Summary Background Maize allergy is not very common especially in Europe. The number of studies that address IgE mediated maize allergy is all too few. Objective Evaluate subjects with a history of maize allergy by double‐blind, placebo‐controlled food challenge; identify the spectrum of symptoms manifested during challenge; determine the lowest provocation dose (PD) during challenge; determine the performance characteristics of maize skin prick test and specific IgE. Methods Twenty‐seven patients with a history of maize allergy were enrolled to be evaluated by skin test, specific IgE and double‐blind placebo‐controlled maize challenge. Results Forty‐eight percent of the patients were challenge positive. PD range was 0.1–25 g. Fifty‐four percent of the maize allergic subjects had a PD that was 2.5 g; two subjects reacted to 100 mg of maize. Comparison of maize specific IgE levels and skin test results to the challenge results revealed the following (specific IgE level/skin testing): sensitivity 1.00/0.846, specificity 0.077/0.384, positive predictive value 0.520/0.579, and negative predictive value 1.00/0.714. Conclusion Maize is a cause of IgE‐mediated allergic reactions to foods in adults and children. Nearly half of the subjects recruited were confirmed by challenge to be allergic to maize. Twenty‐three percent of the positive challenge patients manifested symptoms that involved two organ systems, thus fulfilling the criteria for maize induced anaphylaxis. Maize is allergenic and can pose a risk for symptomatic food allergy at a dose of 100 mg.

Background: Wheat is believed to be an uncommon cause of food allergy in adults; the number of studies that address IgE mediated wheat allergy in adults is all too few.Objective: Determine how many subjects with a history of wheat allergy have real allergy by double-blind, placebo-controlled food challenge; identify the symptoms manifested during the challenge; determine the lowest provocation dose; determine the performance characteristics of wheat skin prick test and specific IgE; identify subjects with real wheat allergy for potential immunoblotting studies.Methods: Patients underwent skin test with commercial wheat extract; specific wheat IgE was determined. Subjects were challenged with 25 g wheat. Subjects who were positive to raw wheat challenge underwent cooked wheat challenge. Results: Thirty-seven double-blind placebo-controlled wheat challenges were performed on 27 patients. A total of 13 of 27 (48%) patients had a positive result. Eleven subjects with positive raw wheat challenge underwent cooked wheat challenge: 10 were positive. The provocation dose range was 0.1 to 25 g. Twenty-seven percent of the subjects allergic to wheat had a provocation dose that was <= 1.6 g.Conclusion: Wheat causes real food allergy in adults. More than a quarter of the patients allergic to wheat reacted to less than 1.6 g wheat. Specific IgE was more sensitive than skin test for wheat; however, specificity and predictive values were low for both tests. Thus, these tests should not be used to validate diagnosis of wheat allergy.

In HIV-1–infected adults, eosinophilia, increased eosinophil cationic protein (ECP), and elevated serum total IgE levels have been observed. 1Paganelli R Scala E Mezzaroma I Pinter E D’Offizi G Fanales-Belasio E et al.Immunologic aspects of hyperimmunoglobulinemia E-like syndrome in patients with AIDS.J Allergy Clin Immunol. 1995; 95: 995-1003Abstract Full Text Full Text PDF PubMed Scopus (55) Google Scholar There is little data with respect to these factors in children. Our previous study showed a relationship between elevated serum total IgE level and HIV-1 disease progression in pediatric patients. 2Viganò A Principi N Crupi L Onorato J Zuccotti GV Salvaggio A. Elevation of IgE in HIV-infected children and its correlation with the progression of disease.J Allergy Clin Immunol. 1995; 95: 627-632Abstract Full Text Full Text PDF PubMed Scopus (88) Google Scholar The objective of the present study was to define whether eosinophil involvement together with IgE elevation could be identified in HIV-1–infected children. The study group consisted of 38 vertically HIV-1–infected subjects (median age, 6.5 years; range, 1 to 13 years; 15 boys), 15 of whom had acute respiratory infections (ARIs) at enrollment. The diagnosis of HIV-1 infection and the clinical and immunologic status of children met the criteria of the 1994 Centers for Disease Control (CDC) HIV classification for children. 