Center for Autoimmune Diseases

Tel Aviv, Israel

Center for Autoimmune Diseases

Tel Aviv, Israel
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Shapira Y.,Zabludowicz Center for Autoimmune Diseases | Agmon-Levin N.,Zabludowicz Center for Autoimmune Diseases | Shoenfeld Y.,Center for Autoimmune Diseases
Nature Reviews Rheumatology | Year: 2010

The accumulative global burden of autoimmune and inflammatory rheumatic diseases is substantial. Studying the distribution of these conditions across various global regions and ethnic groups by means of geoepidemiology might readily provide epidemiological data and also advance our understanding of their genetic and environmental underpinnings. In order to depict the geoepidemiology of autoimmune and inflammatory rheumatic diseases, namely rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, ankylosing spondylitis and Sjögren's syndrome, we present a comprehensive collection of epidemiological reports from various world regions, including the prevalence of each of these conditions. The accumulated data show that the reviewed rheumatic diseases are global phenomena, and, with some variance, seem to be relatively evenly distributed. This finding is in contrast with the obviously uneven distribution of some major nonrheumatic autoimmune conditions. In addition, geoepidemiology demonstrates that ethnogenetic susceptibility interacts with lifestyle and environmental factors, which include socioeconomic status, infectious agents (triggering or protective agents), environmental pollutants, and vitamin D (dependent on sunlight exposure), in determining the risk of developing rheumatic autoimmunity. © 2010 Macmillan Publishers Limited.


Shapira Y.,Center for Autoimmune Diseases | Agmon-Levin N.,Center for Autoimmune Diseases | Agmon-Levin N.,Chaim Sheba Medical Center | Shoenfeld Y.,Center for Autoimmune Diseases | And 2 more authors.
Clinical Reviews in Allergy and Immunology | Year: 2010

Mycobacterium tuberculosis (TB) is a major cause of morbidity and mortality worldwide. Current anti-TB chemotherapies, although effective, are associated with side effects and are limited in treating drug-resistant strands. Autoimmune diseases are a leading cause of morbidity and mortality, with a growing mass of evidence implicating infections (e.g., TB) as their triggers. The burden of TB might further increase by reactivation threats hovering over millions harboring latent infection, thus, calling for novel approaches for this dire ailment. In recent years, the non-calcemic physiological actions of vitamin D have drawn a great deal of attention. In this review, we will focus on the role of vitamin D in the innate immune defense against TB on the one hand and conversely on the immunomodulatory effects of vitamin D on autoimmunity. Taken together, the suggested dual role of vitamin D in treating TB infection and possibly preventing associated autoimmunity will constitute the basis of the current review. © Humana Press Inc. 2009.


Israeli E.,Center for Autoimmune Diseases | Agmon-Levin N.,Center for Autoimmune Diseases | Blank M.,Center for Autoimmune Diseases | Shoenfeld Y.,Center for Autoimmune Diseases | Shoenfeld Y.,Tel Aviv University
Clinical Reviews in Allergy and Immunology | Year: 2011

Macrophagic myofasciitis (MMF) is an immune-mediated condition first reported in 1998. MMF is characterized by post-vaccination systemic manifestations as well as local-stereotyped and immunologically active lesion in the site of inoculation (deltoid muscle). MMF systemic symptoms included myalgias, arthralgias, marked asthenia, muscle weakness, chronic fatigue, and fever. Recently, studies demonstrated that the local lesion is due to persistence for years at site of injection of an aluminum (Al(OH)3) adjuvant commonly used in human vaccines. Time elapsed from last immunization with an Al(OH)3-containing vaccine to muscle biopsy range from 3 months to 8 years; in rare cases, MMF may be diagnosed even 10 years post-vaccination. The discrepancy between the wide applications of aluminum hydroxide-containing vaccines and the very limited number of MMF cases reported may be resolved by observations suggesting that aluminum-containing vaccinations may trigger MMF in genetically susceptible subjects carrying the HLA-DRB1*01. Thus, MMF may be defined as an emerging novel condition that may be triggered by exposure to alum-containing vaccines, in patients with a specific genetic background, and this temporal association may be exhibited from a few months up to 10 years. © 2010 Springer Science+Business Media, LLC.


