Eosinophil cationic protein (ECP), eosinophil chemotactic activity (ECA), neutrophil chemotactic activity (NCA) and tryptase in serum before and during bronchial challenge in cat-allergic children with asthma

In order to study ECP, ECA, NCA and tryptase levels in serum in 18 cat-allergic children with asthma scrum samples were obtained before and during an allergen bronchial challenge. All children were on regular treatment with inhaled steroids (200-800 μg/day) and bronchodilators. Peak expiratory flow (PEF) was recorded twice daily for at least a week before the challenge. The baseline ECP levels were significantly higher in the children who had a baseline PEF 80-95% of pred. compared to those who had PEF >95% of pred. (mean 24. 3 μg/l and 14. 3 μg/l respectively, p <0.02). ECP in serum before the ehallenge correlated significantly to PEF in % of the expected optimal PEF obtained from the PEF curve (r= 0. 48, p <0.05). During the challenge ECA and NCA increased significantly from mean 96. 2% and 97. 9% to 122. 7% and 118. 7% (p <0.05 for both), while ECP did not change significantly, mean 20. 4 μg/l before and 17. 5 μg/l after the challenge. Tryptase levels in serum were not detectable (<0. 5 ng/ml) before or during the asthmatic attack.
We eoncludc that there are significantly raised ECP levels in serum in symptom-free asthmatic children on long-term treatment with topical steroids possibly indicating remaining airway inflammation. Acute asthma results in an increase of ECA and NCA while ECP levels seem to reflect the chronic rather than the acute phase of asthma in children.     

Eosinophil cationic protein in induced sputum as a marker of inflammation in asthmatic children

We evaluated the usefulness of eosinophil cationic protein (ECP) in induced sputum and in serum as markers of asthmatic inflammation in children. We measured ECP in serum and in total indticed sputum samples from 14 children (7-11 years) with newly detected asthma before and after treatment, and from ten healthy non atopic controls of the same age. The patients inhaled budesonide, 800 μg/m2/day for the first month and 400 μg/m2/day for the next 5 months, both divided into two doses, and nedocromil, 4 mg three times daily for the following 6 months. In both sputum and serum, ECP levels were higher in the patients than in the controls, but the difference was more distinct in sputum. Significant clinical improvement during the treatment was accompanied by a decrease in sputum ECP. whereas serum ECP did not change. The results suggest that induced sputum is useful as a non invasive source material for evaluating asthmatic inflammation in children, total sputum ECP being more sensitive than serum ECP for diagnosing and monitoring asthma.     

Leukotriene B4 and C4 generation by human leukocytes after ex vivo stimulation with Ca-ionophore and opsonized zymosan in children with atopic asthma

The ex vivo release of leukotriene B₄ (LTB₄) and leukotriene C₄ (LTC₄) from leukocytes was evaluated after stimulation with both Ca-ionophore (Ca-I) and opsonized zymosan (OZ) in children with atopic asthma. Twenty-seven patients with asthma of varying severity were evaluated and divided into three groups: 1) moderate to severe asthma using inhaled steroids and symptom-free for the last 3 weeks (n = 8), 2) mild asthma with sporadic symptoms, only using inhaled pVagonists < 3 times/week (n = 8), and 3) acute asthmatic attacks admitted to hospital (n = 11). A group of children without atopic disease or any other known disease served as controls (n = 15). Total serum IgE levels were significantly increased in the children with asthma compared with the control group. LTC₄ production was only significantly increased in the group of children with moderate to severe asthma after stimulation with Ca-I, when compared with controls. In the same group, a trend towards increased LTC₄ production after stimulation with OZ was found. LTB₄ was not significantly increased in any patient group compared with the control group. A significant correlation between LTC₄ production after stimulation with Ca-I, but not OZ, and the relative blood eosinophil count was found in all subjects. LTC₄ generation per eosinophilic cell after stimulation with Ca-I or OZ was not statistically different in any patient group compared with the controls. We conclude that the increased leukotriene (LT) levels found after the stimulation of peripheral white blood cells sampled from atopic children with asthma are mainly the result of increased numbers of LT-producing cells, rather than due to increased releasability from these cells.     

