A pilot study on the application of a symptom-based score for the diagnosis of cow’s milk protein allergy

Yvan Vandenplas1

Althera Study Group

Philippe Steenhout2

Dominik Grathwohl3

1. ¹Department of Pediatrics, Universitair Kinderziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium
2. ²Nestlé Nutrition, Vevey, Switzerland
3. ³Nestlé Research Center, Lausanne, Switzerland

1. Yvan Vandenplas, Department of Pediatrics, Universitair Kinderziekenhuis Brussel, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium. Email:yvan.vandenplas@uzbrussel.be

 

Next Section

Abstract

Objective: A challenge is the recommended test to diagnose cow’s milk protein allergy. However, many parents and physicians prefer to not challenge because the procedure may cause (severe) symptoms. In clinical routine, diagnostic testing is only available for IgE-mediated allergy. The aim of this study was to test the diagnostic accuracy of a symptom-based score to select infants at risk of having cow’s milk protein allergy.

Methods: A symptom-based score was developed and consensus was reached that a score of ≥12 would select infants at risk of cow’s milk protein allergy. Diagnosis of cow’s milk protein allergy was demonstrated with a positive challenge after 1-month elimination diet.

Results: An open challenge was performed in 85/116 (73%) infants suspected of cow’s milk protein allergy based on a symptom-based score ≥ 12 and was positive in 59/85 (69%). Although “a challenge test” was planned in the protocol, 27% of the parents refused the challenge. The mean decrease after 1 month of elimination diet with an extensive hydrolysate was −8.07 (95% confidence interval = −8.74, −7.40). If the symptom-based score during the elimination diet decreased to 6 or lower, 80% of the infants had a positive challenge test. If the symptom-based score remained >7, the challenge test was positive in only 48% (p - 0.001).

Conclusion: In daily practice, a symptom-based score of ≥12 is a useful tool to select infants at risk of cow’s milk protein allergy. If an elimination diet reduces the symptom-based score to ≤6, the challenge test is positive in 80%.

• Cow’s milk protein allergy
 
• hydrolysate
 
• symptom-based score

This Article

1. Published February 18, 2014, doi:10.1177/2050312114523423SAGE Open Medicine 2014 vol. 22050312114523423

2. 
3. AbstractOpen Access
4. » Full TextOpen Access
5. Full Text (PDF)Open Access

Epidermal Permeability Barrier Defects and Barrier Repair Therapy in Atopic Dermatitis

Review  Open Access

Allergy Asthma Immunol Res. 2014 Jul;6(4):276-287. English. Published online 2014 March 21.  http://dx.doi.org/10.4168/aair.2014.6.4.276  Copyright © 2014 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease Hae-Jin Lee,1 and Seung-Hun Lee2 1Medical Corps of Sangmudae Army Service Support Group, Republic of Korea Army Training and Doctrine Command, Jangsung, Korea. 2Department of Dermatology, Gangnam Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.  Correspondence to: Seung Hun Lee, MD, PhD, Department of Dermatology, Gangnam Severance Hospital, Yonsei University College of Medicine, 211 Eonju-ro, Gangnam-gu, Seoul 135-720, Korea. Tel: +82-2-2019-3360; Fax: +82-2-3463-6136; Email: ydshderm@yuhs.ac  Received December 08, 2013; Accepted January 06, 2014. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Atopic dermatitis (AD) is a multifactorial inflammatory skin disease perpetuated by gene-environmental interactions and which is characterized by genetic barrier defects and allergic inflammation. Recent studies demonstrate an important role for the epidermal permeability barrier in AD that is closely related to chronic immune activation in the skin during systemic allergic reactions. Moreover, acquired stressors (e.g.,Staphylococcus aureus infection) to the skin barrier may also initiate inflammation in AD. Many studies involving patients with AD revealed that defective skin barriers combined with abnormal immune responses might contribute to the pathophysiology of AD, supporting the outside-inside hypothesis. In this review, we discuss the recent advances in human and animal models, focusing on the defects of the epidermal permeability barrier, its immunologic role and barrier repair therapy in AD. Keywords: Atopic dermatitis, barrier repair therapy, skin barrier. Formats: Abstract Article PubReader PDF Figures + Tables References

Satisfaction level and asthma control among Malaysian asthma patients on Symbicort Maintenance and Reliever Therapy (SMART) in the primary care setting (SMARTEST study)