3Centers for Disease Control Classification system for human immunodeficiency virus (HIV) infection in children under 13 years of age.MMWR Morb Mortal Weekly Rep. 1994; 43: 1-10Google Scholar As regards clinical classification, 26 subjects were in classes N, A, or B (19 without ARIs and 7 with ARIs), whereas 12 were in class C (4 without ARIs and 8 with ARIs); as regards immunologic classification, 24 children were in classes 1 and 2 (18 without ARIs and 6 with ARIs), whereas 14 were in class 3 (5 without ARIs and 9 with ARIs). None of the class N patients was receiving antiretroviral therapy; patients in classes A and B were being treated with zidovudine, whereas patients in class C were taking zidovudine and didanosine. 4Pizzo PA Wilfert C. Antiretroviral therapy for infection due to human immunodeficiency virus in children.Clin Infect Dis. 1994; 19: 177-196Crossref PubMed Scopus (20) Google Scholar When needed, patients were receiving specific prophylaxis for opportunistic infections in agreement with published guidelines. 4Pizzo PA Wilfert C. Antiretroviral therapy for infection due to human immunodeficiency virus in children.Clin Infect Dis. 1994; 19: 177-196Crossref PubMed Scopus (20) Google Scholar According to the definition of Kline et al, 5Kline MW Paul ME Bohannon B Kozinetz CA Shearer WT. Characteristics of children surviving to 5 years of age or older with vertically acquired HIV infection.Pediatr AIDS HIV Infect: Fetus Adolesc. 1995; 6: 350-353PubMed Google Scholar among our HIV-1–infected children, 12 subjects had rapidly progressing disease (4 without ARIs and 8 with ARIs), whereas 26 patients had nonrapidly progressing disease (19 without ARIs and 7 with ARIs). As control subjects, 70 HIV-1–negative children (median age, 5.5 years; range, 1 to 13 years; 28 boys), 26 of whom had ARIs at enrollment, were studied. To avoid the possible increase of eosinophil counts, serum ECP, and IgE concentrations caused by allergic activation, in both HIV-1–infected children and control subjects eligibility criteria included a negative personal and family history of atopy. Each child was concomitantly evaluated for whole blood cell count by means of an automated hematology analyzer (Coulter Electronics, Inc, Miami Lakes, Fla), serum ECP concentrations by means of an RIA (Pharmacia ECP RIA, Pharmacia, Uppsala, Sweden), total serum IgE by immunocapture (Pharmacia CAP System IgE RIA, Pharmacia), allergy to common airborne and food allergens by means of skin prick tests, and individual and family history of atopy by means of a medical history. The diagnosis of ARI (both bacterial and viral) was based on clinical findings, radiologic data, and microbiologic isolation of pathogens, according to standardized conventional methods. A diagnosis of pneumonia was made in 8 HIV-1–infected children and 7 control subjects, rhinosinusitis in 3 HIV-1–infected children and 8 control subjects, acute tracheobronchitis in 2 HIV-1–infected children and 8 control subjects, and acute otitis media in 2 HIV-1–infected children and 3 control subjects. Informed consent was obtained from the parents or legal guardians of all the children. Comparison between groups were performed with the Mann-Whitney U test. In both HIV-1–infected children and control subjects, none of the subjects had a positive family history of atopy, none had allergy since birth, and none had positive skin prick test responses. Table I summarizes eosinophil counts, serum ECP concentrations, and serum IgE levels in the study population. Table IEosinophil counts, serum ECP concentrations, and serum IgE levels in the study populationLaboratory parametersNo ARIARIHIV-1–infected subjects (n = 23)Control subjects (n = 44)HIV-1–infected subjects (n = 15)Control subjects (n = 26)Eosinophil counts (cells/μL) Median130160190180 Range25-330110-27552-50091-492Serum ECP (μg/L) Median9 *12 †2020 Range4-209-1313-3414-41Serum IgE (KU/L) Median58 ‡19166 §29 Range2-18111-2817-200015-40* P < .0001 versus HIV-1–infected children with ARIs † P = .0002 versus control subjects with ARIs. ‡ P = .03 versus control subjects without ARIs § P = .02 versus control subjects with ARIs. Open table in a new tab Eosinophil counts and serum ECP concentrations showed no significant differences between HIV-1–infected children and control subjects either with or without ARIs, whereas IgE levels were significantly increased in HIV-1–infected children. Independent from HIV-1 status, ECP concentrations were significantly higher in patients and control subjects with ARIs in comparison to those without ARIs, whereas eosinophil counts and IgE levels showed no significant differences in the presence or absence of ARIs. Table II describes the relationship between laboratory parameters and CDC setting in HIV-1–infected children. Table IILaboratory parameters