De Carvalho J.F.,University of Sao Paulo | Pereira R.M.R.,University of Sao Paulo | Shoenfeld Y.,Center for Autoimmune Diseases | Shoenfeld Y.,Tel Aviv University
Clinical Reviews in Allergy and Immunology | Year: 2010

Atherosclerosis is an inflammatory disease, and several antigens have been shown to activate the immune response and affect the development of atherogenesis. This suggests that modulation of the immune system could represent a useful approach to prevent and/or treat this disorder. A vaccination approach might be a useful, effective tool in the modern arsenal of cardiovascular therapy and could possibly be used on a large scale at a low cost. Several modalities of vaccines have been tested against lipoproteins, cholesterol, molecules involved in cholesterol metabolism, atherosclerosis- associated microorganisms, and other molecules (heat shock protein, CD99, vascular endothelial growth factor-receptor, interleukin-2), with promising results. Nevertheless, a deeper understanding of the role of immunization in atherosclerosis will be essential to the use of vaccines in clinical medicine. © Humana Press Inc. 2009.


Szekanecz Z.,Debrecen University | Szekanecz E.,Debrecen University | Bako G.,Debrecen University | Shoenfeld Y.,Center for Autoimmune Diseases
Gerontology | Year: 2011

Paraneoplastic symptoms, caused by a malignancy, but not directly related to invasion by the tumor or its metastases, are the result of a wide variety of tumor-derived biologic mediators like hormones, peptides, antibodies, cytotoxic lymphocytes, autocrine and paracrine mediators. Systemic inflammatory rheumatic diseases, such as rheumatoid arthritis, systemic lupus erythematosus, scleroderma or dermatomyositis, may increase the risk for the development of malignancies, predominantly lymphoproliferative disorders. Immunosuppressive drugs and biological agents may also be carcinogenic. However, sustained inflammatory activity seems to be the primary risk factor for malignancies in autoimmune diseases. Tumor-associated antigens may be produced by inflammatory cells and their production may be increased in rheumatoid arthritis and other autoimmune diseases. Copyright © 2010 S. Karger AG, Basel.


Nussinovitch U.,Center for Autoimmune Diseases | Shoenfeld Y.,Center for Autoimmune Diseases | Shoenfeld Y.,Tel Aviv University
Heart | Year: 2010

Autoimmunity plays a role in the pathogenesis of numerous cardiac diseases such as dilated cardiomyopathy (DCM), myocarditis, rheumatic fever and atherosclerosis. An autoimmune response may appear following myocardial injury and exposure to self-antigens. Anti-heart autoantibodies have been identified in patients with heart disease and in low titres of healthy individuals. Troponin is the preferred marker in detecting acute coronary syndrome. In recent years, anti-troponin autoantibodies were identified in patients with DCM and ischaemic cardiomyopathy. The presence of anti-troponin autoantibodies in the serum may cause a false-negative evaluation of troponin levels and delay treatment of acute coronary syndrome. The role of anti-troponin autoantibodies in humans and their possible involvement in the pathogenesis of heart disease remains controversial. Previous studies have demonstrated that anti-troponin autoantibodies can cause cardiac dysfunction in animal models. This paper reviews current knowledge on anti-troponin autoantibodies. Future research should focus on the pathogenic role of anti-troponin autoantibodies and reactive T cells and the possible benefits of targeted therapy in acute coronary syndrome, post-myocardial infarction, myocarditis, DCM and heart failure.


Katz U.,Maccabi Healthcare Services | Shoenfeld Y.,Center for Autoimmune Diseases | Zakin V.,Israel Agricultural Research Organization | Sherer Y.,Hospital Management | Sukenik S.,Ben - Gurion University of the Negev
Seminars in Arthritis and Rheumatism | Year: 2012

Objectives: The Dead Sea, the deepest and most saline lake on earth, has been known from biblical times for its healing properties. The aim of this systematic review was to present critically the level of evidence for the claims of therapeutic effects of Dead Sea treatments in several rheumatologic diseases and psoriasis as well as to review these treatments' safety. Methods: All articles cited in MEDLINE under the query, "Dead Sea," were reviewed. Results: We found bona fide evidence that Dead Sea treatments are especially effective in psoriasis due to both the special characteristics of solar ultraviolet radiation in the Dead Sea and the Dead Sea water balneotherapy. Dead Sea mud and Dead Sea balneotherapy have been found to be beneficial in rheumatologic diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and knee osteoarthritis. In the safety analysis, we found no evidence for an increase in skin neoplasia, although skin actinic damage seems to be increased in patients treated in the Dead Sea. Dead Sea treatments do not lead to worsening of blood pressure. Substantial ingestion of Dead Sea water (generally in unusual near-drowning cases) is toxic and can result in cardiac rhythm disturbances because of electrolyte concentration abnormalities. Laboratory analysis of Dead Sea mud did not reveal mineral concentrations that could represent a health concern for their intended use. Conclusions: Dead Sea treatments are beneficial in several rheumatologic diseases and psoriasis and have a good safety profile. © 2012 Elsevier Inc.


