Focus on work-related asthma

 

European Annals of Allergy and Clinical Immunology Vol 45, No 3 (2013) > Moscato

Focus on work-related asthma

G. Moscato

Abstract

Work-related asthma, encompassing both occupational asthma and work-exacerbatedasthma, accounts for 10%-25% of adult asthma in Europe and occupational asthma iscurrently one of the most common forms of occupational lung disease in many industrializedcountries. It is cause of direct and indirect costs for the worker, the employer andthe society and it is probably still underdiagnosed. Hence, the possibility of work-relatedasthma should be considered in all adult patients in whom asthma started or worsenedduring their working life. The investigation of WRA includes assessing the presenceof asthma, and demonstrating its work-relatedness, that requires training andexpertise. Due to the frequent association of occupational asthma and rhinitis, thepresence of both upper and lower airway symptoms should be investigated. Furthermore,since is work-related asthma is a preventable disease all efforts should be madefor effective prevention strategies.

Keywords

Work-related-asthma,work-related-rhinitis, diagnosis,management, medicolegal aspects

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Review

Diagnosis and management of non-IgE-mediated cow's milk allergy in infancy - a UK primary care practical guide

Carina Venter, Trevor Brown, Neil Shah, Joanne Walsh and Adam T Fox

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Clinical and Translational Allergy 2013, 3:23 doi:10.1186/2045-7022-3-23

Published: 8 July 2013

Abstract (provisional)

The UK NICE guideline on the Diagnosis and Assessment of Food Allergy in Children and Young People was published in 2011, highlighting the important role of primary care physicians, dietitians, nurses and other community based health care professionals in the diagnosis and assessment of IgE and non-IgE-mediated food allergies in children. The guideline suggests that those with suspected IgE-mediated disease and those suspected to suffer from severe non-IgE-mediated disease are referred on to secondary or tertiary level care. What is evident from this guideline is that the responsibility for the diagnostic food challenge, ongoing management and determining of tolerance to cow's milk in children with less severe non-IgE-mediated food allergies is ultimately that of the primary care/community based health care staff, but this discussion fell outside of the current NICE guideline. Some clinical members of the guideline development group (CV, JW, ATF, TB) therefore felt that there was a particular need to extend this into a more practical guideline for cow's milk allergy. This subset of the guideline development group with the additional expertise of a paediatric gastroenterologist (NS) therefore aimed to produce a UK Primary Care Guideline for the initial clinical recognition of all forms of cow's milk allergy and the ongoing management of those with non-severe non-IgE-mediated cow's milk allergy in the form of algorithms. These algorithms will be discussed in this review paper, drawing on guidance primarily from the UK NICE guideline, but also from the DRACMA guidelines, ESPGHAN guidelines, Australian guidelines and the US NIAID guidelines.

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Ultrastructure of Vascular Permeability in Urticaria

ORIGINAL ARTICLES

Ultrastructure of Vascular Permeability in Urticaria

P.R. Criado, R.F.J. Criado, C.F.H. Takakura, C. Pagliari, J.F. de Carvalho, M.N. Sotto and C. Vasconcellos

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Click on the icon on the upper right hand side for the article written by Paulo R. Criado, MD, Roberta F.J. Criado, MD, Cleusa F.H. Takakura, BS, Carla Pagliari, BS, Jozelio F. de Carvalho, MD, Mirian N. Sotto, MD and Cidia Vasconcellos, MD.
IMAJ 2012: 15: April: 173-177

ABSTRACT

 Background: Few studies have addressed the ultrastructure of vascular permeability in urticaria.

Objectives: To describe the types of endothelial cell organelles involved in vascular permeability in drug-induced acute urticaria (DIAU).

Methods: Seven patients with DIAU were enrolled in the study. Biopsies of urticarial lesions and apparently normal skin were performed. The 14 collected fragments were processed with immunogold electron microscopy using single stains for tryptase and factor XIIIa (FXIIIa) and double immunogold labeling for both tryptase and FXIIIa.

Results: Some sections demonstrated mast cells in the degranulation process, in both anaphylactic and piecemeal degranulation. After double immunogold staining, 10 nm (FXIIIa) and 15 nm (tryptase) gold particles were both present, covering the granules in the mast cells, indicating that both tryptase and FXIIIa were localized within the granules of these cells. Interestingly, we found strong evidence of the presence of caveolae and vesico-vacuolar organelles (VVOs) in the endothelial cells of the biopsies. In addition to these findings, we were able to demonstrate the presence of tryptase and FXIIIa in the endothelial cells, in urticarial lesions and in apparently normal skin.

