High Total IgE Levels Research Articles

Relationships of allergic sensitization, total immunoglobulin E and blood eosinophils to asthma severity in children of the EGEA Study.

Although allergy is highly associated with childhood asthma, it is not well known if there is a relationship between the intensity of allergic sensitization and asthma severity. The objectives of the study were to examine the relationships between several markers of allergy and asthma severity in asthmatic children included in the Epidemiological study on the Genetics and Environment of Asthma, bronchial hyper-responsiveness and atopy (EGEA). The population comprised 216 asthmatic children below 16 years of age. Total IgE and blood eosinophil counts were measured and skin prick tests to 11 aeroallergens were performed. The intensity of the allergic sensitization was assessed by the number of positive skin prick tests and by skin weal sizes. Asthma severity was measured with four criteria: a clinical severity score, history of hospitalization for asthma, FEV1% predicted and inhaled steroid use in the last 12 months. Most of the children were sensitized to at least one aeroallergen (88.2%). Atopy was not related to the severity of asthma, except for a tendency for a more severe clinical score in non-atopic children. The type and intensity of the allergic sensitization were not associated with any criteria of asthma severity. Total IgE was significantly increased in children treated with inhaled corticosteroids and in children ever hospitalized for asthma (P-values 0.009 and 0.04, respectively). Eosinophil counts were not related to asthma severity. Our results suggest that severe childhood asthma may be related to a high level of total IgE but not to blood eosinophil counts. The lack of positive relationships between both atopy and the intensity of allergic sensitization with asthma severity supports the hypothesis of different risk factors being associated with asthma and with the severity of asthma.

Association of polymorphisms in the collagen region of SP-A2 with increased levels of total IgE antibodies and eosinophilia in patients with allergic bronchopulmonary aspergillosis

Background: Studies from our group have shown a protective role of pulmonary surfactant protein A (SP-A) against lung allergy and infections caused by Aspergillus fumigatus . Objective: Present study investigated the association of polymorphisms in the collagen region of SP-A1 and SP-A2 (genes encoding SP-A) with allergic bronchopulmonary aspergillosis (ABPA) and its clinical markers. Methods: Genomic DNA was extracted from blood samples of patients with ABPA and age-matched, unrelated control subjects. The polymorphisms were detected by means of PCR amplification and sequencing of the collagen region of SP-A1 and SP-A2 . Results: Two exonic (SP-A2 G1649C and SP-A2 A1660G, 10 patients and 11 control subjects) and 2 intronic (SP-A2 T1492C, 8 patients and 8 control subjects; SP-A1 C1416T, 5 patients and 7 control subjects) polymorphisms in the collagen region of SP-A2 and SP-A1 showed significant association with patients with ABPA. A significantly higher frequency of the AGA allele (A1660G) of SP-A2 was observed in patients with ABPA in comparison with control subjects (P = .0156, odds ratio [OR] = 4.78, 95% CI = 1.23 < OR < 18.52). This polymorphism, when existing along with a nonredundant polymorphism, SP-A2 G1649C (Ala91Pro) resulted in a stronger association with ABPA (A1660G and G1649C: P = .0079, OR = 10.4, 95% CI = 1.62 < OR < 66.90). Patients with ABPA with GCT and AGG alleles showed significantly high levels of total IgE and percentage eosinophilia versus patients with ABPA with CCT and AGA alleles. Conclusion: The results indicated that SP-A2 G1649C and SP-A2 A1660G, polymorphisms in the collagen region of SP-A2 , might be one of the contributing factors to genetic predisposition and severity of clinical markers of ABPA. (J Allergy Clin Immunol 2003;111:1001-7.)

