Focal lesion in the splenium of the corpus callosum in epileptic patients: antiepileptic drug toxicity?

Although the prevalence of asthma has risen significantly during the last 30 yr, it is not clear whether this has occurred primarily in persons with a strong genetic predisposition to asthma and atopy or in other sections of the population. We have investigated outcomes in children of nuclear families selected through probands previously characterized by studies in 1964 and 1989 as having histories of persistent childhood onset atopic asthma, transient childhood wheezy bronchitis, and no respiratory symptoms or atopy. Children of wheezy bronchitic probands had a significantly better symptomatic outcome in adolescence, irrespective of the atopic status of the parent proband, than do children of either asthmatic or asymptomatic probands, suggesting that this may be a syndrome that shows familial aggregation and is distinct from asthma. Total serum IgE levels were significantly lower in children of nonatopic asymptomatic probands, including those with wheezing symptoms. In contrast children of nonatopic asymptomatic probands had an unexpectedly high prevalence of wheezing (33%), positive skin prick tests (56%), and positive specific serum IgE to common allergens (48%) that was similar to that found in children of atopic asthmatic probands. Our findings support the concept that wheezy bronchitis is a separate syndrome from atopic asthma. High total serum IgE levels within our population appear to be an important marker of genetic predisposition to atopy. Our data also suggest that much of the increase in asthma prevalence is associated with specific IgE sensitization and is occurring in persons previously considered to be at low risk of developing asthma or atopy.     

Treatment of recurrent corneal erosion using phototherapeutic keratectomy with the excimer laser

Tachyphylaxis to methacholine has been reported in nonasthmatic subjects. In a recent study on the prevalence of airway hyperresponsiveness (AHR) and atopy, we performed duplicate methacholine inhalation tests at a 60-min interval, in subjects with symptomatic asthma (n = 33), asymptomatic AHR (AAHR) (n = 72) and in a group of normal subjects (n = 130); 135/235 subjects were atopic. All subjects had a respiratory questionnaire, allergy skin prick tests, blood eosinophil counts and determination of total serum IgE level. In asthmatic subjects, PC20 just failed to be significantly higher on a second methacholine challenge (p = 0.09); when they were stratified according to severity of AHR and use of inhaled corticosteroids, we observed a significant increase in PC20 on the second test in asthmatic subjects with mild AHR not using corticosteroids (p < 0.01). In normal controls, PC20 methacholine was slightly increased on rechallenge (p < 0.01) as it was in those with AAHR (p < 0.01). There was no relationship between the magnitude of the change in PC20 and age, sex, baseline airway responsiveness, percent fall in FEV1 on the first challenge, atopic score, blood eosinophil counts and serum IgE levels. In conclusion, tachyphylaxis to methacholine is observed in normal or mild asthmatic subjects not using inhaled corticosteroids and in subjects with AAHR; however, in most subjects this change is of a small magnitude.     

The effect of T cell depletion with Campath-1M on immune reconstitution after chemotherapy and allogeneic bone marrow transplant as treatment for leukaemia

Thirty asthmatic children were examined allergic reaction against egg white, gelatin and vaccine solution before and after vaccination using skin prick test. We also measured the levels of specific IgE and IgG antibody against gelatin. The changes in clinical symptoms before and after vaccination were investigated in 25 asthmatic children by evaluating symptom and treatment score. The results were as follows; 1. In one subject who had delayed type of skin reaction to gelatin, the adverse reaction was also recognized at the skin site around 24 hrs after vaccination. In this subject, the levels of serum specific IgE and IgG to gelatin became positive after 5 months. 2. Specific IgE antibodies to gelatin were not detected in all subjects before and after vaccination. 3. The mean values of asthma symptom score before and after vaccination were 3.3 +/- 4.2 and 1.5 +/- 3.3 respectively. Those of treatment score before and after vaccination were 75.6 +/- 35.2 and 76.0 +/- 35.0 respectively. These results suggest that skin testing with gelatin and vaccine solution is useful as a screening method for predicting adverse reactions in asthmatic children and that influenza vaccination can be performed safely in skin test negative children.     

