OPEN ACCESS PEER-REVIEWED

RESEARCH ARTICLE

Influence of Initial Treatment Modality on Long-Term Control of Chronic Idiopathic Urticaria

• Sujeong Kim,
 
• Seunghee Baek,
 
• Bomi Shin,
 
• Sun-young Yoon,
 
• So Young Park,
 
• Taehoon Lee,
 
• Yoon Su Lee,
 
• Yun-Jeong Bae,
 
• Hyouk Soo Kwon,
• You Sook Cho,
 
• Hee-Bom Moon,
 
• Tae-Bum Kim mail

Abstract

Background

Chronic idiopathic urticaria (CIU) is a common cutaneous disorder but the influence of initial treatment modality on long-term control is not known. The aim of this study was to evaluate clinical features, and the influence of initial treatment modality on long-term control.

Methods and Results

641 CIU patients were enrolled from the allergy clinic in a tertiary referral hospital. Disease duration, aggravating factors and treatment modality at each visit were evaluated. Times required to reach a controlled state were analyzed according to initial treatment modality, using Kaplan-Meier survival curves, the Cox proportional-hazards model, and propensity scores. Female to male ratio was 1.7: 1; mean age at onset was 40.5 years. The most common aggravating factors were food (33.5%), stress (31.5%) and fatigue (21.6%). Most patients (82.2%) used H1-antihistamines alone as initial treatment while 17% used a combination treatment with oral corticosteroids. There was no significant difference in the time taken to reach a controlled state between patients treated with single vs multiple H1-antihistamines or between those who received H1-antihistamine monotherapy vs. a combination therapy with oral corticosteroids.

Conclusion

The time required to control CIU is not reduced by use of multiple H1-antihistamines or oral corticosteroids in the initial treatment.

Citation: Kim S, Baek S, Shin B, Yoon S-y, Park SY, et al. (2013) Influence of Initial Treatment Modality on Long-Term Control of Chronic Idiopathic Urticaria. PLoS ONE 8(7): e69345. doi:10.1371/journal.pone.0069345

Editor: Salik Hussain, National Institute of Health (NIH), United States of America

Received: February 7, 2013; Accepted: June 7, 2013; Published: July 23, 2013

Copyright: © 2013 Kim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This study was supported by a grant (2011-420) from the Asan Institute for Life Sciences, Seoul, Korea. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

Download

PDF

Citation

XML

Autologous Serum Skin Test versus Autologous Plasma Skin Test in Patients with Chronic Spontaneous Urticaria

Clinical Study

Autologous Serum Skin Test versus Autologous Plasma Skin Test in Patients with Chronic Spontaneous Urticaria

Aysegul Alpay,¹ Nilgün Solak Tekin,¹ Ishak Özel Tekin,² H. Cevdet Altinyazar,³ Rafet Koca,¹ and Saniye Çınar¹

¹Bulent Ecevit University, School of Medicine, Department of Dermatology, Kozlu, 67600 Zonguldak, Turkey
²Bulent Ecevit University, School of Medicine, Department of Immunology, Turkey
³Selcuk University, Selcuklu Medical Faculty, Department of Dermatology, Turkey

Received 7 April 2013; Accepted 19 June 2013

Academic Editor: Elizabeth Helen Kemp

Copyright © 2013 Aysegul Alpay 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

Previous studies indicate that 25–45% of chronic urticaria patients have an autoimmune etiology. Autologous serum skin test (ASST) and autologous plasma skin test (APST) are simple tests for diagnosing chronic autoimmune urticaria (CAU). However, there are still some questions about the specificity of these tests. This study consisted of 50 patients with chronic spontaneous urticaria (CSU) and 50 sex- and age-matched healthy individuals aged 18 years, and older. A total of 31 (62%) patients and 5 (10%) control patients had positive ASST; 21 (42%) patients and 3 (6%) control patients had positive APST. Statistically significant differences were noted in ASST and APST positivity between the patient and control groups (ASST ; APST ). Thirteen (26%) patients and 5 (10%) control patients had antithyroglobulin antibodies or antithyroid peroxidase antibody positivity. No statistically significant differences were noted in thyroid autoantibodies between the patient and control groups (anti-TG ; anti-TPO ). We consider that the ASST and APST can both be used as in vivo tests for the assessment of autoimmunity in the etiology of CSU and that thyroid autoantibodies should be checked even when thyroid function tests reveal normal results in patients with CSU.