Experimental rhinovirus challenges in adults with mild asthma: Response to infection in relation to IgE

Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV). Young atopic adults with mild asthma were evaluated before and during an experimental HRV infection to test the hypothesis that airway inflammation before virus inoculation may be a risk factor for an adverse response to HRV. Experimental HRV infections were evaluated in 16 allergic volunteers with mild asthma and 9 nonatopic control patients (age, 18 to 30 years). Before virus inoculation, each participant was screened with tests for lung function, prick skin tests for sensitization to common aeroallergens, measurements of total serum IgE, and serum neutralizing antibody to rhinovirus-16 (the serotype used for inoculation). The response to infection was monitored for 21 days by using symptom diary cards, tests for lung function, and markers of airway inflammation in nasal washes, blood, and expired air. During the infection, asthmatic patients had cumulative upper and lower respiratory tract symptom scores that were significantly greater over the course of 21 days than scores from the control patients. At baseline, the asthmatic patients also had increased sensitivity to methacholine and significantly lower values for FEV(1) (percent predicted) than the control patients (geometric mean and intraquartile values: 87% [79% to 91%] for the asthmatic patients and 101% [90% to 104%] for the control patients, P <.03). Among the patients with mild asthma, 6 had levels of total serum IgE that were substantially elevated (range, 371 to 820 IU/mL) compared with 10 who had lower levels (range, 29 to 124 IU/mL). Those with high levels of IgE had significantly greater lower respiratory tract symptom scores during the initial 4 days of the infection than the low IgE group. They also had higher total blood eosinophil counts at baseline, increased eosinophil cationic protein in their nasal washes (>200 ng/mL), and augmented levels of expired nitric oxide at baseline and during peak cold symptoms. In contrast, levels of soluble intracellular adhesion molecule-1 in nasal wash supernatants from the asthmatic patients with high IgE were diminished, both at baseline and during the infection. The reduced lung function and increased markers of inflammation observed before virus inoculation in the asthmatic patients who had high levels of total serum IgE may be risk factors for an adverse response to infections with HRV.

Reduced risk of atopy among school-age children infected with geohelminth parasites in a rural area of the tropics

Background: Childhood infections might protect against the expression of atopy. Geohelminths are among the most prevalent infections of childhood and might contribute to the low prevalence of allergic disease reported from rural areas of the tropics. Objective: We sought to establish whether geohelminth infections protect against atopy and to explore whether this protection is dependent on infection chronicity. Methods: The risk of atopy (measured by means of allergen skin test reactivity) associated with active geohelminth infections (measured by means of the presence of eggs in stool samples) or with chronic geohelminth infections (measured by means of high levels [≥3564 IU/mL] of total serum IgE or the presence of detectable anti-Ascaris lumbricoides IgG4 antibodies) was investigated in an analytic cross-sectional study conducted among school-age children attending rural schools in Pichincha Province in Ecuador. Results: A total of 2865 children aged 5 to 19 years from 55 schools was examined. Active infection with any geohelminth and infections with A lumbricoides or Ancylostoma duodenale were associated with significant protective effects against allergen skin test reactivity. Children with the highest levels of total IgE or with anti-A lumbricoides IgG4 antibodies were protected against skin test reactivity also, and the protective effects of high IgE or anti-A lumbricoides IgG4 and or active geohelminth infections were statistically independent. Conclusion: Active infections with geohelminth parasites and the presence of serologic markers of chronic infections (high levels of total serum IgE or anti-A lumbricoides IgG4) are independent protective factors against allergen skin test reactivity among school-age children living in an endemic region of the rural tropics. (J Allergy Clin Immunol 2003;111:995-1000.)

Factors associated with recurrent hospitalizations in asthmatic children

Objective. – To determine preventable risk factors associated with recurrent hospitalization of children for acute asthma attacks. Methods. – A retrospective analysis of 288 asthmatic children between 6 and 15 years of age who were hospitalized between 31 December 1993 and 1 January 2000 was carried out. Results. – Admissions for asthma were higher in boys than in girls (male to female ratio 1.8). Of 288 children, 68 (23.6%) had multiple admissions, defined as a more than one admission per year during the follow-up period. The following factors were associated significantly with recurrent hospital admissions for asthma attacks: maternal smoking ( P < 0.02); frequent upper respiratory tract infection ( P < 0.001); high levels of total serum IgE ( P < 0.02); high peripheral blood eosinophil count ( P < 0.001); atopic dermatitis ( P < 0.001); and age less than 11 years ( P < 0.05). Using multivariate logistic regression analysis, among others factors only maternal smoking ( r = 0.24, P < 0.001) and frequent upper respiratory tract infection ( r = 0.37, P < 0.001) were significant factors for recurrent admissions. Conclusion. – Prevention of maternal smoking and frequent upper respiratory tract infections may be effective in decreasing re-admission to hospital in asthmatic children.

