize reactive oxygen species and detoxify electrophilic xenobiotics present in SHS and DEPs. We tested the hypotheses that functional GSTM1-null genotype and GSTP1 codon 105 variants (Ile105 and Val105) are determinants of allergic responses to SHS, and that responses to SHS and DEPs are correlated. In a randomized, placebo-controlled crossover trial, 19 ragweed allergen-sensitive subjects who had previously participated in a DEP trial were challenged intranasally with allergen after having been exposed to either clean air or SHS at separate visits. Nasal allergen-specific IgE, histamine, IL-4, and IFN-gamma levels were measured before and after allergen challenge. Individuals with GSTM1-null or GSTP1 Ile105 genotypes showed larger nasal responses to allergens with SHS compared with clean air. GSTM1-null subjects had a larger increase in IgE than GSTM1-present subjects (median, 173.3 vs. 46.7 U/ml; p = 0.03), and the Ile105 GSTP1 genotype subjects had increased histamine (median, 10.2 vs. 4.6 nM; p = 0.01) after SHS plus allergen challenge. Responses to SHS and DEPs were correlated. Enhancement of IgE and histamine was greatest in the subjects with both the GSTM1-null and GSTP1 Ile/Ile genotypes. GSTM1 and GSTP1 are important cytoprotective factors that reduce SHS and DEP exacerbation of allergic responses.

Rhinosinusitis derived Staphylococcal enterotoxin B plays a possible role in pathogenesis of food allergy.

BackgroundStaphylococcal enterotoxin B (SEB) is a potent immunomodulator and implicated with pathogenesis of inflammatory diseases mediated by Th1 or Th2 dominant immune responses. The objective of this study is to determine a possible association between rhinosinusitis derived SEB and pathogenesis of food allergy (FA).MethodsThe study included chronic rhinosinusitis (CRS) patients with FA (N = 46) or without FA (N = 33). Controls included FA patients without CRS (N = 26) and healthy volunteers (N = 25). In CRS patients, we assessed the parameters associated with FA including prick skin test (PST) reactivity to food allergens, serum levels of allergen-specific IgE and cytokines (IL-4, IL-13, IFN-Î3), and the number/reactivity of food-allergen specific Th1/Th2 cells in the peripheral blood before and 2 months after sinus surgery. Changes of these parameters were evaluated in comparison with changes in SEB concentration in the sinus lavage and stool samples and also in vitro reactivity to SEB. In CRS patients with FA, we also assessed changes in reactivity to oral challenge of offending food before and after sinus surgery.ResultsTwo months following sinus surgery, we observed statistically significant reduction in PST and oral challenge reactivity in CRS patients with FA in parallel to decrease in serum levels of Th2 cytokines (IL-4 and IL-13) and allergen specific IgE. Improvement of reactivity to food allergens was positively associated with decline in SEB concentrations in the sinus lavage and stool samples. In vitro study results also indicated a role of SEB in aggravation of Th2 skewed responses to food allergens. Such changes were not observed in CRS-non FA patients or control FA patients.ConclusionThe rhinosinusitis derived SEB plays a certain role in the pathogenesis of FA by augmenting and/or maintaining polarized Th2 responses. Removal of SEB-producing pathogens from the rhinosinuses may be beneficial for attenuating the FA symptoms in patients with CRS-FA.

Common vaccine antigens inhibit allergen‐induced sensitization and airway hyperresponsiveness in a murine model