Analysis of sputum taken from wheezy and asthmatic infants and children, with special reference to respiratory infections

Children who are destined to develop asthma are considered to be susceptible to a variety of respiratory pathogens. To elucidate respiratory inflammation among these children, we measured the levels of eosinophil cationic protein (ECP) and tryptase in sputum taken from three different groups of wheezy infants and young children: those with a first wheeze (n = 15); those with recurrent wheeze (n = 27); and those with recurrent wheeze with respiratory distress, namely asthma (n = 56). The numbers of eosinophils or metachromatic cells determined by microscopic analysis of sputum samples were also evaluated in combination with the ECP and tryptase levels. Although neither sputum ECP nor tryptase was a clear discriminative marker that differentiated the three different types of wheezy disease, ECP levels in sputum from the asthma group were significantly higher (2,269.2 ± 6,216.8 ng/g) than those in the recurrent wheezy group (440.3 ± 1,199.8 ng/g) or in the first‐wheeze group (209.0 ± 172.9 ng/g). A similar trend was observed with tryptase levels in sputum, but there were no significant differences among the three groups. Sputum taken from asthmatic children showed a marked accumulation of eosinophils. However, an accumulation of eosinophils in sputum (even in the presence of an elevated level of sputum ECP) was not identified in the asthmatic infants < 1 year of age. An accumlation of eosinophils in sputum was not evident until children became > 1 year old and thereafter the eosinophils rapidly increased in number until the children reached 5 years of age. It was noteworthy that sputa positive for pathogenic bacteria, taken from the 1‐ and 2‐year‐old asthmatic infants, had a tendency to show high levels of ECP but a reduced number of eosinophils. Along with the wheezy episodes induced by viral infection, primarily and occasionally in combination with secondary bacterial infection, eosinophil activation and infiltration may develop. These predestined immune reactions to various pathogens might be associated with triggering the onset of asthma.     

Serum inflammatory markers and effects of age and tobacco smoke exposure in young non-asthmatic children

Serum eosinophil cationic protein (ECP), but not serum myeloperoxidase (MPO), has been found to reflect disease activity of asthma and eczema, but no reference values exist for young children. Thus, we aimed to provide values of serum-ECP and serum-MPO in young children without obstructive airways disease (OAD), and determine possible influencing factors. Parental interview was performed and serum was collected from a total of 245 children (207 children aged 24-41 months and 76 children aged 0-23 months) with no history of lower respiratory disease. Repeated serum samples were obtained in 38 subjects. Ten percent of the children had active eczema at examination. All children were controls in the"Environment and Childhood Asthma"study in Oslo. Geometric means (GM ± 1.96 SD) for serum ECP were 11.8 μg/l (2.5-56.0) and 7.9 μg/l (2.0-30.4), respectively, in the 0-23 and 24-41-month-old children, with the corresponding values for serum MPO 453 μg/l (153-1349) and 347 μg/l (142–859), respectively. Age was inversely associated with serum-ECP and serum-MPO, most pronounced in the youngest children. Active eczema and maternal daily smoking adversely affected serum-ECP, but not serum-MPO. Gender and parental atopy did not influence the results. We conclude that serum-ECP in very young children is influenced by age and active eczema and is related to maternal smoking in a dose-dependent fashion. These factors should be considered when assessing inflammatory markers in very young children.     

IL-31 significantly correlates with disease activity and Th2 cytokine levels in children with atopic dermatitis

Recently, we could show that IL-31 serum levels are significantly increased in adult patients with atopic dermatitis compared with skin healthy controls. However, the regulation of IL-31 in children with atopic dermatitis so far is not clear. Thus, we analyzed IL-31 serum levels together with IL-4, IL-13, ECP, and total IgE levels in 60 children with extrinsic, in five children with intrinsic atopic dermatitis, and 20 non-atopic healthy children. Further, we determined the SCORAD score, sleeplessness, and pruritus severity in all children with atopic dermatitis. IL-31 was significantly increased in children with the intrinsic and extrinsic type of atopic dermatitis compared with non-atopic healthy children (p?相似文献   

Clinical value of monitoring eosinophil activity in asthma.

