Concomitant chronic pulmonary diseases and their association with hospital outcomes in patients with anaphylaxis and other allergic conditions

BMJ Open 2013;3:e003197 doi:10.1136/bmjopen-2013-003197

• Respiratory medicine
  • Research

Concomitant chronic pulmonary diseases and their association with hospital outcomes in patients with anaphylaxis and other allergic conditions: a cohort study

 Authors

Abstract

Objectives To determine if chronic pulmonary diseases adversely impact selected outcomes in hospitalised patients who have various allergic conditions including anaphylaxis.

Design A population-based cohort study.

Participants A statewide hospital inpatient discharge database from Texas, USA, covering the years 2004–2007 was analysed. Patients with anaphylaxis and other allergic conditions were identified using the International Classification of Diseases, Ninth Revision, Clinical Modification codes. Within each group of patients (the overall group with various selected allergic conditions and the subgroup with anaphylaxis), the exposure variables were 11 chronic pulmonary diseases including asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis.

Primary outcome measures Admission to an intensive care unit, a prolonged (>3 days) hospital stay, receipt of mechanical ventilation and death in hospital. Logistic regression was used to calculate adjusted OR and 95% CI for these four outcomes.

Results 30 390 patients with allergic conditions were identified, of whom 2410 had anaphylaxis. The following results pertain to the subcohort of patients with anaphylaxis. Median age was 50 years (range 0–95 years) and 1470 (61%) were female. The hospital mortality was 2.7%. Although asthma was not associated with hospital mortality (OR=1.27, 95% CI 0.55 to 2.90), asthmatics had more than twice the odds of non-asthmatics of receiving mechanical ventilation (OR=2.45, 95% CI 1.81 to 3.33). Chronic bronchitis, COPD, emphysema and interstitial lung diseases (ILDs) were also associated with an increased risk of requiring mechanical ventilation. Chronic bronchitis and COPD were associated with a prolonged length of stay: OR=2.69 (95% CI 1.45 to 4.98) and OR=1.86 (95% CI 1.30 to 2.66), respectively. ILD was the only chronic pulmonary disease associated with an elevated risk of hospital mortality: OR=8.71 (95% CI 1.48 to 51.20).

Conclusions In this unique analysis of a large database, we found that asthma, COPD and other chronic pulmonary diseases increased the risk of adverse outcomes among hospitalised patients with anaphylaxis.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:http://creativecommons.org/licenses/by-nc/3.0/

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Allergic Bronchopulmonary Aspergillosis with Repeated Isolation of Nontuberculous Mycobacteria

Internal Medicine
Vol. 52 (2013) No. 15 p. 1721-1726

Language:      English     Japanese   

CASE REPORTS

http://dx.doi.org/10.2169/internalmedicine.52.9537

 

DN/JST.JSTAGE/internalmedicine/52.9537

Allergic Bronchopulmonary Aspergillosis with Repeated Isolation of Nontuberculous Mycobacteria

Takashi Ishiguro¹⁾, Noboru Takayanagi¹⁾, Yotaro Takaku¹⁾, Naho Kagiyama¹⁾, Yoshihiko Shimizu²⁾, Tsutomu Yanagisawa¹⁾, Yoshinori Kawabata²⁾, Yutaka Sugita¹⁾

1) Department of Respiratory Medicine, Saitama Cardiovascular and Respiratory Center, Japan 2) Department of Pathology, Saitama Cardiovascular and Respiratory Center, Japan

 Released on J-STAGE 20130801  

Keywords: allergic bronchopulmonary mycosis, aspergillosis, nontuberculous mycobacteria, mycobacteriosis, colonization

•  Full Text PDF [2047K]

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• References(18)