Co-vaccination with cellular pertussis vaccine down-regulates allergic sensitization to diphtheria and tetanus antigens. Using a murine model, we investigated whether vaccination with diphtheria/tetanus toxoids, administered separately or simultaneously with the whole cell vaccine of Bordetella pertussis, inhibits subsequent allergen-induced immune and inflammatory responses. BALB/c-mice were vaccinated intracutaneously with a combination of diphtheria and tetanus toxoids or a combination of diphtheria and tetanus toxoids with a whole cell vaccine of B. pertussis (three times, days -21 to -7) prior to systemic sensitization (days 1-14) and repeated airway challenges (days 28-30) with ovalbumin. Compared with negative controls, systemic sensitization and airway allergen challenges induced high serum levels of allergen-specific IgE, predominant Th2-type cytokine production, airway inflammation and development of in vivo airway hyperreactivity. Vaccination with diphtheria and tetanus toxoids prior to sensitization suppressed IgE formation and development of eosinophilic airway inflammation. Co-vaccination with a whole cell pertussis vaccine inhibited allergen sensitization, airway inflammation and development of in vivo airway hyperreactivity. Prevention was due to an allergen-specific and general shift from a predominant Th2 towards a predominant Th1 immune response. Vaccination with diphtheria and tetanus toxoids alone or in combination with whole cell pertussis vaccine prior to allergen sensitization prevented allergen-induced Th2 immune responses. Vaccine antigens may down-regulate allergic responses to a range of common allergens.

Accuracy of US Food and Drug Administration–cleared IgE antibody assays in the presence of anti-IgE (omalizumab)

Although serological IgE measurements can aid in efficacy assessment of patients with asthma on omalizumab (Xolair [Genentech, Inc., South San Francisco, Calif]; humanized IgG1 antihuman IgE Fc), its effect on clinically used IgE assay performance is unknown. This study investigated the hypothesis that IgE:IgG-anti-IgE immune complex formation after omalizumab administration diminishes accuracy and increases variability of IgE assays performed in diagnostic immunology laboratories. Plasma from 4 atopic adults was incubated with omalizumab (50 or 200 molar excess to IgE) or buffer. Paired specimens were sent masked to 159 clinical laboratories in the College of American Pathologists Diagnostic Allergy Proficiency Survey (cycles SE-C-2003, SE-A-2005). Inhibitory effects produced by omalizumab on accuracy and reproducibility of US Food and Drug Administration (FDA)-cleared total and allergen-specific IgE assays were computed by using national proficiency survey data. Total serum IgE levels measured in the 2 ImmunoCAP assays were minimally reduced (2.4-9.0%) by the presence of omalizumab, whereas 5 other assays showed marked reductions from 12.5% to 67.2% (P < .001) that increased in proportion to total serum IgE levels. The degree of interference was not large enough to produce detectable misclassification of IgE antibody results (positive to negative) in 4 multiallergen screening assays. Of 11 FDA-cleared IgE antibody assays, only 3 (ImmunoCAP, UniCAP, Immulite-2000) generated quantitative IU/mL results that could be assessed for interference. Omalizumab produced 0.8% to 27.8% reduction in allergen-specific IgE levels across 8 allergen specificities. Although as much as 62% loss in accuracy was observed in FDA-cleared human IgE assays, the ImmunoCAP system was sufficiently robust to provide accurate and reproducible total and allergen-specific IgE antibody results in a clinical setting where therapeutic levels of omalizumab are present in serum. Accurate monitoring of total and allergen-specific IgE, together with free IgE levels, in serum from patients on omalizumab may help optimize dosing and maximize the efficacy of Xolair therapy.

CD14 Promoter Polymorphisms in Atopic Families: Implications for Modulated Allergen-Specific Immunoglobulin E and G1 Responses

