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עמוד בית
Sun, 23.06.24

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July 2017
Margherita Zen MD, Mariele Gatto MD, Linda Nalotto MD, Maddalena Larosa MD, Luca Iaccarino MD PhD and Andrea Doria PhD
April 2016
Sara Bindoli MD, José J. Torres-Ruiz MD, Carlo Perricone MD, Mojca Bizjak MD, Andrea Doria MD and Yehuda Shoenfeld MD FRCP MaCR

Sarcoidosis is a chronic multisystem disease with variable course resulting from the interaction between environmental factors and the immune system of individuals genetically predisposed. The evidence linking sarcoidosis with environmental triggers such as metals is increasing. We describe the case of a 44 year old female with a history of smoking since age 30 and previous mercury dental filling who presented at physical examination with numerous subcutaneous nodules. Laboratory data showed accelerated erythrocyte sedimentation rate and high titer of anti-U1 ribonucleoprotein antibodies (U1-RNP). Skin biopsy and chest X-ray suggested the diagnosis of sarcoidosis. In this report we illustrate the different causes involved in the onset of sarcoidosis.

October 2014
Marcella Di Gangi MD, Giorgio Amato MD, Giovanni Converso MD, Alessia Benenati MD, Concetta Leonetti MD, Elisabetta Borella MD, Andrea Doria MD and Rosario Foti MD
Elisabetta Borella MD, Lavinia Palma MD, Margherita Zen MD, Silvano Bettio MD, Linda Nalotto MD, Mariele Gatto MD, Marta Domeneghetti MD, Luca Iaccarino MD, Leonardo Punzi and Andrea Doria MD
Autoinflammatory (AIF) and autoimmune (AIM) diseases are chronic immune disorders characterized by dysregulation of the immune system. Most AIF diseases are monogenic diseases which lead to hyperactivation of the inflammasome and release of pro-inflammatory cytokines, such as interleukin-1 (IL-1) and IL-18, resulting in tissue inflammation. Besides, the main feature of autoimmune diseases is the loss of tolerance of the adaptive immune cells against self antigens. Most AIF diseases are polygenic and numerous immune pathogens are involved in organ damage. The involvement of some AIF-associated mechanisms in AIM diseases, i.e., the activation of the inflammasome and the role of IL-1, was recently recognized. Moreover, some single nucleotide polymorphisms of the inflammasome genes have been proven to be involved in the development of AIF-related inflammatory features in autoimmune patients. These observations raise the possibility of using some anti-inflammatory drugs, like IL-1 antagonists, in autoimmune diseases with autoinflammatory features. 
January 2008
Y. Shoenfeld, G. Zandman-Goddard, L. Stojanovich, M. Cutolo, H. Amital, Y. Levy, M. Abu-Shakra, O. Barzilai, Y. Berkun, M. Blank, J.F. de Carvalho, A. Doria, B. Gilburd, U. Katz, I. Krause, P. Langevitz, H. Orbach, V. Pordeus, M. Ram, E. Toubi and Y. Sherer
N. Bassi, D. Amital, H. Amital, A. Doria and Y. Shoenfeld

Chronic fatigue syndrome is a heterogeneous disorder with unknown pathogenesis and etiology, characterized by disabling fatigue, difficulty in concentration and memory, and concomitant skeletal and muscular pain. Several mechanisms have been suggested to play a role in CFS[1], such as excessive oxidative stress following exertion, immune imbalance characterized by decreased natural killer cell and macrophage activity, immunoglobulin G subclass deficiencies (IgG-1[2], IgG-3) and decreased serum concentrations of complement component. Autoantibodies were also suggested as a possible factor in the pathogenesis of CFS. Recent studies indicate that anti-serotonin, anti-microtubule-associated protein 2 and anti-muscarinic cholinergic receptor 1 may play a role in the pathogenesis of CFS. It has been demonstrated that impairment in vasoactive neuropeptide metabolism may explain the CFS symptoms







[1] CFS = chronic fatigue syndrome

[2] IgG = immunoglobulin G


November 2001
Anna Ghirardello, PhD, Andrea Doria, MD, Sandra Zampieri SciBiol, Pier Franca Gambari, MD and Silvano Todesco, MD
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