 Vol. 32, No. 2, June 2014 > Liam

Chong-Kin Liam, Yong-Kek Pang, Keong-Tiong Chua

Abstract

Objective: To evaluate Malaysian patients’ satisfaction levels and asthma control with Symbicort SMART® in the primary care setting.
Method: This is a cross-sectional, multicentre study involving adult patients with persistent asthma who were prescribed only Symbicort SMART in the preceding one month prior to recruitment. Patients’ satisfaction with Symbicort SMART and asthma control were evaluated using the self-administered Satisfaction with Asthma Treatment Questionnaire (SATQ) and the Asthma Control Test (ACT).
Results: Asthma was controlled (ACT score >20) in 189 (83%) of 228 patients. The mean overall SATQ score for patients with controlled asthma was 5.65 indicating a high satisfaction level, which was positively correlated with high ACT scores. There were differences in asthma control based on ethnicity, number of unscheduled visits and treatment compliance.
Conclusions: Symbicort SMART resulted in a high satisfaction level and asthma control among Malaysian patients treated in the primary care setting and it is an effective and appealing treatment for asthmatic patients.

Full Text: PDF 

Parameters of lung inflammation in asthmatic as compared to healthy children in a contaminated city

Research article

Benigno Linares Segovia, Gabriela Cortés Sandoval, Norma Amador Licona, Juan Manuel Guízar Mendoza, Estela Núñez Lemus, Diana Olivia Rocha Amador, Xóchitl Sofía Ramírez Gómez and Rebeca Monroy Torres

Author Affiliations

For all author emails, please log on.

BMC Pulmonary Medicine 2014, 14:111  doi:10.1186/1471-2466-14-111

Published: 8 July 2014

Abstract (provisional)

Background

The impact of air pollution on the respiratory system has been estimated on the basis of respiratory symptoms and lung function. However; few studies have compared lung inflammation in healthy and asthmatics children exposed to high levels of air pollution. The aim of the study was to elucidate the modulatory effect of air pollution on Cysteinyl-leukotrienes (Cys-LTs) levels in exhaled breath condensate (EBC) among healthy and asthmatic children.

Methods

We performed a cross-sectional comparative study. Children between 7-12 years of age, asthmatics and non-asthmatics, residents of a city with high levels of PM10 were included. In all cases, forced spirometry, Cys-LTs levels in EBC, and the International Study of Asthma and Allergies in Childhood questionnaire were evaluated. We also obtained average of PM10, CO, SO2 and O3 levels during the period of the study by the State Institute of Ecology.

Results

We studied 103 children (51 asthmatics and 52 non-asthmatics). Cys-LTs levels were higher in asthmatics than in non-asthmatics (77.3 +/- 21.6 versus 60.3 +/- 26.8 pg/ml; p = 0.0005). Also, Cys-LTs levels in children with intermittent asthma were lower than in children with persistent asthma (60.4 +/- 20.4 versus 84.7 +/- 19.2 pg / ml; p = 0.0001). In the multiple regression model, factors associated with levels of Cys-LTs were passive smoking (beta = 13.1, p 0.04) and to be asthmatic (beta = 11.5, p 0.03).

Conclusions

Cys-LTs levels are higher in asthmatic children than in healthy children in a contaminated city and its levels are also associated with passive smoking.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Significance of Persistent Inflammation in Respiratory Disorders Induced by Nanoparticles

Journal of Immunology Research
Volume 2014 (2014), Article ID 962871, 8 pages
http://dx.doi.org/10.1155/2014/962871

Review Article

Yasuo Morimoto,¹ Hiroto Izumi,¹ and Etsushi Kuroda²

¹Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan
²Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Japan

Received 22 February 2014; Revised 17 June 2014; Accepted 20 June 2014; Published 7 July 2014

Academic Editor: Mario Di Gioacchino

Copyright © 2014 Yasuo Morimoto et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Pulmonary inflammation, especially persistent inflammation, has been found to play a key role in respiratory disorders induced by nanoparticles in animal models. In inhalation studies and instillation studies of nanomaterials, persistent inflammation is composed of neutrophils and alveolar macrophages, and its pathogenesis is related to chemokines such as the cytokine-induced neutrophil chemoattractant (CINC) family and macrophage inflammatory protein-1 and oxidant stress-related genes such as heme oxygenase-1 (HO-1). DNA damages occur chemically or physically by nanomaterials. Chemical and physical damage are associated with point mutation by free radicals and double strand brake, respectively. The failure of DNA repair and accumulation of mutations might occur when inflammation is prolonged, and finally normal cells could become malignant. These free radicals can not only damage cells but also induce signaling molecules containing immunoreaction. Nanoparticles and asbestos also induce the production of free radicals. In allergic responses, nanoparticles act as Th2 adjuvants to activate Th2 immune responses such as activation of eosinophil and induction of IgE. Taken together, the presence of persistent inflammation may contribute to the pathogenesis of a variety of diseases induced by nanomaterials.