Background: CD14 promoter DNA sequence polymorphisms for the endotoxin receptor gene have been implicated in modulating allergen-specific immunoglobulin (Ig)E responses in randomly selected individuals with atopy. We sought to determine if a single nucleotide polymorphism in the CD14 promoter region is associated with atopy in atopic families, and to assess its influence on serum levels of CD14 and allergen-specific IgE and IgG1 responses. Methods: We screened 367 members of 91 Caucasian nuclear families with a history of asthma for pulmonary function by spirometry, including methacholine challenge to detect bronchial hyperreactivity, and atopy by serum total IgE and skin prick test to 14 allergens. The CD14 promoter single nucleotide polymorphism was analyzed in DNA isolated from peripheral blood mononuclear cells to identify C/C, C/T and T/T genotypes. Serum tests were done for soluble CD14 (sCD14) and dust mite-specific antibody (Der p 1-IgG1). Results: Serum sCD14 levels were not associated with clinical phenotypes (asthma, bronchial hyperreactivity or atopy). However, sCD14 levels were inversely related to both allergen-specific IgE and Der p 1-IgG1 production, but only among those with evidence of atopic sensitization. Linear regression analysis, accounting for random family effects, demonstrated a higher production of allergen-specific IgE or Der p 1-IgG1 associated with the T/T genotype and a lower level of specific IgE and IgG1 production associated with sCD14 levels. Conclusions: An element of the innate immune system (CD14) has profound effects upon modulating the acquired allergen-specific immunoglobulin responses among those with an inherited atopic predisposition.

Absence of systemic immunologic changes during dose build‐up phase and early maintenance period in effective specific sublingual immunotherapy in children

Sublingual immunotherapy (SLIT) has been reported to be a safe treatment for inhalant allergies in children. Yet the immunologic mechanisms resulting in clinical improvement are poorly understood. To identify early systemic immunologic changes during the first 8 weeks of clinically effective SLIT to grass pollen, tree pollen or house dust mite in paediatric patients with allergic rhinoconjunctivitis and/or asthma. Peripheral blood mononuclear cells and plasma samples of 13 children with reduced symptoms after 1 year of SLIT were obtained before therapy and at 2 and 8 weeks after the initiation of SLIT. Allergen-specific lymphocyte proliferation assays were performed, and allergen-induced cytokine production (IL-2, IL-4, IL-10, IFN-gamma, and TGF-beta(1)) was measured by ELISA and flow cytometry. Allergen-specific IgE, IgG1, IgG4, and IgA levels in plasma samples were determined in ELISA. During the first 8 weeks of successful SLIT, allergen-specific lymphoproliferation (n=13) as well as levels of allergen-specific intracellular (n=8) and secreted cytokines (n=9) did not change significantly. In addition, no alterations in levels of allergen-specific Igs (n=7) were observed. We could not find any early systemic immunologic changes during the first 8 weeks of clinically effective SLIT to inhalant allergens in paediatric patients with allergic rhinoconjunctivitis and/or asthma.

Lack of Association between the IL13 Variant Arg110Gln and Susceptibility to Cedar Pollinosis in a Japanese Population

Background:Interleukin (IL)-13 has come to be appreciated as a molecule critically involved in allergic inflammatory responses. Recent studies revealed that a common variant in the coding region of the IL13 gene, Arg110Gln, has been implicated in the development of asthma and atopy. Methods:To assess whether the IL13 variant Arg110Gln is associated with cedar pollinosis, one of the most common atopic diseases in the Japanese population, we examined the Arg110Gln variant using PCR-RFLP to compare the genotype and allele frequencies between 95 patients with cedar pollinosis and 95 healthy control subjects. Relationships between the Arg110Gln variant and the pollinosis-related traits, e.g. rhinitis severity, eosinophil counts in nasal secretion and serum total and allergen-specific IgE levels, were also investigated. Results: The frequencies of the minor allele Gln110 were 25.8% in patients with cedar pollinosis and 30.9% in healthy control subjects (p > 0.05). There was also no significant difference in the genotype frequencies between cases and controls (p > 0.05). In addition, we found no significant association of the Arg110Gln variant with any of the pollinosis-related phenotypes (p > 0.05). Conclusions: Our data suggest lack of evidence for identifying the variant Arg110Glnat the IL13 locus as a genetic risk factor involved in the development of Japanese cedar pollinosis.