Low molecular weight PTP-IL-4RA interaction in atopy predisposition.

We recently described a protective effect of the low molecular weight protein tyrosine phosphatase (LMPTP) BC genotype, associated with the highest total enzymatic activity, against high serum IgE levels both in the English and the Italian populations. Here we test the hypothesis of a role of LMPTP in the negative modulation of IL-4 signal transduction checking for genetic interaction between interleukin-4 receptor alpha chain (IL-4RA) genetic polymorphisms and LMPTP polymorphism in the predisposition to high total IgE levels in the English population. We find a significant interaction between LMPTP polymorphism and the intracellular Gln/Arg polymorphism in position 551 of IL-4RA. Our data support the hypothesis of a direct or indirect biochemical interaction between LMPTP and IL-4RA resulting in different modulation of IL-4 signal transduction among joint genotypes.

Increased parasiticide activity against Trichinella spiralis newborn larvae during pregnancy.

To evaluate whether pregnancy has a synergetic effect on the host's immune response against Trichinella spiralis infection, immunological and parasitological parameters relating to the infection were assessed in pregnant rats and compared to those observed in virgin infected rats. The muscle parasite load was lower in pregnant infected rats but no differences were found in the intestinal worm burdens or the fecundity of female worms. The ability of sera to mediate death in newborn larvae (NBL) in an antibody-dependent cell cytotoxicity assay was higher for pregnant rats, even in the absence of specific anti-NBL antibodies. High levels of total and anti-NBL IgE were found in both groups, however, these levels were higher in the group of pregnant infected animals. No differences were found in anti-NBL IgGAM titers, nevertheless in some pregnant infected rats these antibodies were found earlier. No differences were found in peritoneal or blood eosinophil counts. Offspring born to infected dams were found to be infected. The results obtained in this model demonstrate that during pregnancy there is an enhanced helminthotoxic effect towards the NBL. Despite this immunoactivation, vertical transmission of the parasite is possible.

Adverse respiratory effects and allergic susceptibility in relation to particulate air pollution: flirting with disaster.

Adverse respiratory effects and allergic susceptibility in relation to particulate air pollution: flirting with disaster.

Genome-wide search for atopy susceptibility genes in Dutch families with asthma

Background:Atopy is a phenotype associated with asthma that has a heritable component. However, the role of atopysusceptibility genes in the development and expression of asthma and allergic disorders is not understood. Objective: We sought to study the familial aggregation and co-occurrence of atopic phenotypes within family members of patients with asthma and to identify chromosomal regions that may contain genes that regulate different atopic phenotypes. Methods: In 200 families (n = 1174) ascertained through a proband with asthma, genome-wide screen and linkage analysis was performed for the following atopic phenotypes: (1) specific IgE to common aeroallergens (Phadiatop assay); (2) specific IgE to Der p 1; (3) positive skin test responses to house dust mite; (4) positive skin test responses to 1 or more of 16 allergens; and (5) peripheral blood eosinophils. Results were compared with the linkage results for total serum IgE levels. Results: There was clear familial aggregation of atopy. A high total serum IgE level in combination with a positive Phadiatop result or a normal total IgE level in combination with a negative Phadiatop result was found in 56.1% of the probands and 66.9% of the offspring. Several chromosomal regions that showed evidence for linkage to an atopic phenotype (ie, 2q, 6p, 7q, and 13q) also showed evidence of linkage with total serum IgE (Xu et al. Am J Hum Genet 2000;67:1163-73). Specific regions of interest for atopic traits were also detected on chromosomes 11q, 17q, and 22q. Conclusions: Atopic phenotypes show familial aggregation, although family members may differ in expression of atopy. Specific chromosomal regions appear to be important in susceptibility to different phenotypes of atopic responsiveness. (J Allergy Clin Immunol 2002;109:498-506.)