A 68-year-old woman without asthma presented with a cough and abnormal shadows on a chest X-ray. Computed tomography showed right middle lobe atelectasis and centrilobular nodules with a tree-in-bud appearance in the other lobes. The patient's sputum repeatedly yielded positive cultures of nontuberculous mycobacteria (NTM); however, no fungi were detected. A transbronchial biopsy showed allergic mucin with eosinophils, although the findings were not diagnostic. We suspected that the patient had pulmonary mycobacteriosis; however, treatment for this condition failed. We then performed thoracoscopy for further evaluation and treatment of the NTM infection. The resected specimen obtained from the right middle lobe exhibited the characteristic findings of allergic bronchopulmonary mycosis without evidence of mycobacterial infection. The administration of corticosteroids and itraconazole resulted in improvement of the patient's condition. The NTM appeared to be simply a coincidental colonization of the resected middle lobe bronchus. The absence of asthma, the inability to isolate fungi and the repeated isolation of NTM made it difficult to differentiate allergic bronchopulmonary aspergillosis from NTM infection.

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Copyright © 2013 by The Japanese Society of Internal Medicine

Polypoidal Lesions in the Nasal Cavity

Original Article DOI : 10.7860/JCDR/2013/4718.3025

Year : 2013  |  Month : 06  |  Volume : 7  |  Issue : 6  |  Page : 1040 - 1042

Polypoidal Lesions in the Nasal Cavity

Kalpana Kumari M.K.1, Mahadeva K.C.2 1 Associate Professor, Department of Pathology, M.S. Ramaiah Medical College, Karnataka, India. 2 Professor, Department of Pathology, M.S. Ramaiah Medical College, Karnataka, India. NAME, ADRESS, E-MAIL ID OF THE CORRESPONDING AUTHOR: Dr. Kalpana Kumari M.K, Flat No 710, C Block, Sterling Residency, Dollors Colony, RMV IInd Stage, Bangalore-560094, Karnataka, India. Phone: 9886392301 E-mail: kalpank@gmail.com

Abstract

Introduction: Nasal polyps are polypoidal masses arising from mucous membranes of nose and paranasal sinuses. They are overgrowths of the mucosa that frequently accompany allergic rhinitis. They are freely movable and nontender. Aims and Objectives: The purpose of this study was to study the histopathologic spectrum of polypoidal lesions of the nasal cavity. Materials and Methods: The study comprised of 100 condivutive cases of polypoidal lesions in the nasal cavity, received in the department of pathology. The age and sex of the patients were recorded. The tissues were routinely processed for histopathologic divtions and stained with haematoxylin and eosin stains. Special stains like Periodic acid Schiff (PAS) was done wherever applicable. The cases were classified into neoplastic and nonneoplastic lesions. The neoplastic lesions were further classified according to WHO classification on histopathologic examination. Results: Analysis of 100 polypoidal lesions in the nose and paranasal sinuses with clinical diagnosis of nasal polyps, revealed 66 cases were nonneoplastic and 34 were neoplastic;17 (50%)were benign and 17(50%) were malignant. True nasal polyps both inflammatory and allergic together comprised 44 cases of the 100 polypoidal lesions in the nasal cavity. Angiofibroma and inverted papilloma were the most frequent benign tumour accounting for 12/17(0.7%). The most common malignant tumour was anaplastic carcinoma 7/17(0.4%). Nonneoplastic and benign tumours were common in younger age groups whereas malignant tumours were most common in older males. Conclusion: The majority of polypoidal lesions in the nasal cavity are nonneoplastic.

How to cite this article : Kalpana Kumari M.K., Mahadeva K.C., .POLYPOIDAL LESIONS IN THE NASAL CAVITY.Journal of Clinical and Diagnostic Research [serial online]2013 06[cited:2013 Aug 3] 6 1040 - 1042  » Full text  » Article in PDF  » Audio Visual  » Citation Manager  » Article Statistics  » Link to PUBMED  » Print this Article  » Send to a Friend

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Front. Immunol., 02 August 2013 | doi: 10.3389/fimmu.2013.00208

Do natural T regulatory cells become activated to antigen specific T regulatory cells in transplantation and in autoimmunity?

