妊娠饮食习惯与婴儿湿疹的关系研究及护理干预

目的 探讨孕期饮食习惯与出生婴儿湿疹之间的关系,并通过对孕妇饮食的护理干预来影响婴儿湿疹的发生. 方法筛选我院两年来孕检的118名孕妇,随机分成观察组和对照组,对观察组进行饮食护理干预,通过对脐血和婴儿血清中总IgE抗体(tIgE)含量的检测和嗜酸性粒细胞阳离子蛋白(ECP)变化情况比较,观察其与婴儿湿疹的发生关系;并对发生婴儿湿疹患儿,检测鸡蛋、牛奶和海鲜过敏原特异性IgE(sIgE). 结果脐血清中tIgE和ECP增高与婴儿血清中变化呈正相关(rsIgE=0.67,P<0.01;rECP=0.56,P<0.05);检测过敏原sIgE含量与婴儿湿疹临床诊断之间符合率较高;观察组脐带血清、婴儿血清中tlgE含量和ECP增高均明显低于对照组(P<0.05、P<0.01);且婴儿湿疹发生率也明显低于对照组(P<0.01).婴儿湿疹中鸡蛋血清sIgE阳性率最高(70.8%),其次为牛奶sIgE(46.3%);同时比较118名婴儿纯母乳、混合和人工喂养三种不同喂养方式,经统计学处理,差异无统计学意义(P>0.05). 结论孕妇孕期过多食用大分子食物可能是导致婴儿湿疹的主要原因之一;婴儿湿疹与鸡蛋、牛奶和海鲜过敏原密切相关,尤其是鸡蛋;而婴儿喂养方式不同与婴儿湿疹发生无明显关系.     

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.     

Eosinophil cationic protein and interleukin-8 levels in bronchial lavage fluid from children with asthma and infantile wheeze

It has been shown previously that airway eosinophils characterize childhood asthma and neutrophils contribute to the pathophysiology of both infantile wheezing and asthma. Therefore, eosinophil cationic protein (ECP) and interleukin‐8 (IL‐8) levels in bronchoalveolar lavage fluid (BALF) from asthmatics (n = 16) and infantile wheezers (n = 30) were analyzed as markers of eosinophil‐ and neutrophil‐mediated inflammation. To aid the interpretation, a control group of children (n = 10) with no lower airway pathology were included. Disease severity was assessed by using a symptom score. Surprisingly, no significant difference was found in IL‐8 or ECP levels among asthma, infantile wheeze, and control groups. Asthma was characterized by: a correlation between ECP levels and eosinophil counts (r = 0.618, p = 0.014); a correlation between neutrophil number and IL‐8 levels (r = 0.747, p = 0.002); and increasing IL‐8 levels with symptom score (p = 0.03). In infantile wheezers, IL‐8 levels were poorly related to neutrophil number but were significantly increased when neutrophils were > 10%. Although detectable levels were found in all but one symptomatic infant, IL‐8 concentrations did not reflect the symptom score in infantile wheeze. ECP was unexpectedly correlated to neutrophil percentages (Rho = 0.832, p = 0.001), and a threshold of ECP > 20 ng/ml was associated with persistent symptoms in these infantile wheezers. Hence, in accordance with BALF cellularity, activation of eosinophils was suggested by raised levels of ECP in childhood asthma, but not in infantile wheeze. Neutrophil‐mediated inflammation appeared to better reflect the severity of asthma than that of infantile wheeze. Although its meaning remains to be elucidated, ECP was suggested to be a helpful indicator of persistent infantile wheeze. However, its utility as a marker predicting ongoing asthma remains to be established.     

Eosinophil cationic protein in tracheal aspirates of preterm infants with bronchopulmonary dysplasia

Eosinophil cationic protein was elevated during the first week of life in tracheal aspirates from 11 preterm infants in whom bronchopulmonary dysplasia subsequently developed compared with 8 preterm and 8 term infants without bronchopulmonary dysplasia. Eosinophil cationic protein levels increased progressively with continued intubation in the infants with bronchopulmonary dysplasia but remained low in a comparison group of term infants. We suggest that eosinophils participate in the inflammatory process in bronchopulmonary dysplasia and may contribute to lung injury. (J Pediatr 1997;130:944-7)     