Epidemiology of asthma and recurrent wheeze in childhood

To summarize, wheeze is common throughout childhood, although it decreases as children age. However, the characteristics of wheeze, its relations with asthma, and its risk factors all change with age. Longitudinal studies have shown that "transient early wheezing" predominates during the first years of life. The principal risks for this type of wheezing are largely mechanical, relating to small airways, and infectious, relating to the risk of becoming infected with respiratory viruses. Associated with passive exposure to cigarette smoke, exposure to other children, and not being breastfed, this form of wheezing was unrelated to increased airway liability or atopy in the child. For the majority of children, particularly those with low lung function at birth, wheezing with early LRIs is a benign condition, not associated with subsequent wheeze or risk for asthma. During the middle part of the first decade of life, wheezing appears to reflect a mix of infectious and allergic wheezing. By 6 yr of age, some children have already wheezed persistently. This group is more likely to have high total IgE levels, to be skin-test positive, and to be given a diagnosis of asthma. Further, their immunologic response to their early LRIs was consistent with a Th2 bias: persistent wheezers produced high levels of IgE, and did not demonstrate the normal pattern of decreased eosinophils. Nevertheless, the children who wheeze in middle childhood are a mixed group, with some being less allergic. Thus, although markers of allergy become increasingly important predictors of wheezing for the group as a whole, wheezing in middle childhood is not associated with later methacholine hyperresponsiveness (42). Finally, persistent allergic wheezing, usually associated with a diagnosis of asthma, predominates by the end of the first decade of life. Wheezing at this age is associated with methacholine responsiveness, peak-flow variability, and markers of atopy, such as total IgE and allergy skin-test response. Although children who wheezed early in life are more likely to wheeze later, early wheeze does not increase the risk of atopy, suggesting that early LRIs are markers of increased risk rather than causes. The gender differences in wheeze disappear, with boys becoming less likely to wheeze and to have asthma, whereas both conditions appear to increase in girls. Finally, some of the risk factors for early LRIs, such as exposure to other children in infancy, appear to be associated with protection from later allergic wheezing. Clearly, asthma and wheeze during childhood are complex entities, presenting with different characteristics at different ages, and implicating varied and changing causes. Genetic factors are important determinants of the intermediate phenotypes. However, environmental factors operating at different developmental stages also appear to influence the development of asthma. Additional research regarding these relationships is essential, both to elucidate possible causal mechanisms and to provide insight into the primary prevention of asthma.

Inhibitory effects of local allergen pretreatment on systemic allergen sensitization depends on the presence of lipopolysaccharides (LPS) in a murine model of allergic airway inflammation

Inhibitory effects of local allergen pretreatment on systemic allergen sensitization depends on the presence of lipopolysaccharides (LPS) in a murine model of allergic airway inflammation

Clinical characteristics of so called eosinophilic otitis media

Objective: Although ‘eosinophilic otitis media’ is not as uncommon a condition as was previously believed, its cause and pathogenesis are not yet fully understood. The purpose of this study was to describe the clinical characteristics in patients with ‘eosinophilic otitis media’ to clarify its pathogenesis. Methods: Seven adult patients with persistent and intractable otitis media with viscous middle ear effusion containing many eosinophils, who were also under treatment for bronchial asthma, were studied. The following examinations were conducted: nasopharyngeal endoscopy, pure-tone audiometry, eustachian tube function test, temporal bone CT scan, blood analysis, bacterial and fungal culture of middle ear effusion, histological study of the middle ear and nasal specimens, and measurement of eosinophilic cationic protein (ECP) in middle ear effusion. Results: Some patients had persistent perforation with papillomatous granulation tissue arising from the mesotympanic mucosa, and all the patients had nasal polyposis. The pure-tone audiometry showed the mixed-type of hearing loss in all the patients, and the hearing level deteriorated progressively during the course in some patients. The eustachian tube function was not always poor but was patulous in some cases. The most severely diseased areas were in the eustachian tube and mesotympanum by temporal bone CT images. All the seven patients had the high levels of total serum IgE, but the RAST scores were negative in three patients and low grade in three patients. The accumulation of eosinophils was observed in middle ear effusion, middle ear mucosa and nasal polyps, and the eosinophils were highly activated with degranulation. High level of ECP was also recovered from middle ear effusion. Conclusions: Active eosinophilic inflammation occurs in the entire respiratory tract, including the middle ear in these patients. From our present investigation, we propose the criteria and clinical characteristics of ‘eosinophilic otitis media’.