• Abstract
• Full-Text PDF
• Full-Text HTML
• Full-Text ePUB
• Linked References
• How to Cite this Article
• Complete Special Issue

A Model for the Determination of Pollen Count Using Google Search Queries for Patients Suffering from Allergic Rhinitis

Journal of Allergy
Volume 2014 (2014), Article ID 381983, 9 pages
http://dx.doi.org/10.1155/2014/381983

Research Article

Volker König and Ralph Mösges

Institute of Medical Statistics, Informatics and Epidemiology, University of Cologne, 50924 Cologne, Germany

Received 27 February 2014; Revised 22 May 2014; Accepted 26 May 2014; Published 19 June 2014

Academic Editor: Carlos E. Baena-Cagnani

Copyright © 2014 Volker König and Ralph Mösges. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. The transregional increase in pollen-associated allergies and their diversity have been scientifically proven. However, patchy pollen count measurement in many regions is a worldwide problem with few exceptions. Methods. This paper used data gathered from pollen count stations in Germany, Google queries using relevant allergological/biological keywords, and patient data from three German study centres collected in a prospective, double-blind, randomised, placebo-controlled, multicentre immunotherapy study to analyse a possible correlation between these data pools. Results. Overall, correlations between the patient-based, combined symptom medication score and Google data were stronger than those with the regionally measured pollen count data. The correlation of the Google data was especially strong in the groups of severe allergy sufferers. The results of the three-centre analyses show moderate to strong correlations with the Google keywords (up to >0.8 cross-correlation coefficient, ) in 10 out of 11 groups (three averaged patient cohorts and eight subgroups of severe allergy sufferers: high IgE class, high combined symptom medication score, and asthma). Conclusion. For countries with a good Internet infrastructure but no dense network of pollen traps, this could represent an alternative for determining pollen levels and, forecasting the pollen count for the next day.

• Abstract
• Full-Text PDF
• Full-Text HTML
• Full-Text ePUB
• Linked References
• How to Cite this Article

Long-term dynamics of death rates of emphysema, asthma, and pneumonia and improving air quality

 

International Journal of Chronic Obstructive Pulmonary Disease

Original Research

(2580) Total Article Views

Authors: Kravchenko J, Akushevich I, Abernethy AP, Holman S, Ross Jr WG, Lyerly HK

Published Date June 2014 Volume 2014:9 Pages 613 - 627

DOI: http://dx.doi.org/10.2147/COPD.S59995

Received:	02 January 2014
Accepted:	09 April 2014
Published:	16 June 2014

Julia Kravchenko,¹ Igor Akushevich,² Amy P Abernethy,³ Sheila Holman,⁴ William G Ross Jr,⁵ H Kim Lyerly<sup>1,6

1</sup>Department of Surgery, ²Center for Population Health and Aging, ³Duke Clinical Research Institute, Duke University Medical Center, Duke University, Durham, ⁴Division of Air Quality, North Carolina Department of Environment and Natural Resources, Raleigh, ⁵Nicholas School of the Environment, ⁶Department of Pathology, Duke University Medical Center, Duke University, Durham, NC, USA

Background: The respiratory tract is a major target of exposure to air pollutants, and respiratory diseases are associated with both short- and long-term exposures. We hypothesized that improved air quality in North Carolina was associated with reduced rates of death from respiratory diseases in local populations.
Materials and methods: We analyzed the trends of emphysema, asthma, and pneumonia mortality and changes of the levels of ozone, sulfur dioxide (SO₂), nitrogen dioxide (NO₂), carbon monoxide (CO), and particulate matters (PM_2.5 and PM₁₀) using monthly data measurements from air-monitoring stations in North Carolina in 1993–2010. The log-linear model was used to evaluate associations between air-pollutant levels and age-adjusted death rates (per 100,000 of population) calculated for 5-year age-groups and for standard 2000 North Carolina population. The studied associations were adjusted by age group-specific smoking prevalence and seasonal fluctuations of disease-specific respiratory deaths.
Results: Decline in emphysema deaths was associated with decreasing levels of SO₂ and CO in the air, decline in asthma deaths–with lower SO₂, CO, and PM₁₀ levels, and decline in pneumonia deaths–with lower levels of SO₂. Sensitivity analyses were performed to study potential effects of the change from International Classification of Diseases (ICD)-9 to ICD-10 codes, the effects of air pollutants on mortality during summer and winter, the impact of approach when only the underlying causes of deaths were used, and when mortality and air-quality data were analyzed on the county level. In each case, the results of sensitivity analyses demonstrated stability. The importance of analysis of pneumonia as an underlying cause of death was also highlighted.
Conclusion: Significant associations were observed between decreasing death rates of emphysema, asthma, and pneumonia and decreases in levels of ambient air pollutants in North Carolina.