Oilseed rape flour: another allergen causing occupational asthma among farmers

BACKGROUND: Farmers are exposed to a wide variety of sensitizers. Since occupational asthma (OA) can lead to permanent disability, exposure discontinuation is the preferred treatment. When this is not possible, the identification of the causative allergen may allow an alternative therapy. METHODS: We present three farmers diagnosed with OA as a consequence of handling fodder. We carried out skin tests with common and occupational allergens and with oilseed rape (OSR) extract. Total and specific serum IgE levels were measured. The patients underwent the OSR-bronchial provocation test (OSR-BPT). The day before and 24 h after the OSR-BPT, the methacholine (M)-BPT and induced sputum were performed. Eosinophil percentages and ECP levels were measured in the sputum samples. RESULTS: OSR sensitization (skin tests and specific serum IgE) was detected in all the patients. The OSR-BPT elicited early responses in two subjects. Methacholine sensitivity, sputum eosinophils, and sputum ECP levels increased 24 h after the OSR-BPT in all the patients. CONCLUSIONS: We have demonstrated that inhalation of OSR flour causes bronchoconstriction, induces an eosinophilic inflammatory bronchial response, and increases bronchial hyperresponsiveness in sensitized asthmatics. OSR flour contained in animal fodder should be considered another potential cause of OA among farmers.     

Serum eosinophil cationic protein (ECP) as a marker of disease activity and treatment efficacy in seasonal asthma

This study was carried out to determine whether serum eosinophil cationic protein (ECP) represents a sensitive marker for disease activity in atopic asthmatic patients during the pollen season. The study, in double-blind fashion, was performed between February and June 1994. Two groups of 10 seasonal asthmatic patients randomly received two different treatments. The first group was treated with inhaled beclomethasone dipropionate (BDP) 500 μg bid; the second received a matched placebo (P). At the beginning and every month, blood samples for determination of ECP and eosinophil count were collected and lung function (FEV₁) and methacholine responsiveness (PD₂₀) were performed. Subjects recorded daily symptoms of asthma, salbutamol consumption, and peak expiratory flow (PEF) values. In the P group, all indices, except FEV₁, showed significant changes during the pollen season ( P < 0.001). In the BDP group, significant changes were detected for symptom score ( P < 0.01), salbutamol consumption ( P < 0.01), and eosinophil number ( P < 0.05). Between the two groups, significant differences for symptom score ( P < 0.001), salbutamol consumption ( P < 0.001), ECP levels ( P < 0.05), eosinophil count ( P < 0.02), PD₂₀ methacholine ( P < 0.02), and PEF values ( P < 0.01) were detected. Changes in serum ECP significantly correlated with changes in other parameters ( P < 0.001), except FEV₁. Our results provide evidence that serum ECP is a sensitive marker for monitoring of the disease activity in seasonal asthma. Furthermore, it may offer a useful tool for estimating treatment efficacy.     

Evaluation of IgE antibodies to recombinant pollen allergens (Phl p 1, Phl p 2, and Phl p 5) in a random sample of patients with specific IgE to Phleum pratense

BACKGROUND: We measured specific IgE levels against the recombinant allergens (RAs) rPhl p 1, rPhl p 2, and rPhl p 5 in patients allergic to grass pollen, and examined the existence of different patterns of IgE production to RAs. The seasonal variations of IgE levels to rPhl p 1, rPhl p 2, and rPhl p 5 were considered, too. METHODS: Blood was taken from 276 consecutive patients with allergy to grass pollen diagnosed by patient history and skin prick testing. Total and specific serum IgE was measured by the immunoenzymatic CAP FEIA System. Eosinophil cationic protein (ECP) and myeloperoxidase (MPO) were assessed by radioimmunoassay according to the instructions of the manufacturers. RESULTS: We observed eight different patterns of IgE production to rPhl p 1, rPhl p 2, and rPhl p 5 in patients with specific IgE to timothy grass. A significant difference between the values of IgE levels to timothy and the sum of each level of specific IgE to individual RAs was found (P = 0.039, Wilcoxon matched pairs test) in the whole population (n = 276 subjects). In four subgroups of patients, the sum of each level of specific IgE to individual RAs was equal to the levels of specific IgE to timothy grass extract. In one subgroup, the sum of IgE to RAs was lower than the levels of IgE to the natural counterpart (P = 0.013). A lack of subjects in two subgroups did not permit comparison at all. Finally, three subjects with specific IgE to timothy did not show specific IgE to RAs. Out of 276 patients, blood was taken from two different groups of subjects at different time points: November-January and May-July, respectively. The median values were as follows: total IgE = 139 kU/l, IgE to timothy = 10.2 kUA/l; IgE to rPhl p 1 = 3.6 kUA/l, to rPhl p 2 = <0.35 kUA/l, and to rPhl p 5 = 1.1 kUA/l; ECP = 8.25 microg/l; MPO = 303.08 microg/l (before exposure to grass pollen); total IgE = 159 kU/l, IgE to timothy = 57.2 kUA/l; IgE to rPhl p 1 = 22.1 kUA/l, to rPhl p 2 = 5.9 kUA/l, and to rPhl p 5 = 3.9 kUA/l; ECP = 16.21 microg/l; MPO = 413.09 microg/l (during the pollen season). There were significant variations of specific IgE levels between the patients exposed to pollen and the unexposed patients. Moreover, there were statistical differences in the IgE, ECP, and MPO levels in sera before and during the pollen season P<0.035, P<0.017, and P<0.0062, respectively. CONCLUSIONS: The results suggest that RAs allow establishment of the patient's IgE-reactivity profile, encourage future research, and encourage manufacturers to produce further RAs for precise diagnosis and substantially improved immunotherapy injection of only those allergens against which significant amounts of specific IgE are produced.     

