A blog that publishes updates and open access scientific papers about allergy, asthma and immunology. Editor: Juan Carlos Ivancevich, MD. Specialist in Allergy & Immunology
March 22, 2013
Bacterial Exposure and the Primary Prevention of Asthma: A Model for Gene-Environment Interaction III
Bacterial Exposure and the Primary Prevention of Asthma:
A Model for Gene-Environment Interaction
Harald Renz, MD
Partners Asthma GR 09.07.2012 - 3/3
Bacterial Exposure and the Primary Prevention of Asthma: A Model for Gene-Environment Interaction II
Bacterial Exposure and the Primary Prevention of Asthma:
A Model for Gene-Environment Interaction
Harald Renz, MD
Partners Asthma GR 09.07.2012 - 2/3
Bacterial Exposure and the Primary Prevention of Asthma: A Model for Gene-Environment Interaction I
Bacterial Exposure and the Primary Prevention of Asthma:
A Model for Gene-Environment Interaction
Harald Renz, MD
Partners Asthma GR 09.07.2012 - 1/3
March 21, 2013
Schnitzler's syndrome: diagnosis, treatment, and follow-up
Review Article
You have free access to this content
Schnitzler's syndrome: diagnosis, treatment, and follow-up
Schnitzler's syndrome: diagnosis, treatment, and follow-up
Abstract
Schnitzler's syndrome is characterized by recurrent urticarial rash and monoclonal gammopathy, associated with clinical and biological signs of inflammation and a long-term risk of AA amyloidosis and overt lymphoproliferation. An extensive literature review was performed, and the following questions were addressed during an expert meeting: In whom should Schnitzler's syndrome be suspected? How should the diagnosis of Schnitzler's syndrome be established? How should a patient with Schnitzler's syndrome be treated? How should a patient with Schnitzler's syndrome be followed up?. A diagnosis of Schnitzler's syndrome is considered definite in any patient with two obligate criteria: a recurrent urticarial rash and a monoclonal IgM gammopathy, and two of the following minor criteria: recurrent fever, objective signs of abnormal bone remodeling, elevated CRP level or leukocytosis, and a neutrophilic infiltrate on skin biopsy. It is considered probable, if only 1 minor criterion is present. In patients with monoclonal IgG gammopathies, diagnosis is definite if three minor criteria are present and possible if two are present. First-line treatment in patients with significant alteration of quality of life or persistent elevation of markers of inflammation should be anakinra. Follow-up should include clinical evaluation, CBC and CRP every 3 months and MGUS as usually recommended.
Abstract
Schnitzler's syndrome is characterized by recurrent urticarial rash and monoclonal gammopathy, associated with clinical and biological signs of inflammation and a long-term risk of AA amyloidosis and overt lymphoproliferation. An extensive literature review was performed, and the following questions were addressed during an expert meeting: In whom should Schnitzler's syndrome be suspected? How should the diagnosis of Schnitzler's syndrome be established? How should a patient with Schnitzler's syndrome be treated? How should a patient with Schnitzler's syndrome be followed up?. A diagnosis of Schnitzler's syndrome is considered definite in any patient with two obligate criteria: a recurrent urticarial rash and a monoclonal IgM gammopathy, and two of the following minor criteria: recurrent fever, objective signs of abnormal bone remodeling, elevated CRP level or leukocytosis, and a neutrophilic infiltrate on skin biopsy. It is considered probable, if only 1 minor criterion is present. In patients with monoclonal IgG gammopathies, diagnosis is definite if three minor criteria are present and possible if two are present. First-line treatment in patients with significant alteration of quality of life or persistent elevation of markers of inflammation should be anakinra. Follow-up should include clinical evaluation, CBC and CRP every 3 months and MGUS as usually recommended.
- A. Simon1,
- B. Asli2,
- M. Braun-Falco3,
- H. De Koning4,
- J.-P. Fermand2,
- C. Grattan5,
- K. Krause6,
- H. Lachmann7,
- C. Lenormand8,
- V. Martinez-Taboada9,
- M. Maurer6,
- M. Peters10,
- R. Rizzi11,
- F. Rongioletti12,
- T. Ruzicka3,
- L. Schnitzler13,
- B. Schubert14,
- J. Sibilia15,
- D. Lipsker8
Article first published online: 9 MAR 2013
DOI: 10.1111/all.12129
© 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd
Mast cells and the liver aging process
Mast cells and the liver aging process
Fabio Grizzi1†, Giuseppe Di Caro1, Luigi Laghi1, Paul Hermonat2, Paolo Mazzola3, Diane D Nguyen4, Saba Radhi4, Jose A Figueroa4, Everardo Cobos4,5, Giorgio Annoni3 andMaurizio Chiriva-Internati4,5,6*†
Immunity & Ageing 2013, 10:9 doi:10.1186/1742-4933-10-9
The electronic version of this article is the complete one and can be found online at:http://www.immunityageing.com/content/10/1/9
Abstract
It has now ascertained that the clinical manifestations of liver disease in the elderly population reflect both the cumulative effects of longevity on the liver and the generalized senescence of the organism ability to adjust to metabolic, infectious, and immunologic insults. Although liver tests are not significantly affected by age, the presentation of liver diseases such as viral hepatitis may be subtler in the elderly population than that of younger patients.