and CDC setting in HIV-1–infected childrenCDC settingCDC clinical classesCDC immunologic classesN+A+B (n = 26)C (n = 12)P value1+2 (n = 24)3 (n = 14)P valueEosinophil counts (cells/μL) Median158141.42130142.55 Range46-50025-29046-38025-500Serum ECP (μg/L) Median1420.061119.02 Range4-306-344-306-27Serum IgE (KU/L) Median64197.0229296.02 Range2-147715-20002-14776-2000 Open table in a new tab With respect to clinical setting, patients in clinical class C showed higher, even if not significantly increased, levels of serum ECP and significantly increased concentrations of serum IgE than subjects in clinical classes N, A, and B. On the contrary, eosinophil counts were similar between children in clinical class C and those in clinical classes N, A, and B. With respect to the degree of immunodeficiency, patients in immunologic class 3 showed a significant increase of both serum ECP and IgE concentrations than subjects in immunologic classes 1 and 2. On the contrary, eosinophil counts were similar between children in immunologic class 3 and those in immunologic classes 1 and 2. Table III shows the relationship between laboratory parameters and HIV-1 disease progression. Table IIILaboratory parameters and HIV-1 disease progressionLaboratory parametersHIV-1 disease progressionRapid progression (n = 12)Nonrapid progression (n = 26)P valueEosinophil counts(cells/μL) Median166137.27 Range25-50046-360Serum ECP (μg/L) Median209.0002 Range14-344-30Serum IgE (KU/L) Median31643.004 Range26-20002-545 Open table in a new tab Interestingly, serum ECP and IgE concentrations were significantly higher in subjects with rapidly progressing disease than in those with nonrapidly progressing disease, whereas no significant difference was observed in eosinophil counts between the 2 groups of children. Our findings show that eosinophilia is not a feature of HIV-1–infected children, even in the presence of increased serum ECP and IgE concentrations. There are discordant data on eosinophil involvement in HIV-1–infected patients. In adults an increase of eosinophil counts in peripheral blood during HIV-1 infection has been shown. 1Paganelli R Scala E Mezzaroma I Pinter E D’Offizi G Fanales-Belasio E et al.Immunologic aspects of hyperimmunoglobulinemia E-like syndrome in patients with AIDS.J Allergy Clin Immunol. 1995; 95: 995-1003Abstract Full Text Full Text PDF PubMed Scopus (55) Google Scholar In HIV-1–infected children, Bacot et al, 6Bacot BK Paul ME Navarro M Abramson SL Kline MW Hanson IC et al.Objective measures of allergic disease in children with human immunodeficiency virus infection.J Allergy Clin Immunol. 1997; 100: 707-711Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar in agreement with our results, failed to show a significant increase in eosinophil counts. As regards ECP, increased levels of this protein in both atopic and nonatopic HIV-1–infected adults either in the presence or absence of eosinophilia have been described. 1Paganelli R Scala E Mezzaroma I Pinter E D’Offizi G Fanales-Belasio E et al.Immunologic aspects of hyperimmunoglobulinemia E-like syndrome in patients with AIDS.J Allergy Clin Immunol. 1995; 95: 995-1003Abstract Full Text Full Text PDF PubMed Scopus (55) Google Scholar To our knowledge, this is the first report on the measurement of serum ECP in HIV-1–infected children. In our study serum ECP concentrations seem to be increased in children with ARIs independent of HIV-1 status and in HIV-1 infected children in clinical class C, in immunologic class 3, and with rapid progression of the disease. However, because of the high incidence of ARIs in our children with severe HIV-1 disease, we cannot finally establish whether the increase in serum ECP level is only a consequence of ARI or also represents a marker of HIV-1 disease progression. Further studies are necessary to clarify the significance of these data. Findings regarding IgE levels confirm our previous study in which elevated serum total IgE concentrations appeared as evidence of the immunologic abnormalities caused by HIV-1 infection in pediatric patients. 2Viganò A Principi N Crupi L Onorato J Zuccotti GV Salvaggio A. Elevation of IgE in HIV-infected children and its correlation with the progression of disease.J Allergy Clin Immunol. 1995; 95: 627-632Abstract Full Text Full Text PDF PubMed Scopus (88) Google Scholar In conclusion, HIV-1 infection does not seem to produce eosinophilia in children at baseline and with ARIs. On the contrary, eosinophil activation appears to be related to ARI and may also be associated with severe HIV-1 disease; moreover, serum IgE levels are increased in children with HIV-1 disease progression.