Pathogenicity and lethality of a minute intestinal fluke, Neodiplostomum seoulense, to various strains of mice

Atopy is a genetically determined disorder that affects 10%-20% of the population. Many symptoms of patients with atopy (allergic rhinitis, conjunctivitis, asthma, and anaphylaxis) result from events occurring after crosslinking of cell-bound IgE by per se innocuous environmental antigens. The frequently raised hypothesis that autosensitization can also be a pathogenetic factor in atopy, gained support by our recent demonstration of IgE antibodies against human proteins in atopic dermatitis patients. To unravel the molecular nature of IgE-defined autoantigens, we used serum IgE from atopic dermatitis patients to screen a human epithelial cDNA expression library. One of the cDNA-encoding IgE-reactive products contained 1501 bp of a 2274 bp open-reading frame finally identified by sequence analysis of two additional cDNA clones resulting from oligonucleotide screening. The IgE-defined autoantigen, designated Hom s 1, exhibited an almost complete sequence identity with a recently described antigen recognized by cytotoxic T cells of a squamous cell carcinoma patient. Purified recombinant Hom s 1 specifically bound IgE from patients with severe atopy. When used as immunogen in rabbits, recombinant Hom s 1 gave rise to an anti-serum that reacted with a cytoplasmic protein exhibiting a broad cellular and tissue reactivity (skin, lung > gastrointestinal tract > muscle, brain) and identified a 55 kDa protein in blotted serum IgE preparations. The attractive possibility remains that the Hom s 1-triggered IgE response contributes to the events resulting in allergic tissue inflammation. If so, the respective recombinant molecule may serve as a paradigmatic tool for the diagnosis and treatment of patients with "intrinsic" atopy.     

The current role of high-resolution ultrasonography of the hand and wrist in rheumatic diseases

BACKGROUND: We have started a large birth cohort study in which pregnant women with and without atopy are differentially included. In view of the large number of subjects to be screened (12000), a simple questionnaire was developed for the assessment of atopy in pregnant women. OBJECTIVE: The objective of our study was to evaluate the efficacy of a questionnaire using serum IgE tests. METHODS: During a antenatal visit to the midwife clinic, 175 expecting mothers completed a questionnaire and from each subject blood was obtained in which total and specific IgE against house dust mite, cat, dog, birch and grass was determined. RESULTS: When atopy was defined as the presence of a positive test for IgE against at least one allergen, seven questions from the questionnaire had a sensitivity and specificity of 55.0% and 88.7%, respectively. With the use of the questionnaire it was possible to select about 50% of the subjects with specific IgE to one or more common inhalant allergens. The positive predictive value of the screening questions was 71.7%. Taking total IgE into account did not change these results. CONCLUSION: The screening questionnaire is an efficient tool for differential inclusion of subjects with and without atopy in epidemiological studies.     

Anti-IgE autoantibodies in asthma: a diagnostic artefact or an explanation for non-allergic asthma?

Autoantibodies to IgE can be detected in sera of individuals with atopic disease, but occasionally elevated levels are also found in sera of normal individuals. During the last years we studied therefore the functional properties of such autoantibodies. Depending on the studied in vitro system one can always detect minimally two different antibody types. Antibodies have been found that either trigger or inhibit mediator release from basophils, that enhance or inhibit binding of IgE to the low IgE receptor and either stimulate or inhibit human IgE synthesis. Based on such in vitro experiments one may conclude that also in vivo autoantibodies exist that either neutralize IgE or have no effect on IgE mediated clinical events. Thus, anti-IgE autoantibodies may hide IgE as for example in those bee sting allergic individuals where we could not detect specific IgE but found IgE hidden within immune complexes, suggesting that the biological activity of IgE was not neutralized. A similar phenomenon may exist in asthmatic individuals. In a recent study we found that non-atopic asthmatic children had indeed low levels of serum IgE, but showed the same levels of autoantibodies to IgE, against suggesting that IgE was hidden within immune complexes. Thus, our ongoing research addresses the question whether in diseases of unclear atopic origin IgE may nevertheless play a critical role but based on possible artefacts in the IgE detection assays some of the clinically relevant IgE may escape.     

