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The epidemiology of adverse food reactions (AFRs), including the potentially life-threatening food allergy (FA), in Asia is unclear. AFR is believed to be less prevalent than in Caucasians. This study determines the prevalence, clinical features and risk factors for parent-reported AFR in Chinese pre-school children in Hong Kong. Children aged 2–7 yr living in Hong Kong were recruited through local nurseries and kindergartens to ascertain the occurrence and clinical spectrum of AFR and other atopic disorders. Subjects’ parents answered a self-administered questionnaire that was modified and validated based on the International Study of Asthma and Allergy in Childhood. A total of 3827 children from 21 nurseries and kindergartens returned the study questionnaires, and information on AFR was analyzable for 3677 (96.1%) children. The prevalence rates of parent-reported AFR and parent-reported, doctor-diagnosed AFR were 8.1% and 4.6%, respectively, whereas 5.0% of pre-schoolers had doctor-diagnosed asthma. The six leading causes of AFR were shellfish (15.8%), egg (9.1%), peanut (8.1%), beef (6.4%), cow’s milk (5.7%), and tree nuts (5.0%). When compared with children born and raised in Hong Kong, children born in mainland China (n = 253) had less parent-reported AFR (4.0% vs. 6.7%; p = 0.016). On logistic regression, parent-reported AFR was associated with younger age (p = 0.010), born in mainland China (p = 0.038), and AFR history in father (p = 0.001), mother (p < 0.001), siblings (p = 0.020), and paternal history of rhinitis (p = 0.044). This study shows that AFR is a common atopic disorder in Hong Kong pre-school children, and prevalence rates are comparable to the Caucasians. [ABSTRACT FROM AUTHOR]

Abstract: The primary objective of our study was to provide a simple and reliable assay for identifying the majority of G6PD genetic variants in the Chinese population. We optimized the multiplex primer extension reaction (MPER) assay for simultaneous screening of 14-point mutations in 98 G6PD-deficient subjects. Our data demonstrated that this method is precise, cost-effective and has successfully identified mutations in 97 out of 98 subjects, including all heterozygous mutants. We also detected a relatively high incidence (12.3%) of c.871G>A, and all of them harbored the silent mutation c.1311C>T. Apart from the screening program, the pharmacogenetic relationship between G6PD level and residual reduced glutathione (GSH) level was studied upon oxidative challenge by α-naphthol. The GSH levels were correlated with their status of G6PD deficiency, but no significant difference was observed between individual G6PD-deficient groups. Our data demonstrated the potentials of the MPER assay for characterization of G6PD deficiency and other genetic diseases. [Copyright &y& Elsevier]

Background: Domestic endotoxin enhances airway inflammation and increases asthma severity in Caucasian children, but little data are published on indoor endotoxin exposure in Asian countries. This study investigated house dust endotoxin and Der p 1 levels in Hong Kong families with asthmatic children, and their effects on asthma severity. Methods: 115 asthmatics from a pediatric clinic underwent fractional exhaled nitric oxide (FeNO) and spirometric measurements. Home visits were then made within 2 weeks, during which parents completed the International Study of Asthma and Allergies in Childhood questionnaire. Settled dust was collected from patients’ mattresses, bedroom floors and living room floors. Endotoxin and Der p 1 were measured by limulus amebocyte lysate and immunoassay, respectively. Results: Endotoxin was detectable in all locations from all families, whereas Der p 1 was detectable in 58–70% of indoor sites. Floors of both bedroom and living rooms had higher endotoxin but lower Der p 1 levels than mattresses (p < 0.001 for both). Mattress endotoxin level correlated inversely with Der p 1 level (r = –0.308, p = 0.001). Household smoker, feather bedding and vacuum cleaning were independent determinants of indoor endotoxin. Timing of last bedding change was associated with Der p 1 levels at all sites. Mattress endotoxin level was associated with frequency of wheezing episodes (p = 0.044), but neither endotoxin nor Der p 1 was associated with FeNO and spirometric parameters. Conclusions: Domestic endotoxin levels are associated with frequency of wheezing episodes in asthmatic children but not their FeNO or spirometric measurements. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: Glucose-6-phosphate dehydrogenase (G6PD)-deficient subjects are susceptible to chemical-induced oxidative haemolysis. Little is known concerning the haemolytic properties of Chinese herbal medicine on G6PD-deficient subjects. Our objective was to investigate the pro-oxidative effect of 18 commonly used Chinese herbal medicine (CHM) on human G6PD-deficient red blood cells. G6PD-deficient (n =10) and normal (n =10) whole blood samples were incubated with water extracts of CHM. The resulting levels of reduced glutathione (GSH) and methaemoglobin (MetHb) were determined by biochemical assays. Rhizoma Coptidis significantly reduced GSH level by 48.9±5.4% (at 1mg/mL) in the G6PD-deficient erythrocytes (P <0.001) compared with the respective control group without challenge. Similar dose-dependent responses were observed at higher concentrations of Cortex Moutan, Radix Rehmanniae, Radix Bupleuri, Rhizoma Polygoni Cuspidati and Flos Chimonanthi (P <0.01, 5–10mg/mL). In addition, the levels of MetHb were elevated significantly when challenged with Rhizoma Coptidis (2.8 fold at 5mg/mL) and Cortex Moutan (3.4 fold at 10mg/mL). This is the first report on the pro-oxidative action of CHM on G6PD-deficient blood samples in vitro as demonstrated by the decrease of GSH and increase of MetHb. G6PD-deficient subjects should restrain from excessive consumption of these pro-oxidative herbs. [Copyright &y& Elsevier]