To evaluate the use of eosinophil cationic protein (ECP) in monitoring disease activity in childhood asthma, serum ECP in 175 asthmatic children was assessed. Forty five patients with cystic fibrosis, 23 with lower respiratory tract infections (LRTI), and 87 healthy children were used as controls. Serum ECP concentrations (34.3 micrograms/l v 9.8 micrograms/l) were significantly higher in children with bronchial asthma than in healthy control subjects. In symptomatic patients with asthma serum ECP concentrations were increased compared with those from asymptomatic patients (40.2 micrograms/l v 14.4 micrograms/l), irrespective of treatment modalities (that is steroids, beta 2 agonists, or sodium cromoglycate). Moreover, atopy and infection appeared to be factors enhancing eosinophil activity in bronchial asthma as measured by serum ECP (58.4 micrograms/l v 36.8 micrograms/l and 68.8 micrograms/l v 42.2 micrograms/l, respectively). In a longitudinal trial, antiasthmatic treatment modalities (that is steroids) reduced serum ECP within four weeks (42.2 micrograms/l v 19.0 micrograms/l). In conclusion, the data indicate that (1) eosinophils also play a central part in childhood asthma; (2) serum concentrations of ECP in children with bronchial asthma are related to the disease severity and may thus be used for monitoring inflammation in childhood asthma; (3) eosinophil activity appears to be enhanced by atopy and infection; and (4) longitudinal measurements of serum ECP concentrations may be useful for optimising anti-inflammatory treatment in children with bronchial asthma.     

Evaluation of a clinical algorithm involving serum eosinophil cationic protein for guiding the anti‐inflammatory treatment of bronchial asthma in childhood

A pilot study was performed to investigate a clinical algorithm using serum‐eosinophil cationic protein level (S‐ECP) as an objective parameter for tapering the anti‐inflammatory treatment in chronic childhood asthma. We studied 21 outpatient asthmatic children (6 girls and 15 boys, mean age 9 yr, range 3–12 yr, all with initial S‐ECP ≥ 15 µg/l) over a period of 12 months at monthly intervals. At each visit a short history, clinical examination, blood sample for S‐ECP and eosinophil count, lung function tests and drug compliance were assessed. According to the initial S‐ECP, patients were allocated to two anti‐inflammatory treatment groups: patients with S‐ECP between 15 µg/l and 30 µg/l were treated with Budesonide 200 µg twice daily, while patients with S‐ECP of 30 µg/l and above received Budesonide 400 µg twice daily. After this induction treatment the anti‐inflammatory medication was tapered at monthly intervals according to actually measured S‐ECP: patients with S‐ECP < 15 µg/l received sodium cromoglycate (SCG) 10 mg twice daily per inhalation via spacer, patients with S‐ECP ≥ 15 µg/l and < 30 µg/l received Budesonide 200 µg twice daily via spacer, and patients with S‐ECP ≥ 30 µg/l received Budesonide 400 µg twice daily. Prior to inhalation of topical steroids or SCG all patients had to inhale 500 µg Terbutaline twice daily for optimal bronchodilatation. The use of medication was assessed by weighing the metered dose inhaler containers each month. Our results showed a decrease in symptoms (p = 0.0001) and in S‐ECP (p = 0.02) and MEF50% predicted (p = 0.02) after the initial month of Budesonide treatment. During a total of 246 months of investigation there was no need for emergency room treatment or hospital admission, and no need for oral steroids. During the whole study period there was a tendency for inhaled steroids to be more effective than SCG in reduction of markers of airway inflammation, improvement of symptoms and lung function. Inadequate use of medication was related to an increase in S‐ECP in all treatment groups. From this open pilot study it is concluded that a clinical algorithm including S‐ECP for tapering the anti‐inflammatory treatment may be helpful in childhood asthma. These first observations should be confirmed by a controlled long‐term study.     

Does the severity of atopic dermatitis correlate with serum IgE levels?

Recent studies suggest an association between atopic phenotypes and serum IgE levels. In contrast to asthma, this association has not been proven for atopic dermatitis. For 345 children (mean age 2.9 years), we investigated a correlation of the severity of eczema (defined by SCORAD score) and serum IgE levels. Additionally, the data was analyzed for differences between children with high and low SCORAD quartile. Parameters such as genetic background, the prevalence of other atopic phenotypes such as bronchial asthma, allergic rhinoconjunctivitis, and allergic sensitization were recorded. Our results indicate a significant correlation between SCORAD and serum IgE levels (R = 0.31, p < 0.001), but the standard deviation was large. Children with atopic dermatitis showed a high prevalence of sensitization to foods independent of the IgE levels; children with high SCORAD levels showed a sensitization to aeroallergens significantly more often (p < 0.02). No differences were found in prevalences of atopic family background, or a number of additional atopic symptoms such as asthma and allergic rhinoconjunctivitis. These results suggest that serum IgE levels seem to correlate with the degree of eczema. Children with severe atopic dermatitis and high IgE levels are at risk for sensitization to food allergens and aeroallergens.     