Allergy to Dermatophagoides in a Group of Spanish Gypsies: Genetic Restrictions

Background: Spanish gypsies have traditionally lived as nomads, a reason why few epidemiological studies were done in this ethnic group. However, the high prevalence of asthmatic diseases demonstrated in a population residing in the North of Spain induces us to analyse whether it was due to the influence of genetic loci previously implicated in other population studies as causing the disorders. Methods: DRB1* and DQB1* HLA class II, TCR-Vα8.1, FcΕRI-β Rsa I exon 7 and intron 2, TNF-β (LTα-Nco I) and CD14, were tested for association with asthma and atopy by multiple regression analysis, in 5 families comprising 87 individuals. Results: Significant associations were found with DQB1*02 (p = 0.02) and DQB1*0301 (p = 0.008) and elevated levels of total serum IgE. A negative association (p = 0.02) was found between total serum IgE and DRB1*14. FcΕRI-β Rsa I-In2 allele 1 was associated with high levels of total serum IgE (p = 0.04). Levels of Der p 1 IgE antibodies were negatively associated with DRB1*11-DQB1*0301 (p = 0.007), and positively with TCR Vα-8 allele 1 (p = 0.04) and with FcΕRI-β Rsa I-In2 allele 1 (p = 0.009). Conclusions: Our results do not show any association between asthma and the genetic loci studied although they do suggest the existence of multiple genetic influences on the allergic response in these families.

Lacto-N-fucopentaose III found on Schistosoma mansoni egg antigens functions as adjuvant for proteins by inducing Th2-type response.

We have recently demonstrated that induction of Th2 responses by Schistosoma mansoni egg Ag is largely due to carbohydrates on the Ag functioning as adjuvants. Lacto-N-fucopentaose III (LNFPIII), a polylactosamine sugar, is the predominant carbohydrate found in S. mansoni egg Ag. Therefore, using neoglycoprotein, we investigated whether LNFPIII induces in vivo Th2 response and functions as an adjuvant. Following intranasal immunization with LNFPIII linked to human serum albumin (HSA) (HSA-LNFPIII), BALB/c mice mounted a strong Th2 response and produced significantly higher levels of total IgE as well as HSA-specific IgG, IgG1, and IgE. HSA-LNFPIII was over 1000-fold more potent in inducing Ab production as compared with HSA alone. Although LNFPIII itself did not function as an epitope for either IgG or IgE, its conjugation with protein was essential for the adjuvant activity. Moreover, fucose residue on LNFPIII was crucial for induction of Ab production. Nasal lymphocytes from mice immunized with HSA-LNFPIII produced IL-4, IL-5, and IL-10, but not IFN-gamma following in vitro stimulation with HSA or HSA-LNFPIII. In addition, these activated nasal lymphocytes also showed a significant increase of B7-2 expression on B220-positive cells. Furthermore, not only intranasal but also both i.p. and s.c. immunization with HSA-LNFPIII induced significant production of HSA-specific Abs compared with the immunization with HSA alone, suggesting that the activity of LNFPIII was not restricted on particular route of immunization. These results demonstrate that Lewis type carbohydrate LNFPIII can function as an adjuvant by their ability to induce a Th2 response.

Glutathione S-transferase genotypes and allergic responses to diisocyanate exposure.