Background: Vascular endothelial growth factor (VEGF), AA isoform of platelet-derived growth factor (PDGF-AA), and epidermal growth factor (EGF) are involved in the pathogenesis of airway inflammation in asthma. These molecules are closely associated with cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-4. This study investigates the relation between childhood asthma and levels of these mediators in exhaled breath condensate (EBC). Methods: EBC was collected from asthmatic children and controls using a disposable collection kit, and the concentrations of VEGF, PDGF-AA, EGF, TNF-α and IL-4 in EBC were measured using sandwich enzyme immunoassays. Exhaled nitric oxide concentration was measured by a chemiluminescence analyzer. Results: Thirty-five asthmatic patients aged between 7 and 18 years and 11 controls were recruited. Sixteen patients had intermittent asthma (IA) whereas 19 of them suffered from persistent asthma (PA). A significant correlation was found between IL-4 and TNF-α in EBC (ρ = 0.374, p = 0.010). PDGF-AA levels in EBC were higher in subjects with diminished FEV1 (p = 0.023) whereas IL-4 concentrations were increased in asthmatics (p = 0.007) as well as subjects with increased plasma total IgE (p = 0.033). Patients with PA receiving high-dose inhaled corticosteroid (ICS) had higher EBC IL-4 concentration than those on low-dose ICS (p = 0.007). Linear regression revealed that PDGF-AA levels in EBC were negatively associated with FEV1 percentage (β = –0.459, p = 0.006) among the asthmatic patients. Conclusions: IL-4 in EBC is increased in childhood asthma, and growth factors are detectable in a significant proportion of these children. Increased PDGF-AA is found in asthmatics with more severe airflow limitation. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Leung TF, Li CY, Lam CWK, Au CSS, Yung E, Chan IHS, Wong GWK, Fok TF. The relation between obesity and asthmatic airway inflammation. Pediatr Allergy Immunol 2004: 15: 344–350. © 2004 Blackwell Munksgaard Epidemiologic studies suggest increased asthma prevalence in obese subjects. However, the relation between obesity and airway inflammation remains unclear. This cross-sectional study aims to investigate the relation between obesity indices and exhaled nitric oxide (ENO) and leukotriene B4 (LTB4) in children with asthma. Asthmatic patients aged 7–18 yr old were recruited. Weight-for-height Z score was calculated from anthropometry. ENO was measured by online single-breath method using a chemiluminescence analyzer, whereas LTB4 concentrations in exhaled breath condensate (EBC) were quantified using competitive enzyme immunoassay. Ninety-two asthmatics and 23 controls were recruited. The mean ENO and LTB4 concentrations in EBC were higher in asthmatic patients (87 p.p.b. and 40.5 pg/ml) than controls (25 p.p.b. and 18.7 pg/ml) (p < 0.0001 for both). Obesity, as defined by weight >120% median weight-for-height, was not associated with any alteration in ENO or LTB4 concentrations in patients with asthma. Besides, these inflammatory markers did not differ between asthmatics in the highest and lowest quartiles of weight-for-height Z score. On multivariate analysis, ENO showed significant correlation with age ( β = 0.511, p < 0.0001), peripheral blood eosinophil count ( β = 0.222, p = 0.019), plasma total IgE concentration ( β = 0.187, p = 0.050) and forced expiratory volume in 1-s (FEV1; β = −0.221, p = 0.014). None of the factors was associated with LTB4 concentration in EBC. In conclusion, ENO and LTB4 concentration in EBC are increased in childhood asthma. However, these inflammatory markers did not differ between obese and non-obese children with asthma. [ABSTRACT FROM AUTHOR]