Cord blood house dust mite allergen in newborns: relationship to maternal blood levels of allergen and allergen specific IgG and IgE

House dust mite allergen has previously been detected in the cord blood of some newborns but not others. The factors that affect the presence and levels in cord blood of this and possibly other allergens are unknown. To test the hypothesis that the levels of maternal allergen and allergen specific IgG affect the presence and levels of newborn allergen. Enzyme-linked immunosorbent assays were used to measure the levels of house dust mite allergen Der p 1 and Der p 1 specific IgG and IgE in paired blood samples from 98 mothers and full-term newborns. Der p 1 was detected in 27 mothers and 12 newborns. None of the 71 mothers who lacked Der p 1 had Der p 1-positive newborns. When present, cord blood Der p 1 levels correlated with and were approximately one third of Der p 1 levels in maternal blood. Cord blood Der p 1 levels also tended to correlate with maternal blood levels of Der p 1 specific IgG but showed little, if any, correlation with maternal blood levels of Der p 1 specific IgE. When detectable, the levels of an allergen in the blood of newborns correlate with the levels of that allergen in the blood of their mothers and tend to be related to maternal levels of allergen specific IgG.

Beyond Our Pages

Beyond Our Pages

Airway Hyperresponsiveness in the Absence of CD4+ T Cells after Primary but Not Secondary Challenge

CD4+ T cells have been shown to play a role in the development of airway hyperresponsivness (AHR) and airway eosinophilia in mice using ablation as well as adoptive transfer experiments. However, as other T cell subsets (CD8, NKT) may play a role in these models, we examined the responses of sensitized CD4-deficient mice after either primary or secondary airway allergen challenge. After sensitization, CD4-deficiency in mice was not associated with airway eosinophilia, allergen-specific IgE, or elevated levels of interleukin (IL)-4 or IL-13. Increases in lung CD8 T cells and IL-5 were observed and shown to be essential for AHR as demonstrated after CD8 T cell depletion or anti-IL-5 treatment. In contrast to the response of sensitized CD4-deficient mice to primary allergen challenge, they failed to develop AHR after secondary allergen challenge. Although the importance of this CD4+ T cell-independent pathway in normal mice is unclear at this time, these studies identify the diversity of the cellular pathway, which may contribute to the development of AHR after primary allergen exposure of sensitized mice.

Interleukin-2–Inducible T Cell Kinase Regulates Mast Cell Degranulation and Acute Allergic Responses

Bruton's tyrosine kinase (Btk) is thought to positively regulate mast cell activation, implying a role in allergic responses. We have compared acute and late phase allergic airway reactions in mice lacking either Btk or interleukin-2-inducible T cell kinase (Itk), another Tec kinase expressed in mast cells. Btk(-/-) mice showed minor protection against allergic symptoms when challenged with allergen via the airways. In sharp contrast, both acute and late phase inflammatory allergic responses were markedly reduced in Itk(-/-) mice. Notably, airway mast cell degranulation in Itk(-/-) mice was severely impaired, despite wild-type levels of allergen-specific IgE and IgG1. The degranulation defect was confirmed in DNP-conjugated human serum albumin-challenged mice passively sensitized with anti-DNP IgE antibodies, and was also observed after direct G-protein stimulation with the mast cell secretagogue c48/80. Moreover, late phase inflammatory changes, including eosinophilia, lymphocyte infiltration, and Th2 cytokine production in the lungs, was eliminated in Itk(-/-) mice. Collectively, our data suggest a critical role of Itk in airway mast cell degranulation in vivo that together with an impaired T cell response prevents the development of both acute and late phase inflammatory allergic reactions.

Poor association between allergen‐specific serum immunoglobulin E levels, skin sensitivity and basophil degranulation: a study with recombinant birch pollen allergen Bet v 1 and an immunoglobulin E detection system measuring immunoglobulin E capable of binding to FcɛRI