Diisocyanates are the most common low molecular weight chemicals to cause occupational asthma. However, only some 5-10% of exposed workers develop asthma, which suggests an underlying genetic susceptibility. Diisocyanates and their metabolites may be conjugated with glutathione by glutathione S-transferases (GSTs). We examined whether polymorphisms in the GSTM1, GSTM3, GSTP1 and GSTT1 genes modify allergic responses to diisocyanate exposure. The study population consisted of 182 diisocyanate exposed workers, 109 diagnosed with diisocyanate-induced asthma and 73 without asthma. Lack of the GSTM1 gene (null genotype) was associated with a 1.89-fold risk of diisocyanate-induced asthma [95% confidence interval (CI) 1.01-3.52]. Moreover, among the asthma patients, the GSTM1 null genotype was associated with lack of diisocyanate-specific immunoglobulin (Ig)E antibodies [odds ratio (OR) 0.18, 95% CI 0.05-0.61] and with late reaction in the specific bronchial provocation test (OR 2.82, 95% CI 1.15-6.88). Similarly, GSTM3 AA genotype was related to late reaction in the specific bronchial provocation test (OR 3.75, 95% CI 1.26-11.2). The GSTP1 Val/Val genotype, on the other hand, was related to high total IgE levels (OR 5.46, 95% CI 1.15-26.0). The most remarkable effect was seen for the combination of GSTM1 null and the GSTM3 AA genotype which was strongly associated with lack of diisocyanate-specific IgE antibodies (OR 0.09, 95% CI 0.01-0.73) and with late reaction in the bronchial provocation test (OR 11.0, 95% CI 2.19-55.3). The results suggest, for the first time, that the polymorphic GSTs, especially the mu class GSTs, play an important role in inception of ill effects related to occupational exposure to diisocyanates.

Total and specific IgE in nasal polyps is related to local eosinophilic inflammation

Background: Nasal polyps (NPs) are characterized by eosinophilic inflammation and often coexist with asthma. However, the role of atopy and IgE in NP pathogenesis is unclear. Objective: We sought to determine whether there is an association between total and specific IgE to a variety of allergens in polyp and nonpolyp tissue and markers of eosinophilic inflammation or skin test results. Methods: Homogenates were prepared from nasal tissue of 20 patients with NPs and 20 patients without NPs and analyzed for concentrations of IL-5, IL-4, eotaxin, leukotriene (LT) C4/D4/E4, sCD23, and histamine (ELISA). Eosinophil cationic protein (ECP), tryptase, and total and specific IgE for inhalant allergens and Staphylococcus aureus enterotoxins were measured (ImmunoCAP). Results: The concentrations of total IgE, IL-5, eotaxin, ECP, LTC4/D4/E4, and sCD23 were significantly higher in NP tissue compared with nonpolyp tissue. Total IgE was significantly correlated to IL-5, ECP, LTC4/D4/E4, and sCD23 and to the number of eosinophils in NPs. On the basis of the presence of specific IgE antibodies in tissue, 3 NP groups were defined. NP group 1 demonstrated no measurable specific IgE, and NP group 2 selected specific IgE. The third group demonstrated a multiclonal specific IgE, including IgE to S aureus enterotoxins, a high total IgE level, and a high prevalence of asthma. Conclusions: These studies suggest that there is an association between increased levels of total IgE, specific IgE, and eosinophilic inflammation in NPs, which may be of relevance in the pathophysiology of nasal polyposis. Similarly, the presence of specific IgE to staphylococcal enterotoxins A and B also points to a possible role of bacterial superantigens. (J Allergy Clin Immunol 2001;107:607-14.)

The role of cockroach allergens in asthma.

Cockroach allergy has been recognized as an important cause of asthma. Cockroach asthma has been described as a more severe disease, associated with perennial symptoms and high levels of total IgE. Cockroaches produce several allergens that induce sensitization, and exposure to high levels of cockroach allergens in the home is a major risk factor for symptoms in sensitized individuals. Previously identified allergens from Blattella germanica and Periplaneta americana, the most important domiciliary species, include Bla g 2 (inactive aspartic protease), Bla g 4 (calycin), Bla g 5 (glutathione-S-transferase), Bla g 6 (troponin), the Group 1 cross-reactive allergens Bla g 1 and Per a 1, Per a 3 (arylphorin), and Per a 7 (tropomyosin). Strategies for decreasing environmental exposure to cockroach have been recently investigated. The results suggest that a sustained decrease in cockroach allergen levels is difficult to accomplish, even after successful extermination of cockroach populations. Cockroach allergens have been cloned and produced as recombinant proteins in high-level expression vectors. The use of recombinant cockroach allergens should allow mechanisms of cockroach-induced asthma to be investigated and may lead to the development of new approaches to asthma treatment in the future.