Serum IgE levels in atopic diseases in childhood

The serum IgE levels were determined according to the radioimmunosorbent technique (RIST), in 208 children aged between 1 and 14 years, with atopic diseases alone or in combination. Geometric mean IgE levels were significantly increased and rose progressively from the atopic dermatitis "alone" to the allergic rhinitis, the allergic asthma and the combination of asthma with rhinitis, with the highest values in patients where atopic dermatitis was combined with respiratory allergy. IgE levels rose slowly with age. For the atopy diagnosis in vitro, two criteria were chosen and compared: a fixed IgE-level of 100 U/ml, and one standard deviation below the geometric mean of the atopic children.     

Local production of total IgE and specific antibodies to the house dust mite in adenoid tissue

Adenoids are known as immunosecretory organs and those in atopic children present cellular and cytokine profiles different from those of non‐atopic children. We hypothesized that locally produced total IgE and allergen‐specific antibodies could be involved in the inflammatory responses in adenoid tissue. Local productions of total IgE and Dermatophagoides pteronyssinus (DP)‐specific IgE, IgA, IgG1, and IgG4 antibodies were evaluated, as well as their relationships with the markers of allergic inflammation within adenoid tissue. Eighteen atopic subjects, who were sensitized to more than one common aeroallergen, and 22 non‐atopic subjects undergoing adenotonsillectomy, were recruited. Immunoassays using adenoid tissue homogenate were performed to quantify the levels of total IgE, eosinophil cationic protein (ECP), and mast cell tryptase. DP‐specific IgE, IgA, IgG1, and IgG4 antibodies, soluble IL‐2 receptors (sIL‐2R), soluble CD23 (sCD23), and IL‐6 were measured by ELISA. All parameters measured in adenoid tissue homogenate were presented as a ratio to the albumin level found in the adenoid. Median level of total IgE in adenoid tissue homogenate was significantly higher in atopic individuals than in non‐atopic individuals. Median values of DP‐specific IgE and IgA antibodies were significantly higher in atopics than in non‐atopics (p = 0.001, p = 0.006, respectively), while no differences were seen in DP‐specific IgG1 and IgG4 antibodies. ECP and sCD23 levels in adenoid homogenate were significantly higher in atopics than in non‐atopics (p = 0.026, p = 0.048, respectively), while no significant differences were noted in tryptase, sIL‐2R, and IL‐6 levels. The levels of DP‐specific IgE, IgA, IgG1, and IgG4 antibodies in adenoid homogenate correlated significantly with ECP levels, but not with those of sIL‐2R, sCD23, and IL‐6. The presence of total IgE and DP‐specific antibodies in adenoid tissue was confirmed to be more prominent in atopics. In conclusion, locally‐produced total IgE and DP‐specific antibodies may contribute to eosinophilic inflammation in adenoid tissue in atopic children.     

Exhaled breath condensate pH measurement in children with asthma, allergic rhinitis and atopic dermatitis

Recent studies have shown that the pH of exhaled breath condensate (EBC) could be predictive of asthma exacerbation. Moreover, it has been documented that both allergic rhinitis and atopic dermatitis constitute risk factors for the occurrence of asthma in a progression of disease known as atopic march. The aim of our study was to establish if condensate pH could be used as a valuable mean of monitoring of asthma in atopic children. We studied 34 atopic children with acute asthma, 70 with stable asthma, 35 children with allergic rhinitis, and 17 with atopic dermatitis. Thirty healthy children were used as controls. All children underwent skin prick tests and lung function tests. Exhaled breath condensate samples were collected with a condensing device and de-aerated with argon. The pH of EBC was measured using a pH meter. Children with acute asthma were treated with inhaled steroids and bronchodilators. We found that the pH of condensate in patients with acute asthma was lower than that of patients with stable asthma, rhinitis, and controls (7.25 vs. 7.32, p < 0.05; 7.25 vs. 7.48, p < 0.02; 7.25 vs. 7.78, p < 0.0001, respectively). Patients with stable asthma, rhinitis, and eczema had also lower pH than that of controls (7.32, 7.48, and 7.44 vs. 7.78; p < 0.0001, p < 0.006, p < 0.04, respectively). Patients with acute asthma normalized their pH after treatment (7.82 vs. 7.25; p < 0.0001). Finally, patients with acute asthma showed a positive correlation between pH and lung functional parameters (forced expiratory volume in 1 s; r = 0.39, p = 0.04). Our study shows that EBC pH measurement may be a promising marker for assessing airway inflammation and monitoring response to anti-inflammatory treatment in asthmatic children. Furthermore, we report the first evidence of airways acidification in children with allergic rhinitis and atopic dermatitis. Therefore, EBC pH assessment may be useful in the evaluation of progression of the atopic march toward the development of asthma later in life. Further studies are recommended in order to confirm this indication.     