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

ORIGINAL RESEARCH ARTICLE

Share0

Like0

Comment0

Facebook

Linkedin

0Share

views119

Front. Immunol., 12 August 2013 | doi: 10.3389/fimmu.2013.00230

Binding of soluble yeast β-glucan to human neutrophils and monocytes is complement-dependent

Nandita Bose*, Anissa S. H. Chan, Faimola Guerrero, Carolyn M. Maristany, Xiaohong Qiu, Richard M. Walsh, Kathleen E. Ertelt, Adria Bykowski Jonas, Keith B. Gorden, Christine M. Dudney, Lindsay R. Wurst, Michael E. Danielson, Natalie Elmasry, Andrew S. Magee, Myra L. Patchen and John P. Vasilakos

• Biothera, Eagan, MN, USA

The immunomodulatory properties of yeast β-1,3/1,6 glucans are mediated through their ability to be recognized by human innate immune cells. While several studies have investigated binding of opsonized and unopsonized particulate β-glucans to human immune cells mainly via complement receptor 3 (CR3) or Dectin-1, few have focused on understanding the binding characteristics of soluble β-glucans. Using a well-characterized, pharmaceutical-grade, soluble yeast β-glucan, this study evaluated and characterized the binding of soluble β-glucan to human neutrophils and monocytes. The results demonstrated that soluble β-glucan bound to both human neutrophils and monocytes in a concentration-dependent and receptor-specific manner. Antibodies blocking the CD11b and CD18 chains of CR3 significantly inhibited binding to both cell types, establishing CR3 as the key receptor recognizing the soluble β-glucan in these cells. Binding of soluble β-glucan to human neutrophils and monocytes required serum and was also dependent on incubation time and temperature, strongly suggesting that binding was complement-mediated. Indeed, binding was reduced in heat-inactivated serum, or in serum treated with methylamine or in serum reacted with the C3-specific inhibitor compstatin. Opsonization of soluble β-glucan was demonstrated by detection of iC3b, the complement opsonin on β-glucan-bound cells, as well as by the direct binding of iC3b to β-glucan in the absence of cells. Binding of β-glucan to cells was partially inhibited by blockade of the alternative pathway of complement, suggesting that the C3 activation amplification step mediated by this pathway also contributed to binding.

Article Info

Abstract

Full Text

PDF

Supplemental Data

• Presentation 1.PDF

Export Citation

XML

View Article Impact

Keywords: C3, opsonization, CR3, β-glucans, neutrophils, monocytes

Citation: Bose N, Chan ASH, Guerrero F, Maristany CM, Qiu X, Walsh RM, Ertelt KE, Jonas AB, Gorden KB, Dudney CM, Wurst LR, Danielson ME, Elmasry N, Magee AS, Patchen ML and Vasilakos JP (2013) Binding of soluble yeast β-glucan to human neutrophils and monocytes is complement-dependent. Front. Immunol. 4:230. doi: 10.3389/fimmu.2013.00230

Received: 06 May 2013; Accepted: 22 July 2013;
Published online: 12 August 2013.

Edited by:

Zvi Fishelson, Tel Aviv University, Israel

Reviewed by:

Anna M. Blom, Lund University, Sweden
Joana Vitte, Aix Marseille Université, France
Zsuzsa Bajtay, Lorand Eotvos University, Hungary

Copyright: © 2013 Bose, Chan, Guerrero, Maristany, Qiu, Walsh, Ertelt, Jonas, Gorden, Dudney, Wurst, Danielson, Elmasry, Magee, Patchen and Vasilakos. 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: Nandita Bose, Biothera, 3388 Mike Collins Drive, Eagan, MN 55121, USA e-mail: nbose@biothera.com

Share0

Like0

Comment0

Facebook

Linkedin

0Share

views119

Research

Hereditary angioedema with C1 inhibitor deficiency: delay in diagnosis in Europe

Andrea Zanichelli, Markus Magerl, Hilary Longhurst, Vincent Fabien and Marcus Maurer

For all author emails, please log on.

Allergy, Asthma & Clinical Immunology 2013, 9:29 doi:10.1186/1710-1492-9-29

Published: 12 August 2013

Abstract (provisional)

Background

Hereditary angioedema (HAE) is a rare, debilitating, and potentially life-threatening disease characterized by recurrent edema attacks. Important advances in HAE treatment have been made, including the development of new therapies for treating or preventing attacks. Nevertheless, the disease is still frequently misdiagnosed and inappropriately treated, potentially exposing patients with laryngeal attacks to the risk of asphyxiation.

Methods

The Icatibant Outcome Survey (IOS) is an international, observational study that documents the clinical outcome of HAE patients eligible for treatment with icatibant. Patient ages at first symptoms and at diagnosis were recorded at enrolment, and the delay between first symptoms and diagnosis was calculated.

Results

The median [range] diagnostic delay in HAE type I and II patients across eight countries was 8.5 years [0--62.0]. The median delay in diagnosis was longer for HAE type II versus type I (21 versus 8 years, respectively), although this did not quite reach statistical significance.

Conclusions

Although it can be difficult to differentiate HAE symptoms from those of more common angioedema sub-types (e.g. idiopathic or acquired angioedema), our results show that HAE type I and II patients have an unacceptable delay in diagnosis, even those with a family history of the disease. Raising physician awareness of this disabling and potentially fatal disease may lead to a more accurate diagnosis and timely treatment.

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