Conclusions: VVOs are present in the endothelial cells of post-capillary venules in DIAU. This is the first report on the expression of FXIIIa and tryptase in the cytoplasm of endothelial cells in urticaria. 

Schnitzler syndrome - an under diagnosed clinical entity

1. Tania Jain1, 
2. Chetan P. Offord2, 
3. Robert Kyle2 and 
4. David Dingli2,*

+Author Affiliations

1. ¹ Wayne State University, USA;
2. ² Mayo Clinic, USA

1. ↵* Corresponding author; email: dingli.david@mayo.edu

Abstract

Schnitzler syndrome is considered to be a rare disorder characterized by a monoclonal IgM protein and chronic urticaria that is associated with considerable morbidity. We hypothesized that the syndrome may be under recognized and patients may be deprived of highly effective therapy in the form of anakinra. We performed a retrospective search of the dysproteinemia database at Mayo Clinic as well as the medical records of all patients with chronic urticaria to determine the true incidence of the disease. We compared patients with the diagnosis of Schnitzler syndrome and those who met the criteria but in whom the syndrome was not recognized. Comparisons between groups were performed and survival curves determined. We identified 16 patients with diagnosed Schnitzler syndrome and an additional 46 patients who met diagnostic criteria. The monoclonal protein was IgMκ in 94% of patients. Therapy with anakinra in 4 patients led to rapid and complete resolution of symptoms. The median overall survival for this syndrome is greater than 12.8 years. Progression to lymphoma was only observed in 8% of patients which is lower than what has previously been reported. Schnitzler syndrome may be present in up to 1.5% of patients with a monoclonal IgM in their serum and likely under-recognized as a clinical syndrome.

• Monoclonal Gammopathy of Undetermined Significance
 
• Quality of Life
• Clinical and Molecular Epidemiology

• This Article

  1. Published online before print June 28, 2013, doi:10.3324/haematol.2013.084830haematol June 28, 2013haematol.2013.084830
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• Received January 31, 2013.
• Accepted June 10, 2013.

• Copyright © 2013, Ferrata Storti Foundation

Correlation of Increased Blood Levels of GITR and GITRL with Disease Severity in Patients with Primary Sjögren’s Syndrome

Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 340751, 9 pages
http://dx.doi.org/10.1155/2013/340751

Research Article

Correlation of Increased Blood Levels of GITR and GITRL with Disease Severity in Patients with Primary Sjögren’s Syndrome

Xiaoxia Gan, Xiaoke Feng, Lei Gu, Wenfeng Tan, Xiaoxuan Sun, Chengyin Lv, and Miaojia Zhang

Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, China

Received 3 May 2013; Accepted 20 June 2013

Academic Editor: Guixiu Shi

Copyright © 2013 Xiaoxia Gan 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

Glucocorticoid-induced tumor necrosis factor receptor family-related protein (GITR) is a type I transmembrane protein belonging to the TNFR superfamily. After activated by its ligand GITRL, GITR could influence the activity of effector and regulatory T cells, participating in the development of several autoimmune and inflammatory diseases included rheumatoid arthritis and autoimmune thyroid disease. We previously reported that serum GITRL levels are increased in systemic lupus erythematosus (SLE) patients compared with healthy controls (HC). Here, we tested serum soluble GITR (sGITR) and GITRL levels in 41 primary Sjögren’s syndrome (pSS) patients and 29 HC by ELISA and correlated sGITR and GITRL levels with clinical and laboratory variables. GITR and GITRL expression in labial salivary glands was detected by immunohistochemistry. pSS patients had significantly increased serum levels of sGITR and GITRL compared with controls (GITR: 5.66 ± 3.56 ng/mL versus 0.50 ± 0.31 ng/mL; ; GITRL: 6.17 ± 7.10 ng/mL versus 0.36 ± 0.28 ng/mL; ). Serum sGITR and GITRL levels were positively correlated with IgG (GITRL: , ; sGITR: , ) and ESR (GITRL:  ; sGITR: , ). Moreover, GITR and GITRL are readily detected in the lymphocytic foci and periductal areas of the LSGs. In contrast, the LSGs of HC subjects did not express GITR or GITRL. Our findings indicate the possible involvement of GITR-GITRL pathway in the pathogenesis of pSS. Further studies may facilitate the development of targeting this molecule pathway for the treatment of pSS.