Eosinophil cationic protein in nasal secretion and in serum and myeloperoxidase in serum in respiratory syncytial virus bronchiolitis: relation to asthma and atopy

Eosinophil cationic protein (ECP) in nasal secretions was determined in 34 infants with respiratory syncytial virus (RSV) bronchiolitis during the acute infection stage and one and six months later. ECP in serum was determined in 19 of these children at the same time. Myeloperoxidase (MPO) was determined in the same 19 children at the acute infection stage and after one month. All children were followed prospectively for two years after the infection with regard to the development of bronchial obstructive symptoms. Asthma, defined as three or more episodes of bronchial obstruction verified by a physician, developed in 18% of children and less severe obstructive symptoms in 29%. A screening test for food IgE antibodies in serum was performed six months and a skin prick test two years after the acute infection. Nasal ECP/albumin ratios after six months were significantly higher than during the acute RSV infection. MPO, but not ECP, levels in serum were significantly elevated at the time of acute infection compared with levels after one month. Nasal ECP/albumin ratios at the acute infection were compared to a control group of 27 infants with non-RSV upper respiratory tract infections and did not differ. It was not possible to predict, either from ECP/albumin ratios in nasal secretion or from ECP and MPO in serum, which children would develop asthma, other bronchial obstructive symptoms or positive IgE tests.     

Seasonal differences of peak expiratory flow rate variability and mediators of allergic inflammation in non-atopic adolescents

Variations in peak expiratory flow (PEF) and serum eosinophil mediators were studied in healthy adolescents. Twenty‐five boys and 31 girls, 11–16 years of age (mean age 14.3 years), were selected and investigated during the birch pollen season of 1995; 45 were also investigated during the autumn of the same year. The PEF was measured twice daily and eosino‐phil mediators in serum and in urine were measured by radioimmunoassay (RIA) once during the birch pollen season and once in autumn. The type values of the daily PEF variation, expressed in amplitude percentage mean, were 6.4 and 3.9%, mean values were 7.35 and 6.74%, and the 95th percentiles were 18 and 14%, during the birch pollen season and autumn, respectively. The 95th percentiles were 41 and 38 µg/l for serum eosinophil cationic protein (s‐ECP), 74 and 62 µg/l for serum eosinophil protein X (s‐EPX), 987 and 569 µg/l for serum myeloperoxidase (s‐MPO), and 165 and 104 µg/mmol for urinary eosinophil protein X/urinary creatinine (u‐EPX/u‐creatinine), during the birch pollen season and autumn, respectively. The levels of the eosinophil mediators decreased significantly from May (n = 56) to November (n = 45), for s‐ECP from a median value of 14 µg/l to 7 µg/l (p= 0.001), for s‐EPX from a median value of 28 µg/l to 20 µg/l (p= 0.001), and for the neutrophil mediator, s‐MPO, from a median value of 440 g/l to 292 g/l (p< 0.001). The PEF variability decreased significantly (p= 0.037), from spring (n = 55; median 8%, 95% confidence interval [CI] 7.8–10.19) to autumn (n = 44; median 6%, 95% CI 6.1–8.9). A significant correlation was found between the levels of s‐ECP and s‐EPX (r_s = 0.7, p< 0.001), between s‐ECP and s‐MPO (r_s = 0.6, p< 0.001), between s‐EPX and s‐MPO (r_s = 0.4, p< 0.005), and between s‐EPX and u‐EPX/u‐creatinine (r_s = 0.6, p< 0.0001), in the birch pollen season (n = 56) and in the autumn (n = 45). There was a positive correlation found in PEF variability between the two seasons (n = 43; r_s = 0.5, p= 0.0006). No other correlation was found between PEF variability and any other parameters. The difference in the levels of eosinophil mediators between seasons in non‐atopic, healthy children is unexplained. Normal limits for mediators were higher and PEF variability was almost the same as has been reported in adults. When using normal values, seasonal influences should be considered.     