Paz Z.,Center for Autoimmune Diseases | Paz Z.,Tel Aviv University | Shoenfeld Y.,Center for Autoimmune Diseases | Shoenfeld Y.,Tel Aviv University
Clinical Reviews in Allergy and Immunology | Year: 2010

Fibrosis is a pathological process that includes scar formation and overproduction of extracellular matrix by the connective tissue as a response to tissue damage. The fibrotic process involves multiple organs and results in progressive life-threatening diseases. Today, we know more about the molecular mechanism that leads to fibrosis involving different type of cells, cytokines, chemokines, and tissue enzymes. Fibrosis was considered an irreversible process, at least clinically, and is still usually treated by anti-inflammatory and immunosuppressive agents. No proven antifibrotic therapy has shown efficacy in ameliorating the clinical course of fibrotic diseases, but our current understanding led to the development of different drugs with promising results, like: mycophenolate mofetil, interferon, relaxin, and intravenous immunoglobulin. This review will provide a glance to this heavily investigated subject. © Humana Press Inc. 2009.


Shaye K.,Sheba Medical Center | Shaye K.,Center for Autoimmune Diseases | Amir T.,Sheba Medical Center | Shlomo S.,Institute for Preventive Medicine | Yechezkel S.,Sheba Medical Center
American Heart Journal | Year: 2012

Background: Diabetes mellitus and impaired glucose metabolism are associated with increased risk for cardiovascular disease (CVD). However, it is still not clear whether glucose levels can predict CVD risk among patients without diabetes. The primary aim of this study is to assess whether normoglycemic fasting plasma glucose (FPG) is associated with increased risk of CVD outcomes in healthy patients. Methods: We obtained blood measurements, data from physical examination, and medical and lifestyle information from 10,913 men and women who were evaluated in the Institute for Preventive Medicine of Sheba Medical Center. Enrolled were participants with FPG < 100 mg/dL as well as 100 to 125 mg/dL, who were free of diagnosis of CVD. The participants were actively screened for coronary disease using a stress test. Primary end points were coronary heart disease or self-reported cerebral vascular disease. Results: A total of 1,119 incident cases of CVD occurred during a mean follow-up of 4.3 years. Subjects with fasting glucose levels in the high normal range (95-99 mg/dL) had an increased CVD risk when compared with levels < 80 mg/dL, (HR 1.53;CI 95% [1.22-1.91], P < .001). A multivariate model, adjusted for age, sex, family history of CVD, blood pressure, body mass index, smoking status, pharmacologic treatment, serum triglycerides, and high-density lipoprotein and low-density lipoprotein cholesterol levels, revealed an independent increased risk of CVD with rising FPG levels in the normal range. Conclusion: Elevated CVD risk is strongly and independently associated with glucose levels within the normoglycemic range. Fasting plasma glucose may help in identifying apparently healthy persons with early metabolic abnormalities who are at increased risk for CVD before progression to prediabetes and overt diabetes mellitus. © 2012 Mosby, Inc. All rights reserved.


Shapira Y.,Center for Autoimmune Diseases | Agmon-Levin N.,Center for Autoimmune Diseases | Agmon-Levin N.,Sheba Medical Center | Shoenfeld Y.,Center for Autoimmune Diseases | And 2 more authors.
Journal of Autoimmunity | Year: 2010

Autoimmune diseases cumulatively affect 5-10% of the industrial world population and are a significant cause of morbidity and mortality. In recent decades rates are rising worldwide, and autoimmunity can no longer be associated solely with the more developed "Western" countries. Geoepidemiology of autoimmune diseases portrays the burden of these illnesses across various regions and ethnic populations. Furthermore, Geoepidemiology may yield important clues to the genetic and triggering environmental mechanisms of autoimmunity. In this review we compiled and discuss in depth abundant geoepidemiological data pertaining to four major autoimmune conditions, namely type-1 diabetes mellitus, multiple sclerosis, autoimmune thyroid disease, and inflammatory bowel disease. The following key results manifested in this review: 1) Ethno-geographic gradients in autoimmune disease risk are attributable to a complex interplay of genetic and environmental pressures. 2) Industrial regions, particularly Northern Europe and North America, still exhibit the highest rates for most autoimmune diseases. 3) Methods particularly useful in demonstrating the significant influence of genetic and environmental factors include comparative ethnic differences studies, migration studies, and recognition of 'hotspots'. 4) Key environmental determinants of geographical differences include diminished ultraviolet radiation exposure, Western or affluence-related lifestyle, infection exposure, environmental pollutants, nutritional factors and disease-specific precipitants (e.g., iodine exposure). © 2009 Elsevier Ltd. All rights reserved.

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