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MicroRNAs Implicated in the Immunopathogenesis of Lupus Nephritis

Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 430239, 13 pages
http://dx.doi.org/10.1155/2013/430239

Review Article

MicroRNAs Implicated in the Immunopathogenesis of Lupus Nephritis

Cristen B. Chafin¹ and Christopher M. Reilly^1,2

¹Department of Biomedical Sciences & Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA
²Edward Via College of Osteopathic Medicine, Blacksburg, VA 24060, USA

Received 12 February 2013; Revised 20 May 2013; Accepted 12 June 2013

Academic Editor: Richard J. Quigg

Copyright © 2013 Cristen B. Chafin and Christopher M. Reilly. 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

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the deposition of immune complexes due to widespread loss of immune tolerance to nuclear self-antigens. Deposition in the renal glomeruli results in the development of lupus nephritis (LN), the leading cause of morbidity and mortality in SLE. In addition to the well-recognized genetic susceptibility to SLE, disease pathogenesis is influenced by epigenetic regulators such as microRNAs (miRNAs). miRNAs are small, noncoding RNAs that bind to the 3′ untranslated region of target mRNAs resulting in posttranscriptional gene modulation. miRNAs play an important and dynamic role in the activation of innate immune cells and are critical in regulating the adaptive immune response. Immune stimulation and the resulting cytokine milieu alter miRNA expression while miRNAs themselves modify cellular responses to stimulation. Here we examine dysregulated miRNAs implicated in LN pathogenesis from human SLE patients and murine lupus models. The effects of LN-associated miRNAs in the kidney, peripheral blood mononuclear cells, macrophages, mesangial cells, dendritic cells, and splenocytes are discussed. As the role of miRNAs in immunopathogenesis becomes delineated, it is likely that specific miRNAs may serve as targets for therapeutic intervention in the treatment of LN and other pathologies.

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Acute eosinophilic pneumonia leading to acute respiratory failure in a current systemic corticosteroid user

Case Report  Open Access

|    Allergy Asthma Immunol Res. 2013 Jul;5(4):242-244. English. Published online 2013 April 05.  http://dx.doi.org/10.4168/aair.2013.5.4.242  Copyright © 2013 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease Acute Eosinophilic Pneumonia Leading to Acute Respiratory Failure in a Current Systemic Corticosteroid User Hwa Yong Shin,1 Ju Won Choe,2 Minsuk Kwon,3 Ju Young Jang,3 Jae Woo Jung,3 Jae Chol Choi,3 Jong Wook Shin,3 In Won Park,3 Byoung Whui Choi,3 and Jae Yeol Kim3 1Department of Anesthesiology & Pain Medicine, Chung-Ang University College of Medicine, Seoul, Korea. 2Department of Chest Surgery, Chung-Ang University College of Medicine, Seoul, Korea. 3Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea. Correspondence to: Jae Yeol Kim, MD, PhD, Department of Internal Medicine, Chung-Ang University Hospital, 102 Heukseok-ro, Dongjak-gu, Seoul 156-755, Korea. Tel: +82-2-6299-1396, Fax: +82-2-825-7571, Email: jykimmd@cau.ac.kr Received August 20, 2012; Revised October 11, 2012; Accepted November 06, 2012. 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 A 69-year-old female patient visited the emergency room with fever (38.3℃) and dyspnea. She had been taking prednisolone (5 mg once per day) and methotrexate (2.5 mg once per week) for rheumatoid arthritis for 2 years. Chest computed tomography (CT) showed bilateral, multifocal ground glass opacity with interlobular septal thickening. Peripheral blood leukocyte count was 6,520/mm3 (neutrophils, 77.4%; eosinophils, 12.1%). During the night, mechanical ventilation was initiated due to the development of severe hypoxemia. Bronchoalveolar lavage fluid showed a high proportion of eosinophils (49%). Her symptoms improved dramatically after commencement of intravenous methylprednisolone therapy. This is the first report of idiopathic acute eosinophilic pneumonia developing in a current user of systemic corticosteroids. Keywords: Acute eosinophilic pneumonia, respiratory failure, corticosteroid.