Specific IgE antibodies and serum eosinophil cationic protein in children with atopic dermatitis alone

Both eosinophils and specific immunoglobulin E (IgE) to foods and mites have been considered involved in the pathogenesis of atopic dermatitis (AD). The relationship between eosinophils and specific IgE, however, remains to be elucidated. Blood eosinophil counts, serum eosinophil cationic protein (ECP) and IgE to egg white, cow's milk, soybean, rice and Dermatophagoides pteronyssinus (Dp) were measured in subjects with AD alone or bronchial asthma (BA) alone. Subjects with positive IgE titers (Pharmacia radioallergosorbent test (RAST) units > 0.7) of one or more items were defined as RAST-positive. Immunoglobulin E titers to egg white, cow's milk and soybean of subjects with AD were high in early childhood and declined with aging, whereas the titers of subjects with BA were negative or low. Immunoglobulin E titers to Dp were elevated after 1 year of age in both disease groups. Eosinophil cationic protein (ECP) levels and blood eosinophil counts in the AD and BA groups were significantly higher than those of non-atopic controls. No difference in ECP levels or blood eosinophil counts were observed between RAST-positive and negative groups. It is concluded that IgE to foods such as egg white, cow's milk and soybean might have a role in the pathogenesis of AD of young children, while IgE to mites might be involved in older children. Eosinophils may also participate in AD. However, different mechanisms may be responsible for the rise in specific IgE and high ECP levels and blood eosinophil counts.     

Prediction of allergy from family history and cord blood IgE levels

Screening of total IgE in 1189 cord blood samples was conducted by Phadebas IgE PRIST in a one-year birth cohort 1983-1984 in Viborg. Denmark. 113 children with cord blood IgE levels ≥ 0.5 kU/l and 138 children chosen at random among those with cord blood IgE levels < 0. 5 kU/l were seen at a follow-up at 5 years of age. Based upon history and physical examination a diagnosis of definite atopy or no atopy was established. Allergy (IgE mediated) was defined as atopic disease combined with increased total IgE levels at 5 years of age. The cumulative prevalence of atopic disease was not influenced by cord blood IgE levels or atopic predisposition. Cord blood IgE levels had a low sensitivity as a predictor of atopic disease. A statistically significant correlation between serum levels of IgE at birth and at 5 years was however found (p < 0.001), and a significantly greater number of children with elevated cord blood IgE levels developed allergic disease before 5 years of age (p < 0.01). A cut-off limit of 0. 3 kU/l was superior to the originally suggested limit of 0. 5 kU/l. A total IgE level > 63 kU/l (geometric mean + 1 SD) at the age of 5 years can be regarded as being an elevated level. A cord blood IgE level ≥ 0.3 kU/l in combination with atopic predisposition was predictive of allergic disease, especially allergic bronchial asthma. With regard to allergic disease, the positive predictive value was 26%, the sensitivity 33% and the rate ratio for development of allergic disease 4. In the case of the most serious atopic disease, allergic bronchial asthma, the positive predictive value was 20%, the sensitivity 87% and the rate ratio 68.     

Serum levels of eosinophilic cationic protein (ECP), myeloperoxidase (MPO), lipid peroxidation products, interleukin (IL)-5 and interferon (IFN)-gamma in children with bronchial asthma at acute asthma attack and remission

We determined serum levels of myeloperoxidase (MPO), eosinophilic cationic protein (ECP), reactive oxygen species measured as thiobarbituric acid reactive substances (TBARS), interleukin (IL)-5, and interferon (IFN)-gamma in 14 asthmatic children during an asthma attack and remission. Twelve healthy children served as controls. In atopic asthmatics, asthma attack resulted insignificant elevations of ECP, MPO, and TBARS compared to remission. TBARS levels were also higher at remission compared to controls. However, there was a great deal of overlap in the values of asthmatics and controls. IL-5 and IFN-gamma were detectable at low levels and only in a few patients. These results provide further evidence for participation of eosinophils, neutrophils and reactive oxygen species in the pathogenesis of acute asthma, and suggest that their products may be used in monitoring asthma attack. Serum IL-5 and IFN-gamma levels are not appropriate for use in the follow-up of asthmatic children.     