The prevalence of atopy and hypersensitivity to latex in medical laboratory technologists

Members of the Alberta Society of Medical Laboratory Technologists were invited to take part in a study of sensitivity to latex gloves. A total of 230 persons volunteered; 108 (47%) had no problems with gloves, and 122 (53%) reacted to latex gloves. A history was obtained regarding atopy, smoking, years in laboratory medicine, and the nature of the problem with latex gloves. Serum was assayed for the total IgE level and the presence of IgE with specificity to common inhalant allergens and to latex. The affected group had an increased population of subjects with an atopic history and a higher incidence of a raised IgE level and a positive screen for inhalant allergens. In the affected group, there was no relationship between the total IgE level and severity of skin reaction. However, smoking was related to severity of reaction and was more common in the groups with a more severe reaction. Three subjects were positive for IgE specific for latex; there were no other data distinguishing them from latex-negative subjects.     

Spontaneous IgE production in asthmatic children

In this study, we demonstrated spontaneous IgE production by peripheral blood mononuclear cells of asthmatic children. In 26 asthmatic children, the level of spontaneous IgE ranged 0.1-15.0 IU/ml and in 5 healthy normal children showed under 0.051 IU/ml. In 5 of asthmatic children, specific antibody of Dermatophagoides farinae was detected from PBMC by CAP RAST. In healthy normal children, specific antibody of Df was not detected. Spontaneous IgE production by PBMC and serum IgE level showed well correlation (gamma = 0.835, p < 0.001). Spontaneous IgE production and specific antibody of Df by PBMC also showed well correlation (gamma = 0.717, p < 0.001) IgE production of asthmatic children was inhibited by IFN-gamma.     

Atopy and IgE in a pediatric allergy practice

In children under six years of age referred to a pediatric allergy practice the usefulness of serum IgE assay was evaluated in relation to age, symptoms, nasal eosinophilia, skin tests and family history. In more than 60% of the children the initial symptom, usually rhinorrhea, had occurred before one year of age. In infancy the diagnosis was more difficult, gastrointestinal complaints were more frequent and nasal eosinophilia less frequent than in the older children. Many infants had positive skin tests to foods and to environmental allergens. There was a significant correlation between elevated serum IgE level and age, nasaeosinophilia, the number of positive skin tests and the probability of immunotherapy being prescribed. Although no clear diagnostic level is seen, an IgE level above 100 micron/ml at any age and an IgE level above 20 micron/ml in infants strongly suggest the possibility of atopic disease. However, a low IgE level does not exclude atopic disease.     

The relationship between bronchial histamine reactivity and atopic status

It has been proposed that increased production of IgE, a feature of atopy, is a cause of the non-specific bronchial hyper-reactivity that is characterisitc of asthma. This hypothesis was examined by selecting groups of subjects with asthma or rhinitis and a group of healthy control subjects and studying the relationship between their bronchial histamine reactivity and their atopic status. In none of the groups tested was there a significant association between the degree of bronchial histamine reactivity and either the serum level of total IgE or the number of extracts of aeroallergens giving positive prick test reactions.     

Outcome of wheeze in childhood: the influence of atopy

We have previously demonstrated that the adult outcome of childhood asthma differs from that of wheeze occurring only in the presence of infection. This paper examines the role of atopy in relation to outcome. We investigated the atopic status, current symptoms and bronchial reactivity to methacholine of 235 subjects aged 34-40 yrs, originally classified at age 10-15 yrs as having asthma (asthma group), wheeze only in the presence of infection (wheezy group), or no respiratory symptoms (comparison group). Subjects from the original asthma group were more likely to be atopic as defined by skin test reactivity, total serum immunoglobulin E (IgE) measurement or specific IgE radio allergosorbent test (RAST) measurement than those from the wheezy group. The wheezy group differed significantly from the reference group only in RAST results, when other variables were taken into account. In a logistic regression model, the important independent predictors for adult wheezing symptoms were original group, atopy and current smoking. Methacholine responsiveness was independently associated with original group (the asthma group were more likely to respond positively), atopy and female gender. The results suggest that atopy is an important predictor for wheeze and bronchial hyperreactivity in middle age. However, the difference in outcome for children who had asthma compared to those who had wheeze only in the presence of infection cannot be explained by atopy alone.     

Basophil count in neonates is not suitable for atopy predictivity

Basophil granulocytes and their mediators are involved in the pathogenesis of allergic inflammation. We evaluated basophil count, blood histamine content, eosinophil count and serum total IgE levels in one hundred-thirteen healthy newborns at birth. 102 children were prospectively studied with a follow up to 18 months of age for development of atopic disorders. No difference was found in newborns with biparental family history of atopy (FHA) in comparison with newborns with monoparental FHA and with newborns without FHA. Children who developed atopic disorders had neonatal basophil counts higher than those who did not develop atopic symptoms (p = 0.03). No significant correlation was found between basophil and eosinophil counts (rs = 0.013), between basophil count and serum total IgE levels (rs = 0.012) and between basophil count and blood histamine content. Positive predictive value and sensitivity of basophil count for allergy up to 18 months of age was only 33% and 27%, respectively. Our data indicate that an increased basophil count at birth is not associated with FHA and is not a good predictive marker of atopy.     