Prevalence of IgE antibodies to an extract from rubber tree (Hevea brasiliensis) latex and recombinant pollen allergens (Phl P 1, Phl P 2, Phl P 5, Bet v 1 and Bet v 2) in the sera of Italian atopic patients

Previous studies have reported cross-reactivity between latex and grass allergens. Inhibition studies have indicated cross-reactivity of IgE with latex and grass pollen proteins. A panel consisting of a few recombinant allergens, namely rPhI p 1, rPhl p 2, rPhl p 5 and profilin, was sufficient to diagnose grass pollen allergy in patients allergic to grass pollen. Serum samples from 528 consecutive outpatients with IgE antibodies towards at least one allergen (IgE level > 0.35 kAU/L) were selected for this retrospective study. Total and specific serum IgE to rPhl p 1, rPhl p 2, rPhl p 5, rBet v 1, rBet v 2, latex, birch, hazel, mugwort, wall pellitory, Dermatophagoides pteronissinus, Alternaria tenuis, cat and apple were measured by the immunoenzymatic capsulated hydrophilic carrier polymer (CAP) FEIA system (Pharmacia & Upjohn). Of 123 polysensitized patients with antilatex Ig1E, 12 (9.76%) had symptoms after latex exposure. Ten of 12 subjects monosensitized to latex had symptoms after latex exposure. Symptomatic patients had higher IgE levels to latex than symptomless patients (P = 0.046). A higher prevalence of antilatex IgE was seen in sera containing specific IgE to rPhl p 1, rPhl p 5 and rBet v 2. A good correlation (Spearman's r = 0.52; P = 0.001) between high levels of antilatex IgE and total serum IgE was found. The findings of the present study may support the concept that a high proportion of sera containing IgE to rBet v 2, rPhl p 1 and rPhl p 5 simultaneously contain antilatex IgE. Therefore, patients with specific IgE to these recombinant allergens with no history of current latex exposure may need additional evaluation.

What are the candidate groups for pharmacotherapeutic intervention to prevent asthma?

Despite the development of many new therapies for the treatment of asthma, the prevalence of this disease is still increasing in many areas of the world. Today no intervention is able to completely cure asthma but chronic therapies could decrease its severity. Moreover, asthma is one of the most common chronic diseases of childhood and its pharmacoeconomic burden is huge. Epidemiologic studies have identified some of the major factors involved in the pathogenesis and evolution of asthma. Several prevention programs have been developed in different countries with various success rates. Most of those interventions were based on allergen avoidance. From studies aimed at controlling early asthma and from epidemiologic data, we have learned to identify high-risk groups, e.g, the atopic child with allergic asthma, with a family history of asthma or allergy-related disease and early sensitization to aeroallergens. Only a few prospective studies aimed at preventing the onset of asthma have been published. With ketotifen, Iikura et al. could prevent the onset of asthma after a 1-year period in patients suffering from atopic dermatitis. Another study has been published by Bustos et al. concerning children with a family history of allergy and high total IgE levels. Those studies involved about 100 patients. No follow-up data has been published for either of them. Recently, the first results from the ETAC (Early Treatment of the Atopic Child) trial have been reported. This study involved 817 atopic children with atopic dermatitis and a family history of atopy: cetirizine halved the number of patients developing asthma in the subgroups (200 children) sensitized to house dust mite (51.5% versus 28.6%) or pollen (58.8% versus 27.8%). The optimal target for pharmaceutical intervention to prevent asthma would seem to be high risk patients: children with atopic dermatitis, a family history of asthma or atopic disease and early sensitization to aeroallergens. Primary prevention in whole populations (e.g. starting even before the onset of atopic dermatitis or allergen sensitization) does not at present appear to be a realistic approach.

Atopy and asthma genes--where do we stand?

Atopy and asthma genes--where do we stand?