Bruce M. Hall*, Giang T. Tran, Nirupama D. Verma, Karren M. Plain, Catherine M. Robinson, Masaru Nomura and Suzanne J. Hodgkinson

• Immune Tolerance Laboratory, Medicine, University of New South Wales, Sydney, NSW, Australia

Antigen specific T regulatory cells (T_reg) are often CD4⁺CD25⁺FoxP3⁺ T cells, with a phenotype similar to natural T_reg (nT_reg). It is assumed that nT_reg cannot develop into an antigen specific T_reg as repeated culture with IL-2 and a specific antigen does not increase the capacity or potency of nT_reg to promote immune tolerance or suppress in vitro. This has led to an assumption that antigen specific T_reg mainly develop from CD4⁺CD25⁻FoxP3⁻ T cells, by activation with antigen and TGF-β in the absence of inflammatory cytokines such as IL-6 and IL-1β. Our studies on antigen specific CD4⁺CD25⁺ T cells from animals with tolerance to an allograft, identified that the antigen specific and T_reg are dividing, and need continuous stimulation with specific antigen T cell derived cytokines. We identified that a variety of cytokines, especially IL-5 and IFN-γ but not IL-2 or IL-4 promoted survival of antigen specific CD4⁺CD25⁺FoxP3⁺T_reg. To examine if nT_reg could be activated to antigen specific T_reg, we activated nT_reg in culture with either IL-2 or IL-4. Within 3 days, antigen specific T_reg are activated and there is induction of new cytokine receptors on these cells. Specifically nT_reg activated by IL-2 and antigen express the interferon-γ receptor (IFNGR) and IL-12p70 (IL-12Rβ2) receptor but not the IL-5 receptor (IL-5Rα). These cells were responsive to IFN-γ or IL-12p70. nT_reg activated by IL-4 and alloantigen express IL-5Rα not IFNGR or IL-12p70Rβ2 and become responsive to IL-5. These early activated antigen specific T_reg, were respectively named Ts1 and Ts2 cells, as they depend on Th1 or Th2 responses. Further culture of Ts1 cells with IL-12p70 induced Th1-like T_reg, expressing IFN-γ, and T-bet as well as FoxP3. Our studies suggest that activation of nT_reg with Th1 or Th2 responses induced separate lineages of antigen specific T_reg, that are dependent on late Th1 and Th2 cytokines, not the early cytokines IL-2 and IL-4.

Keywords: antigen specific T_reg, nT_reg, Th1-like T_reg, Th2-like T_reg, immune tolerance

Citation: Hall BM, Tran GT, Verma ND, Plain KM, Robinson CM, Nomura M and Hodgkinson SJ (2013) Do natural T regulatory cells become activated to antigen specific T regulatory cells in transplantation and in autoimmunity? Front. Immunol. 4:208. doi: 10.3389/fimmu.2013.00208

Received: 03 April 2013; Accepted: 08 July 2013;
Published online: 02 August 2013.

Edited by:

Eyad Elkord, United Arab Emirates University, UAE; University of Salford, UK; University of Manchester, UK

Reviewed by:

Dominique M. A. Bullens, KU Leuven, Belgium
Jocelyne Demengeot, Instituto Gulbenkian de Ciencia, Portugal

Copyright: © 2013 Hall, Tran, Verma, Plain, Robinson, Nomura and Hodgkinson. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Bruce M. Hall, Immune Tolerance Laboratory, Medicine, University of New South Wales, Suite 206 National Innovation Centre, 4 Cornwallis Street, Australian Technology Park, Eveleigh, Sydney, NSW 1430, Australia e-mail: b.hall@unsw.edu.au

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Fibroblasts: the missing link between fibrotic lung diseases of different etiologies?