We evaluate correlations among airway resistance measured by the interrupter method with a new device (Microlab 4000, Micromedical) with those of standard pletismography. Twenty-two healthy children (mean age 10 +/- 3 yrs) without any remote or recent history of lung disease were enrolled in this study. All baseline values of lung function were within normal limits confirming health conditions. A highly significant degree of linear correlation was found between inspiratory (Rint-i) resistance of the interrupter method and all the pletismographic measurments (Raw-i r = 0.74, Raw-e r = 0.82, Raw-t r = 0,81, s-Gaw r = 0,73) and to a lesser extent with flows (FEV1 r = 0,61, FEF50 r = 0,73). A similar correlation was found with reciprocal of Rint, Gint-i except for FEV1; in contrast no statistical correlations were found between expiratory resistance (Rint-e) and pletismographic parameters except for Raw-i (r = 0,64); on the contrary Gint-e shows significant correlations with all parameters measured except for s-Gaw.These results,obtained in normal healthy well collaborating children, allow us to conclude that eventhough more and larger studies are necessary to better standardize the interrupter technique, this new device is able to bring new informations about the lung function in children.

Serum level of pro-inflammatory cellular markers such as eosinophil cationic protein (s-ECP), neutrophil myeloperoxidase (s-MPO) and mast cell tryptase (s-TRI) have been analysed in a group of 80 children who were subdivided in 3 subgroups according to the underline pathology: a) allergic asthma, b) infective wheezing, c) atopic dermatitis or eczema. These children were compared with an adeguate sex-, age mathched group of normale controls. Each patient was further assigned to symptomatica (S) or asymptomatic (As) subgroups on the basis of the presence or absence of specific acute symptoms. At entry, illness severity was accurately assessed to correlate clinical status with the markers serum levels. s-ECP has been found elevated in all the symtomatic groups unregardless of the type of disease (asthma, wheezing or atopic dermatitis) and of the etiology (allergic asthma or infective wheezing) (s-ECP: mu g/L allergic asthma S = 43 +/- 34; AS = 22 +/- 12; C = 8 +/- 3; S vs As p < 0.05; S vs C p < 0.0005; As vs C NS; infective wheezing S = 28 +/- 13, As = 17 +/- 12, C = 10 +/- 3, S vs As p < 0.01, As vs C NS, atopic dermatitis S = 49 +/- 13, As = 20 +/- 11, C = 10 +/- 3, S vs As p < 0.01, S vs C p < 0.002, As vs C NS). s-MPO has been found statistically significant only in acute wheezing and acute atopic dermatitis vs normal controls, whereas no statistically differences has been found in allergic asthma (s-MPO mu g/l: allergic asthma S = 1180 +/- 448; As = 841 +/- 500; C = 596 +/- 217; S vs As NS; S vs CNS; As vs CNS; infective wheezing S = 1142 +/- 385; As = 1386 +/- 364; C = 665 +/- 384; S vs As NS; S vs C p < 0.005; As vs C p < 0.01; atopic dermatitis S = 1474 +/- 292; As = 1011 +/- 604; C = 665 +/- 384; S vs As NS; S vs C p < 0.005; As vs C NS); those results on one side confirm the role of neutrophils during infections even viral one's, but on the other side demonstrate a lesser involvement in allergic diseases. s-Tryptase was always found at lower levels of the capacity detenction of the test in all situations analysed; this surprisingly result confirm same other data present in literature. In conclusion our results confirm the usefulness, at least for s-ECP and s-MPO, as pro-inflammatory activity markers well correlated with disease activity; nevertheless, our data that at least for s-ECP a not specific rise according to etiology (allergy or infection). s-MPO seems more reliable as an activity marker of infective processes than allergic one's More data are necessary to better define the role of neutrophils in allergic diseases. Data about s-TRY from our study didn't allow us to consider it as a reliable marker of allergic disease activity. Therefore more data on larger number of patients are needed to better define the role and usefulness of these markers both in allergic and infectious diseases.