The Gordon phenomenon induced by the eosinophil cationic protein and eosinophil protein X

Cerebellar Purkinje cell degeneration after intracerebral injection of eosinophil granulocytes or extracts thereof is known as the Gordon phenomenon. The reaction is said to be highly selective. An eosinophil-derived neurotoxin (EDN) has recently been reported to induce the Gordon phenomenon. However, we report here that two eosinophil-derived proteins, eosinophil cationic protein (ECP) and eosinophil protein X (EPX), may induce the Gordon phenomenon after intraventricular injection. The potency of ECP is far greater than that of EPX and the latter is possibly identical to EDN. The Fink-Heimer staining for degenerating nerve fibers and boutons, however, indicated that the selectivity of the Gordon phenomenon is not as specific as was previously thought, since this method revealed degeneration of all brain areas in proximity to the ventricular system.     

Intranasal challenge with aspirin induces cell influx and activation of eosinophils and mast cells in nasal secretions of ASA-sensitive patients

Background Although the mechanism of aspirin-sensitivity seems to be related to inhibition of cyclo-oxygenase by aspirin (ASA), the chain of biochemical events leading to the ASA-induced adverse reaction is not clear, and the contribution of particular mediators and inflammatory cells has not been elucidated. Objectives To investigate the involvement of secretory, vascular and cellular mechanisms in the pathophysiology of nasal reactions to aspirin. Methods Six patients with ASA-sensitive asthma/rhinosinusitis and seven ASA-tolerant patients were challenged intranasaly with saline and lysine-acetylsalicylic acid (Lys-ASA) 12mg, on separate occasions. Nasal lavages were obtained before, and then every 15min after challenges, and analysed for biochemical and cellular composition. Results Lys-ASA challenge caused rhinorrhoea. sneezing and nasal congestion with parallel increases in total protein and albumin concentration, albumin % and lysozyme activity in the nasal secretions of ASA-sensitive patients. Concomitant with clinical symptoms, an influx of leucocytes into nasal secretions occurred with significant enrichment in eosinophils (mean prechallenge: 24 ± 12%, postsatine 27±9%, postLys-ASA 51 ± 10%; P < 0.03). The influx of eosinophils into nasal secretions was associated with a remarkable increase in Eosinophil Cationic Protein (ECP) immunoreactivity in five of six patients (mean 9.3 ± 3.8 μg/L and 140.9 ± 45.8 μg/mL before and after Lys-ASA, respectively). At the peak of ASA-induced symptoms an increase in the tryptase level was also observed in five of six patients (mean prechallenge: 2 ± 0.1 U/L; postLys-ASA 16 ± 5 U/L; P < 0.01) suggesting activation of mucosal mast cells. In ASA-tolerant patients Lys-ASA did not induce significant symptoms or changes in the biochemical and cellular composition of nasal secretions. Conclusion The results show that the ASA-induced nasal adverse reaction involves changes in vascular permeability and serous cell secretion. Both activated eosinophils and mast cells may contribute to the pathophysiology of the ASA-induced reaction in the nasal mucosa.