Bruno Crestani, Valerie Besnard, Laurent Plantier, Keren Borensztajn and Arnaud Mailleux

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Respiratory Research 2013, 14:81 doi:10.1186/1465-9921-14-81

Published: 2 August 2013

Abstract (provisional)

Fibrotic lung disorders, either idiopathic, or associated with a specific etiology or a specific condition such as scleroderma, are increasingly recognized. As a whole they constitute a group of diseases characterized by the progressive destruction of the lung which ultimately leads to chronic respiratory failure and death. Improving the prognosis of these disorders requires the identification of drugs capable of inhibiting partially or totally the progression of lung fibrosis, and perhaps to reversing established fibrosis. This has been the focus of huge efforts from academic groups and pharma companies, and more than 20 different molecules are being investigated in clinical trials in idiopathic pulmonary fibrosis (IPF) a well defined and relatively frequent fibrotic lung disease of unknown etiology. However, until now, only one drug has been approved for lung fibrosis treatment. This drug, pirfenidone, has been shown to slow the decline of lung function in IPF, but no drug has demonstrated on the survival of patients with lung fibrosis (1). The effort must be prolonged and intensified. Beside IPF, scleroderma-associated lung fibrosis is a well recognized fibrotic disorder. With pulmonary hypertension, lung fibrosis is now the main cause of death of patients with scleroderma (2). The nature and pathophysiology of lung fibrosis in IPF and scleroderma are different. For instance, scleroderma affects mainly women, whereas IPF predominates in men; usual interstitial pneumonia is the pathological pattern of IPF, whereas non specific interstitial pneumonia is the main pattern in patients with scleroderma ; the MUC5B promotor polymorphism is associated with IPF whereas it is not observed in patients with IPF (3); IPF is rapidly progressive disorder as compared with the slowly moving scleroderma-associated lung fibrosis (2).

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

Research

Microarray profiling reveals suppressed interferon stimulated gene program in fibroblasts from scleroderma-associated interstitial lung disease

Gisela E Lindahl, Carmel JW Stock, Xu Shi-Wen, Patricia Leoni, Piersante Sestini, Sarah L Howat, George Bou-Gharios,Andrew G Nicholson, Christopher P Denton, Jan C Grutters, Toby M Maher, Athol U Wells, David J Abraham andElisabetta A Renzoni

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Respiratory Research 2013, 14:80 doi:10.1186/1465-9921-14-80

Published: 2 August 2013

Abstract (provisional)

Background

Interstitial lung disease is a major cause of morbidity and mortality in systemic sclerosis (SSc), with insufficiently effective treatment options. Progression of pulmonary fibrosis involves expanding populations of fibroblasts, and the accumulation of extracellular matrix proteins. Characterisation of SSc lung fibroblast gene expression profiles underlying the fibrotic cell phenotype could enable a better understanding of the processes leading to the progressive build-up of scar tissue in the lungs. In this study we evaluate the transcriptomes of fibroblasts isolated from SSc lung biopsies at the time of diagnosis, compared with those from control lungs.

Methods

We used Affymetrix oligonucleotide microarrays to compare the gene expression profile of pulmonary fibroblasts cultured from 8 patients with pulmonary fibrosis associated with SSc (SSc-ILD), with those from control lung tissue peripheral to resected cancer (n=10). Fibroblast cultures from 3 patients with idiopathic pulmonary fibrosis (IPF) were included as a further comparison. Genes differentially expressed were identified using two separate analysis programs following a set of pre-determined criteria: only genes significant in both analyses were considered. Microarray expression data was verified by qRT-PCR and/or western blot analysis.

Results

A total of 843 genes were identified as differentially expressed in pulmonary fibroblasts from SSc-ILD and/or IPF compared to control lung, with a large overlap in the expression profiles of both diseases. We observed increased expression of a TGF-beta response signature including fibrosis associated genes and myofibroblast markers, with marked heterogeneity across samples. Strongly suppressed expression of interferon stimulated genes, including antiviral, chemokine, and MHC class 1 genes, was uniformly observed in fibrotic fibroblasts. This expression profile includes key regulators and mediators of the interferon response, such as STAT1, and CXCL10, and was also independent of disease group.

Conclusions

This study identified a strongly suppressed interferon-stimulated gene program in fibroblasts from fibrotic lung. The data suggests that the repressed expression of interferon-stimulated genes may underpin critical aspects of the profibrotic fibroblast phenotype, identifying an area in pulmonary fibrosis that requires further investigation.

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