Enhanced IL-4 but normal interferon-gamma production in children with isolated IgE mediated food hypersensitivity

Atopic disorders such as atopic dermatitis and asthma have been characterised by an imbalance in interferon-gamma (INF-γ) and IL-4. Whether similar imbalances are found in atopic disorders with different clinical manifestations, such as IgE mediated immediate food hypersensitivity, is not clear. We have examined the in vitro production of INF-γ and IL-4 in peripheral blood mononuclear cells (PBMC) following phytohaemagglutinin stimulation from children with isolated immediate IgE mediated food hypersensitivity (egg, milk, "nut"), children with moderate and severe atopic dermatitis, and normal children. Children with immediate food reactions were excluded if they had a history or evidence of atopic dermatitis or asthma. PBMC from children with IgE mediated food hypersensitivity produced significantly more IL-4 (p = 0.013) but equivalent INF-γ (p=0.26) compared to PBMC from control children. In contrast, PBMC from children with atopic dermatitis produced significantly less INF-γ (p < 0.001) and more IL-4 (p < 0.008) than PBMC from normal children. In addition, there was no difference in IL-4 (p = 0.74) but significantly less INF-γ (p < 0.001) produced by PBMC from the children with atopic dermatitis than food hypersensitivity. We demonstrate that children with IgE mediated food hypersensitivity and no other manifestation of atopic disease have enhanced IL-4 production without the defect in INF-γ production observed in childhood AD and asthma. We postulate that isolated IL-4 enhancement promotes the development of IgE mediated hypersensitivity disorders such as food allergy, whilst the combination of defective INF-γ and enhanced IL-4 production promotes inflammatory atopic disorders such as AD and asthma.     

Asthma severity and atopy: how clear is the relationship?

BACKGROUND: The relationship between asthma severity and atopy is complex. Many studies have failed to show significant relationships between clinical severity or lung function and markers of atopic sensitisation. AIM: To determine whether increasing asthma severity is related to atopic sensitisation in a population of children with asthma. METHODS: A total of 400 children (7-18 years) with asthma were recruited as part of a multicentre study of the genetics of asthma. Detailed phenotypic data were collected on all participants. Associations between measures of asthma severity and atopic sensitisation were sought using multilevel models allowing variation at the individual and family level. RESULTS: Children recruited to the study had a range of asthma severities, with just over a third having mild persistent asthma. The logarithm of total serum IgE was associated with increased asthma severity score, decreased FEV1, increased airways obstruction, risk of hospital admission, and inhaled steroid use. Increasing skin prick test reactivity to a panel of seven aeroallergens was associated with increased risk of hospital admission, use of an inhaled steroid, and airways obstruction. The results remained highly significant after corrections for age, gender, and birth order. CONCLUSIONS: In children with asthma, increasing atopy is associated with increasing asthma severity. However, the relationships between asthma severity and skin prick tests, and asthma severity and total serum IgE values, appear subtly different.     

温州地区402例哮喘患儿特应质现象分析

目的 对温州地区15岁以下哮喘患儿特应质现象进行分析,探讨其临床及理论价值.方法 回顾性分析402例哮喘患儿皮肤过敏原诊断试验、血清特异性IgE、总IgE、个人过敏史、家族史、过敏原检出率、类型及与年龄关系.结果 哮喘发病有家族聚集倾向,家族过敏史总阳性率为52.74%.个人过敏史总阳性率为61.69%.过敏原皮肤诊断试验和过敏原血清特异IgE阳性率达83.58%,吸人性过敏原阳性人数占检测患儿的74.13%,其中以粉尘螨(61.44%)、屋尘螨(58.96%)为主;食人性过敏原阳性占24.38%,以小虾(16.67%)、牛奶(8.46%)为主.血清总IgE阳性率87.9%,总IgE阳性组和阴性组的哮喘患儿血清嗜酸性细胞阳离子蛋白(ECP)、户尘螨sIgE(D1)、粉尘螨sIgE(D2),皮肤过敏原诊断试验(pt)、家族过敏史、个人过敏史差异有统计学意义(P均≤0.05).哮喘患儿3岁前、后过敏原分布不同,3岁以后吸人性过敏原阳性为主.发病诱因中以上呼吸道感染为最多,哮喘症状发作的时间主要集中在临睡、夜晚、清晨.结论 儿童哮喘存在明显特应质现象,对其的正确认识和诊断对哮喘免疫机制的深入研究、综合治疗如在糖皮质激素吸入治疗的基础上,增加患儿教育、过敏原避免、特异性的免疫治疗等具有实用和理论指导意义.