Results from several studies indicate that the magnitude of immediate symptoms of type I allergy caused by allergen-induced cross-linking of high-affinity Fc epsilon receptors on effector cells (mast cells and basophils) is not always associated with allergen-specific IgE levels. To investigate the association of results from intradermal skin testing, basophil histamine release and allergen-specific IgE, IgG1-4, IgA and IgM antibody levels in a clinical study performed in birch pollen-allergic patients (n = 18). rBet v 1-specific IgEs were measured by quantitative CAP measurements and by using purified Fc epsilon RI-derived alpha-chain to quantify IgE capable of binding to effector cells. Bet v 1-specific IgG subclasses, IgA and IgM levels were measured by ELISA, and basophil histamine release was determined in whole blood samples. Intradermal skin testing was performed with the end-point titration method. Our study demonstrates on the molecular level that the concentrations of allergen-specific IgE antibodies capable of binding to Fc epsilon RI and biological sensitivities are not necessarily associated. A moderate association was found between cutaneous and basophil sensitivity. Our results highlight the quantitative discrepancies and limitations of the present diagnostic tools in allergy, even when using a single allergenic molecule. The quantity of allergen-specific serum IgE is only one component of far more complex cellular systems (i.e. basophil-based tests, skin tests) used as indirect diagnostic tests for IgE-mediated allergic sensitivity.

Macrophage inflammatory protein–1α as a costimulatory signal for mast cell–mediated immediate hypersensitivity reactions

Regulation of the immune response requires the cooperation of multiple signals in the activation of effector cells. For example, T cells require signals emanating from both the TCR for antigen (upon recognition of MHC/antigenic peptide) and receptors for costimulatory molecules (e.g., CD80 and CD60) for full activation. Here we show that IgE-mediated reactions in the conjunctiva also require multiple signals. Immediate hypersensitivity reactions in the conjunctiva were inhibited in mice deficient in macrophage inflammatory protein-1alpha (MIP-1alpha) despite normal numbers of tissue mast cells and no decrease in the levels of allergen-specific IgE. Treatment of sensitized animals with neutralizing antibodies with specificity for MIP-1alpha also inhibited hypersensitivity in the conjunctiva. In both cases (MIP-1alpha deficiency and antibody treatment), the degranulation of mast cells in situ was affected. In vitro sensitization assays showed that MIP-1alpha is indeed required for optimal mast cell degranulation, along with cross-linking of the high-affinity IgE receptor, FcepsilonRI. The data indicate that MIP-1alpha constitutes an important second signal for mast cell degranulation in the conjunctiva in vivo and consequently for acute-phase disease. Antagonizing the interaction of MIP-1alpha with its receptor CC chemokine receptor 1 (CCR1) or signal transduction from CCR1 may therefore prove to be effective as an antiinflammatory therapy on the ocular surface.

Sensitivity of the Skin Prick Test and Specificity of the Serum-Specific IgE Test for Airway Responsiveness to House Dust Mites in Asthma

Background. The concept that asthma diagnosis based on allergen-specific IgE levels in serum is more accurate than diagnosis based on skin test reactivity is controversial. Objective. To determine the atopy parameter that correlates most closely with airway reactivity to house dust mites in asthma. Methods. Forty-three asthma cases were examined retrospectively for data on Dermatophagoides farinae-specific bronchoprovocation, serum-specific IgE, and skin prick tests. Results. The maximal decreases in FEV1 following bronchoprovocation were correlated significantly with both the IgE levels and skin test scores. The accuracies of the tests were highest at a cutoff value of class 4 or higher for the IgE and of 3 + or higher for the skin test. At the cutoff values, the accuracies of both tests were similar (70% vs. 70%). The sensitivity of the skin test (81%) was higher than that of the IgE test (67%), whereas the specificity of the IgE test (71%) was higher than that of the skin test (52%). The sensitivity of the skin test was 91% at 2 + or higher, and the specificity of the IgE test was 95% at class 6 or higher. Conclusion. These results suggest that both the specific IgE level and the skin test reactivity are useful parameters in the prediction of positive airway responses to house dust mites in asthma. However, the skin test is more sensitive, whereas the IgE test is more specific. Therefore, these tests can be used in a complementary fashion (i.e., the skin test for screening and the specific IgE test for confirmation of the relevant allergen).