Airways remodeling is a distinctive feature of asthma and is related to severity of disease

PURPOSE: Airways remodeling, evaluated as the subepithelial layer thickness, was compared in asthmatic patients with that of healthy subjects, and was related to clinical grading of disease, presence of atopy, and length of asthmatic history. SUBJECTS AND METHODS: Thirty-four patients with stable asthma (mean age+/-SD: 26.5+/-9.2 years; 10 female) treated with only inhaled beta2-agonists and eight healthy volunteers (mean age+/-SD: 24.6+/-2.5 years; four female) were recruited for the study. Twenty-seven of 34 asthmatics had atopy. Eleven patients had newly diagnosed conditions (duration of disease < or = 1 year), nine patients had long asthmatic history (> 1 year and < or = 10 years), and 14 had prolonged asthmatic history (> 10 years). Bronchial responsiveness to methacholine (M) was expressed as provocative concentration of M causing a 20% fall in FEV1 (PC20) (mg/mL). Degree of asthma severity was assessed using a 0- to 12-point score based on symptoms, bronchodilator use, and daily peak expiratory flow variability over a 3-week period. Bronchoscopy and bronchial biopsy were performed successfully for all subjects; the subepithelial layer thickness, in biopsy samples, was measured from the base of bronchial epithelium to the outer limit of reticular lamina. RESULTS: In asthmatics, baseline FEV1 values (percent of predicted) ranged from 75.7 to 137.0%, and PC20 M ranged from 0.15 to 14.4 mg/mL. According to the asthma severity score, 14 asthmatics were classified as having mild disease, 14 as having moderate disease, and six as having severe disease. The mean values of subepithelial layer thickness were 12.4+/-3.3 microm (range, 6.8 to 22.1 microm) in asthmatics, and 4.4+/-0.5 microm (range, 3.8 to 5.2 microm) in healthy subjects (p<0.001). Subepithelial layer thickness of those with severe asthma differed significantly from that of patients with moderate and mild asthma (16.7+/-3.1 microm vs 12.1+/-2.7 microm and 10.8+/-2.4 microm, p<0.01 and p<0.003, respectively). Moreover, in asthmatics, degree of thickening was positively correlated to asthma severity score (Spearman rank correlation coefficient [rs]=0.581; p<0.001), and negatively correlated with baseline FEV1 (rs=-0.553; p<0.001) and PC20 M (rs=-0.510; p<0.01). No difference was found between degree of thickening observed in atopic asthmatics, compared with that of nonatopic asthmatics, or between degree of thickening in patients with different lengths of asthmatic history. Lastly, multiple regression analysis revealed that asthma severity score was the significant predictive factor for thickness of subepithelial layer. CONCLUSIONS: We confirmed that airways remodeling is a very distinctive and characteristic pathologic finding of asthma. We also demonstrated that it is related to the clinical and functional severity of asthma, but not to atopy or length of asthmatic history.     

The interaction of IgE antibody with human alveolar macrophages and its participation in the inflammatory processes of lung allergy

After the initial observation that human and animal mononuclear phagocytes can be activated into specific killer cells against larvae of the parasite Schistosoma mansoni by seric IgE antibody from infected patients, a possible interaction of IgE with human alveolar macrophages in asthmatic patients was investigated. In vitro, alveolar macrophages from non-atopic individuals can bind monoclonal IgE molecules, as well as IgE antibody from the serum of patients with respiratory allergy. A subsequent contact with anti-IgE antibody or with the specific allergen induces the extracellular release of a variety of mediators, such as lysosomal enzymes, neutral proteases, or superoxide anion. Due to the presence of allergen-specific IgE antibody on the macrophage surface in situ, the same results were obtained in vitro with freshly purified alveolar macrophages from allergic patients. Disodium cromoglycate, corticosteroids, or beta-adrenergic stimulants are strong inhibitors of this specific exocytosis of physiological mediators. The atopic cells formed rosettes with allergen-coated erythrocytes at 4 degrees C, except after pretreatment with aggregated monoclonal IgE or with the allergen.     