Keywords: chronic obstructive pulmonary disease, sulfur dioxide, carbon monoxide, nitrogen dioxide, particulate matter


 This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution - Non Commercial (unported, v3.0) License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on how to request permission may be found at: http://www.dovepress.com/permissions.php

Effects of BMI, Fat Mass, and Lean Mass on Asthma in Childhood: A Mendelian Randomization Study

PLoS Med. Jul 2014; 11(7): e1001669.

Published online Jul 1, 2014. doi:  10.1371/journal.pmed.1001669

PMCID: PMC4077660

Raquel Granell,1,* A. John Henderson,1 David M. Evans,2,3 George Davey Smith,2 Andrew R. Ness,4,5 Sarah Lewis,1,2 Tom M. Palmer,2,6 and Jonathan A. C. Sterne1

Cosetta Minelli, Academic Editor

Author information ► Article notes ► Copyright and License information ►

Abstract

Background

Observational studies have reported associations between body mass index (BMI) and asthma, but confounding and reverse causality remain plausible explanations. We aim to investigate evidence for a causal effect of BMI on asthma using a Mendelian randomization approach.

Methods and Findings

We used Mendelian randomization to investigate causal effects of BMI, fat mass, and lean mass on current asthma at age 7½ y in the Avon Longitudinal Study of Parents and Children (ALSPAC). A weighted allele score based on 32 independent BMI-related single nucleotide polymorphisms (SNPs) was derived from external data, and associations with BMI, fat mass, lean mass, and asthma were estimated. We derived instrumental variable (IV) estimates of causal risk ratios (RRs). 4,835 children had available data on BMI-associated SNPs, asthma, and BMI. The weighted allele score was strongly associated with BMI, fat mass, and lean mass (all p-values-0.001) and with childhood asthma (RR 2.56, 95% CI 1.38–4.76 per unit score, p=0.003). The estimated causal RR for the effect of BMI on asthma was 1.55 (95% CI 1.16–2.07) per kg/m2,p=0.003. This effect appeared stronger for non-atopic (1.90, 95% CI 1.19–3.03) than for atopic asthma (1.37, 95% CI 0.89–2.11) though there was little evidence of heterogeneity (p=0.31). The estimated causal RRs for the effects of fat mass and lean mass on asthma were 1.41 (95% CI 1.11–1.79) per 0.5 kg and 2.25 (95% CI 1.23–4.11) per kg, respectively. The possibility of genetic pleiotropy could not be discounted completely; however, additional IV analyses using FTO variant rs1558902 and the other BMI-related SNPs separately provided similar causal effects with wider confidence intervals. Loss of follow-up was unlikely to bias the estimated effects.

Conclusions

Higher BMI increases the risk of asthma in mid-childhood. Higher BMI may have contributed to the increase in asthma risk toward the end of the 20th century.

Formats:

Article
 | 
PubReader
 | 
ePub (beta)
 | 
PDF (739K)

Go to:

Abstract

Background

Observational studies have reported associations between body mass index (BMI) and asthma, but confounding and reverse causality remain plausible explanations. We aim to investigate evidence for a causal effect of BMI on asthma using a Mendelian randomization approach.

Methods and Findings

We used Mendelian randomization to investigate causal effects of BMI, fat mass, and lean mass on current asthma at age 7½ y in the Avon Longitudinal Study of Parents and Children (ALSPAC). A weighted allele score based on 32 independent BMI-related single nucleotide polymorphisms (SNPs) was derived from external data, and associations with BMI, fat mass, lean mass, and asthma were estimated. We derived instrumental variable (IV) estimates of causal risk ratios (RRs). 4,835 children had available data on BMI-associated SNPs, asthma, and BMI. The weighted allele score was strongly associated with BMI, fat mass, and lean mass (all p-values<0 .001="" 1.38="" 2.56="" 95="" and="" asthma="" childhood="" ci="" em="" nbsp="" per="" score="" unit="" with="">p