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Esposito S.,University of Milan | Bosis S.,University of Milan | Semino M.,University of Milan | Rigante D.,University Cattolica Sacro Cuore
European Journal of Clinical Microbiology and Infectious Diseases | Year: 2014

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that presents a protean spectrum of clinical manifestations, and may affect any organ. The typical course of SLE is insidious, slow, and progressive, with potential exacerbations and remissions, and even dramatically acute and rapidly fatal outcomes. Recently, infections have been shown to be highly associated with the onset and/or exacerbations of SLE, and their possible causative and/or protective role has been largely emphasized in the medical literature. However, the etiopathogenesis of SLE is still obscure and far from being completely elucidated. Among infections, particularly Epstein-Barr virus (EBV), parvovirus B19, retrovirus, and cytomegalovirus (CMV) infections might play a pivotal pathogenetic role. The multifaceted interactions between infections and autoimmunity reveal many possibilities for either causative or protective associations. Indeed, some infections, primarily protozoan infections, might confer protection from autoimmune processes, depending on the unique interaction between the microorganism and host. Further studies are needed in order to demonstrate that infectious agents might, indeed, be causative of SLE, and to address the potential clinical sequelae of infections in the field of autoimmunity. © 2014 Springer-Verlag. Source

Rigante D.,University Cattolica Sacro Cuore | Vitale A.,University of Siena | Lucherini O.M.,University of Siena | Cantarini L.,University of Siena
Autoimmunity Reviews | Year: 2014

There is a thriving interest in the field of hereditary autoinflammatory disorders (HAID), a gamut of heterogeneous conditions deriving from an aberrant orchestration of innate immunity, unified by the common feature of seemingly unprovoked inflammation, which might be systemic or occur in localized niches of the organism. Recurrent fever and episodic inflammation in the joints, serosal membranes, skin, gut, and other organs are the common denominator of HAID. Mutations in the inflammasome-related genes have been associated with different HAID, showing the intimate link existing between interleukin-1 (IL-1)-structured inflammasome and their pathogenesis. Differential diagnosis of HAID can be challenging, as there are no universally accepted diagnostic protocols, and near half of patients may remain without any genetic abnormality identified. The use of IL-1-antagonists has been associated with beneficial effects in a large number of HAID associated with excessive IL-1 signalling, such as cryopyrin-associated periodic syndromes, familial Mediterranean fever, and deficiency of IL-1 receptor antagonist. This review will discuss about the key-clues of HAID which might guide for an early recognition and drive decisions for treatment. © 2014 Elsevier B.V. Source

Ansuini V.,University of Milan | Rigante D.,University Cattolica Sacro Cuore | Esposito S.,University of Milan
BMC Infectious Diseases | Year: 2013

Background: Hemophagocytic syndrome (HPS) is clinically defined as a combination of fever, liver dysfunction, coagulation abnormalities, pancytopenia, progressive macrophage proliferation throughout the reticuloendothelial system, and cytokine over-production, and may be primary or secondary to infectious, auto-immune, and tumoral diseases. The most consistent association is with viral infections but, as it is still debated whether any micro-organisms are involved in its pathogenesis, we critically appraised the literature concerning HPS and its relationship with infections.Discussion: Infection-dependent HPS has been widely observed, but there are no data concerning its incidence in children. A better understanding of the pathophysiology of HPS may clarify the interactions between the immune system and the variously implicated potential infectious agents. Epstein-Barr virus (EBV) infection has been prominently associated with HPS, with clonal proliferation and the hyperactivation of EBV-infected T cells. However, a number of other viral, bacterial, fungal, and parasitic infections have been reported in association with HPS. In the case of low-risk HPS, corticosteroids and/or intravenous immunoglobulin or cyclosporine A may be sufficient to control the biological process, but etoposide is recommended as a means of reversing infection-dependent lymphohistiocytic dysregulation in high-risk cases.Summary: HPS is a potential complication of various infections. A polymerase chain reaction search for infectious agents including EBV, cytomegalovirus and Leishmania is recommended in clinical settings characterised by non-remitting fever, organomegaly, cytopenia and hyperferritinemia. © 2013 Ansuini et al.; licensee BioMed Central Ltd. Source

Rigante D.,University Cattolica Sacro Cuore | Mazzoni M.B.,University of Milan | Esposito S.,University of Milan
Autoimmunity Reviews | Year: 2014

The underlying trigger for systemic lupus erythematosus (SLE) has remained elusive, and multiple interacting environmental and genetic factors likely contribute to the onset and perpetuation of the disease. Among environmental influences, infectious agents have been suggested to play a pivotal role in driving autoimmunity pathogenesis via structural or functional molecular mimicry, the expression of proteins that induce cross-reactive responses against self-antigens, and the aberrant activation or apoptosis of different immune system cells in the context of a peculiar genetic background. The increased viral load and changing subsets of lytic or latent viral proteins observed in selected populations with SLE have indicated that common viruses, such as Epstein-Barr virus, parvovirus B19, cytomegalovirus, retroviruses and transfusion-transmitted viruses, might be triggers for this disease. Alternatively, some infectious agents might exert a protective effect from autoimmunity. Existing achievements have not been fully investigated and clarified. Thus, the aim of this review is to analyze the medical literature within the last 15. years regarding the role of infectious agents in the pathogenesis of SLE. © 2013 Elsevier B.V. Source

Rigante D.,University Cattolica Sacro Cuore | Esposito S.,University of Milan
International Journal of Immunopathology and Pharmacology | Year: 2013

Fever of unknown origin (FUO) in adults is conventionally defined by the occurrence of body temperatures above 38.3°C (101°F) for a period of 3 weeks without any identified etiology after a period of 1-week hospitalization. The issue of FUO in pediatrics is rather hazy and still represents a challenging diagnostic dilemma. Most of the available data are limited to nationwide cohorts of patients of any age. The major difficulty in establishing a diagnosis is that the characteristic features rendering specific disorders clinically recognizable are absent or subtle, hence only a painstaking questioning on family background may elicit the correct investigative path. No diagnostic algorithms are actually available and clinicians must rely on a very careful step-by-step evaluation of the single patient. The need for invasive diagnostic techniques should be closely taken into consideration when laboratory tests or simple imaging procedures fail to discern the origin of FUO. Fevers with no reasonable explanation and no localizing signs often conceal different common diseases in children, which tend to display an unusual or atypical pattern. The principal causes behind FUO in pediatric age remain infections, followed by collagen vascular diseases and neoplastic disorders, although most children with malignancies present other systemic signs or suggestive laboratory abnormalities. The possibility of autoinflammatory syndromes, drug fever, and factitious fever should also be taken into account. Copyright © by BIOLIFE, s.a.s. Source

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