Human immunosenescence is a situation in which the immune system, particularly T lymphocyte function, deteriorates with age, while innate immunity is negligibly affected and in some cases almost up-regulated.
We here briefly review the relationships between the liver aging process and mast cells, the key effectors in a more complex range of innate immune responses than originally though.
An evidence-based approach for providing cautionary recommendations to sulfonamide-allergic patients and determining cross-reactivity among sulfonamide-containing medications
Review Article
You have free access to this content
- S. Ghimire MPharm1,
- E. Kyung PharmD MPharm1,
- J. H. Lee MD PhD2,
- J. W. Kim MD3,
- W. Kang PhD4,*,
- E. Kim PharmD PhD5,*
Article first published online: 13 MAR 2013
DOI: 10.1111/jcpt.12048
© 2013 Blackwell Publishing Ltd
Issue
Journal of Clinical Pharmacy and Therapeutics
Summary
What is known and Objective
Prescribing sulfonamide-containing medications for patients with sulfonamide allergy continues to complicate medical decisions. We examined the cautionary recommendations in the approved drug monographs and primary literature, and formulated an evidence-based grading of cautionary recommendations for sulfonamide allergy and cross-reactivity among sulfonamide-containing medications.
Methods
Drug monographs were collected from six countries and three drug compendia. Two reviewers independently extracted the data from the contraindication, warning and/or precaution sections of drug monographs. Evidence for cross-reactivity was examined in the primary literature and compared with drug monograph recommendations. Consequently, medications were categorized based on the strength of recommendation and level of evidence by consensus.
Results and Discussion
We identified wide variability in cautionary recommendations ranging from no warning or precaution to contraindication among the sources reviewed. The recommendations were located mainly in the contraindication section of monographs for France (65·2%), United Kingdom (51·9%), Italy (50·0%), South Korea (43·5%), United States (38·2%) and Canada (37·0%), whereas in drug compendia, the recommendations were found in the precaution section for Martindale (51·4%) and Micromedex-Drugdex (33·3%), and contraindication and precaution section for the American Hospital Formulary Service Drug Information 2010 (30·8%). Evidence from the primary literature varied with recommendation included in drug monographs. Evidence-based categorization was carried out for 16 medications. Two sulfonamide-moiety-containing drugs were considered safe, six non-sulfonylarylamines required precaution, and eight medications from all three sulfonamide chemical classes were considered mostly unsafe.
What is new and Conclusion
There are significant discrepancies in cautionary recommendations included in drug-labels and drug compendia. Statements concerning cross-reactive hypersensitivity with other sulfonamides generally suggest theoretical possibilities. The consensus evidence-based grading instrument developed may be useful for deriving cautionary recommendations for sulfonamide-allergic patients.
Cogan's syndrome: An autoimmune inner ear disease
Review
Cogan's syndrome: An autoimmune inner ear disease
Open Access Article
- A. Grecoa,
,
,
- A. Galloa,
- M. Fusconia,
- G. Magliuloa,
- R. Turchettab,
- C. Marinellia,
- G.F. Macria,
- A. De Virgilioa,
- M. de Vincentiisa
- a ENT Department, Policlinico “Umberto I”, University of Rome “Sapienza”, Italy
- b Audiology Department, Policlinico “Umberto I”, University of Rome “Sapienza”, Italy
Abstract
Objectives
The objective of our study was to review our current knowledge of the aetiopathogenesis of Cogan's syndrome, including viral infection and autoimmunity, and to discuss disease pathogenesis with relevance to pharmacotherapy.
Systematic review methodology
Relevant publications on the aetiopathogenesis and pharmacotherapy of Cogan's syndrome from 1945 to 2012 were analysed.
Results and conclusions
Cogan's syndrome is a rare autoimmune vasculitis, and its pathogenesis is unknown. Infection, but primarily autoimmunity, may play contributing roles in the pathogenesis of this disease. It is characterised by ocular and audiovestibular symptoms similar to those of Meniere's syndrome. Approximately 70% of patients have systemic disease, of which vasculitis is considered the pathological mechanism. The immunologic theory is based on the release of auto-antibodies against corneal, inner ear and endothelial antigens, and of anti-nuclear cytoplasmic auto-antibodies (ANCA).
Corticosteroids are the first line of treatment, and multiple immunosuppressive drugs have been tried with varying degrees of success. Tumour necrosis factor (TNF)-alpha blockers are a category of immunosuppressive agents representing a recent novel therapeutic option in Cogan's syndrome.
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