Allergen-induced cytokine production in atopic disease and its relationship to disease severity

The Th2 cytokines, interleukin (IL)-4 and IL-5, have an important role in atopic disease. CD30 is a transmembrane molecule that may be expressed on a proportion of activated T-lymphocytes and has been reported to be a marker for Th2 phenotype. Our objective was to compare the in vitro cytokine responses and CD30 expression of peripheral blood mononuclear cells (PBMCs) to stimulation with house dust mite antigen (Dermatophagoides pteronyssinus) in atopic asthmatics, atopic nonasthmatics, and normal subjects, and to see if atopic asthmatic cytokine production correlated with symptomatic disease activity and whether cytokine production was allergen-specific. Eighteen atopic asthmatics (all were allocated a symptomatic disease score), 6 atopic nonasthmatics, and 7 healthy nonatopic individuals were studied. Resting serum IL-4 levels were measured, then PBMCs were separated using Lymphoprep density centrifugation and cultured in modified RPMI 1640 medium. PBMCs were stimulated with IL-2 alone or with D. pteronyssinus (1,000 subcutaneous units/ml) with IL-2 and harvested after 5 and 10 d. Using monoclonal antibodies and flow cytometry we obtained the percentage of CD4+ T cells expressing CD30 and the intensity of CD30 staining. Culture supernatants were analyzed for IL-4 and interferon gamma (IFN-gamma) using an enzyme-linked immunosorbent assay. In 9 atopic asthmatics PBMCs were also stimulated nonspecifically using phytohemagglutinin (PHA). IL-4 was detectable in the serum of atopic subjects but not in normal subjects. Stimulation of PBMCs with D. pteronyssinus produced significant amounts of IL-4 in atopic asthmatics and atopic nonasthmatics, but minimal quantities in normal subjects. Much lower levels of IFN-gamma were produced by atopic asthmatics in response to D. pteronyssinus compared to atopic nonasthmatics. IFN-gamma levels had an inverse correlation with asthmatic symptom score. CD4+ T-cell expression of CD30 also correlated inversely with IFN-gamma production and IFN-gamma:IL-4 ratio. PHA produced minimal levels of IL-4 compared to specific allergen stimulation. It is concluded that different groups of atopic patients exhibit different patterns of allergen-induced cytokine production. In vitro allergen-induced cytokine production in atopic asthmatics correlated with symptomatic disease activity, and is allergen-specific.     

Local IgE production in nasal allergy

IgE mediates allergic reactions by binding to the high-affinity receptor, Fc epsilonR1, on mast cells and basophils at mucosal surfaces; then cross-linking of the receptor by multivalent antigen triggers the allergic response. We demonstrate here that B cells in the nasal mucosa of patients with hay fever express IgE. The results also suggest that allergen-induced heavy-chain switching to IgE occurs locally within the nasal mucosa. Local IgE synthesis may explain why some 'atopic' patients develop rhinitis whereas others have either no clinical manifestations or develop atopic disease elsewhere.     

Further evidence for the presence of cannabinoid CB1 receptors in mouse vas deferens

Basophil granulocytes and their mediators are involved in the pathogenesis of allergic inflammation. We evaluated basophil count, blood histamine content, eosinophil count and serum total IgE levels in one hundred-thirteen healthy newborns at birth. 108 children were prospectively studied with a follow-up to 18 months of age for development of topic disorders. No difference was found in newborns with biparental family history of atopy (FHA) in comparison with newborns with monoparental FHA and with newborns without FHA. Children who developed atopic disorders had neonatal basophil count higher than those who did not develop atopic symptoms (p = 0.03). No significant correlation was found between basophil and eosinophil counts (r = 0.013), between basophil count and serum total IgE levels (r = 0.012) and between basophil count and blood histamine content. Positive predictive value and sensitivity of basophil count for allergy up to 18 months of age was respectively only 33% and 27%. Our data indicate that an increased basophil count at birth is not associated with FHA and is not a good predictive marker of atopy.     

Dermatophagoides sp. and IgE anti-D. pteronyssinus and D. farinae detection in a Venezuelan community at more than 2000 m above the sea level

BACKGROUND: It has been reported that the concentration of Dermatophagoides sp. population, the main trigger of asthma in sensitized atopic subjects, is inversely related with altitude and probably directly with humidity and that this population are scarcely found over 1750 m above sea level. OBJECTIVE: We studied the presence of Dermatophagoides sp. in a Venezuelan community between 2040 and 2600 m above sea level, and also the IgE response to D. pteronnyssinus and D. farinae in atopic subjects living on that region. METHODS: The presence of Dermatophagoides sp. was determined by microscopic identification of mites in dust, obtained by brushing the mattresses surface in 93 randomly selected houses between 2040 and 2600 m above sea level. The indoor relative humidity was also measured. The specific IgE serum levels were studied in 65 subjects classified as asthmatics, allergic non-asthmatics and non-allergic. RESULTS: A mean concentration of 188 mites/g of room dust was determined in 82.4% of houses with an indoor relative humidity ranging from 89% and 92% independently of altitude. The density of Dermatophagoides sp. was sufficiently high to sensitize the atopic subjects, IgE levels were 6.8 PRU mean value for asthmatic, against 0.38 PRU in non-atopic. CONCLUSIONS: We conclude that: (a) Dermatophagoides sp. can be found up to 2600 m above sea level in a Venezuelan neotropical region where a high indoor relative humidity is characteristic of most dwellings; (b) sensitization by D. pteronyssinus and D. farinae were demonstrated in atopic subjects resident at that region.     

Predictability of early atopy by cord blood-IgE and parental history

BACKGROUND: Atopic family history and cord blood IgE have been used as predictors of atopic disease in newborns for about 20 years, but at least for cord blood IgE the sensitivity has been shown to be very low. The objective of this paper was to evaluate whether parental history and cord blood-IgE were more accurate predictors for the appropriate atopic phenotypes in the infants rather than for any atopy. METHODS: A total of 1314 newborn infants was recruited in six German obstetric departments in 1990 and followed-up for 2 years. Four hundred and ninety-nine (38%) were at high risk for atopy with at least two first degree atopic family members and/or elevated cord-blood IgE concentrations. RESULTS: The cumulative incidence of atopic dermatitis over the first 2 years of life (AD24) amounted to 20.1%, and there was a significant association with AD history of the mother (OR 2.5, 95%CI 1.46-4.26) and of the father (OR 3.53, 95%CI 1.90-6.54). The cumulative incidence of recurrent wheezing in the first 2 years of life (RW24) amounted to 16.1%, and was positively associated with asthma history (OR 2.11, 95%CI 1.33-3.60) and sensitization history (OR 1.64, 95%CI 1.34-2.36) of the mother, but with neither for the father. RW24 was less prevalent in girls than in boys (OR 0.64, 95%CI 0.47-0.89). Thirty-one per cent of infants were sensitized (CAP test value > 0.35 kU/L) against at least one of nine food or inhalative allergens (S24) and this was significantly associated with cord blood-IgE value (OR 2.43, 95%CI 1.69-3.49), and sensitization history of the mother (OR 1.64, 95%CI 1.18-2.41). Using multiple logistic regression analysis, the prediction of AD24 by AD of parents, of RW24 by asthma of parents, and of sensitization by cord blood IgE was of low accuracy. CONCLUSION: The predictive capacity of parental history and cord blood IgE is not high enough to recommend them as screening instruments for primary prevention. The majority of atopic manifestations and of sensitization occur in infants with no demonstrable risk at birth.     

Analysis of polyunsaturated fatty acids in newborn sera: a screening tool for atopic disease?

It has been demonstrated that patients with atopic disease have anomalies of fatty acid composition, as a result of altered metabolism or abnormal incorporation of fatty acids into the tissues. In the present study, in 57 newborns 'at risk' for atopic disease, the polyunsaturated fatty acid (PUFA) levels were found to be lower in cord blood in infants who subsequently developed atopic disease than in non-atopics. In all babies, levels of arachidonic acid and dihomo-gamma-linolenic acid in sera at 1 and 3 months of age were lower than those in cord blood. These changes were more marked in children who subsequently developed atopic disease, and in those who, independently of signs and/or symptoms of atopic disease, were formula-fed. A comparison between IgE and PUFA levels revealed no significant differences at any tested time interval. In conclusion, our data suggest that in children 'at risk' for atopy, PUFA levels may be predictive of atopic disease.