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Dive into the research topics where E. Lazaro is active.

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Featured researches published by E. Lazaro.


Joint Bone Spine | 2015

Management of neutropenia in patients with rheumatoid arthritis

E. Lazaro; Jacques Morel

Neutropenia is defined as a neutrophil count lower than 1.5g/L, with categorization as mild, moderate, or severe when the count is 1.5-1g/L, 1-0.5g/L, or<0.5g/L, respectively. The main complication is infection, whose risk increases with the depth and duration of the neutropenia. Comprehensive etiological investigations are mandatory to determine the best treatment strategy. Constitutional neutropenia is rarely seen in everyday rheumatology practice. It predominantly affects patients of African descent and is usually moderate and well tolerated. Congenital neutropenia due to genetic abnormalities is severe and chiefly seen in the pediatric population. Most cases of neutropenia in patients with rheumatoid arthritis (RA) are acquired. Medications are the most common causes, making detailed history-taking crucial. Many medications used to treat RA can induce neutropenia. Folic acid deficiency should be sought routinely in patients taking methotrexate. A less common cause of neutropenia is an RA-related autoimmune reaction. Splenomegaly suggests Feltys syndrome, which is accompanied with large granular lymphocytic (LGL) leukemia in 40% of cases. The treatment depends on the depth of the neutropenia and findings from the etiological workup. A neutrophil count below 0.5g/L, a fever, and the presence of clinical signs indicate a life-threatening condition requiring emergent treatment. In other patients, the first step is immediate discontinuation of any possibly involved drugs, simultaneously with the etiological workup.


Revue de Médecine Interne | 2012

Lymphome à grandes cellules B intravasculaire : trois cas et mise au point

T. Chroboczek; E. Lazaro; C. Greib; Marie Parrens; M.-S. Dilhuydi; J.L. Pellegrin; J.-F. Viallard

PURPOSE Intravascular large B cell lymphoma (IVLBCL) is a rare and aggressive variant of non-Hodgkins lymphoma, characterized by multifocal proliferation of lymphoma cells exclusively within small and medium blood vessels. IVLBCL can be systemic and quite polymorphic, which often makes it difficult to diagnose, thus delaying appropriate treatment. PATIENTS AND METHODS We report three patients of atypical IVLBCL, through the study of which we overview recent knowledge about IVLBCL. RESULTS The first patient initially presented with peripheral thrombocytopenia and splenic destruction of platelets, later completed with an interstitial pulmonary syndrome. The second patient, of African origin, we believe is the first case of a black patient with IVLBCL described in the medical literature. The third belongs to the rare group of occidental patients that present an IVLBCL associated with a hemophagocytic syndrome. CONCLUSION Intravascular large B cell lymphoma is a systemic and polymorphic disease. Awareness of this entitiy should allow rapid and appropriate management.


Arthritis & Rheumatism | 2016

IgE Inhibits Toll-like Receptor 7- and Toll-like Receptor 9-Mediated Expression of Interferon-α by Plasmacytoid Dendritic Cells in Patients With Systemic Lupus Erythematosus.

Liliane Khoryati; Jean-François Augusto; Emilie Shipley; Cécile Contin-Bordes; Isabelle Douchet; Stéphane Mitrovic; Marie-Elise Truchetet; E. Lazaro; P. Duffau; Lionel Couzi; Clément Jacquemin; Thomas Barnetche; Pierre Vacher; Thierry Schaeverbeke; Patrick Blanco; Christophe Richez

Plasmacytoid dendritic cells (PDCs) play a central role in pathogenesis of systemic lupus erythematosus (SLE) through their unique ability to produce large amounts of type I interferon (IFN) upon Toll‐like receptor 7 (TLR‐7) and TLR‐9 triggering. PDCs express specific surface regulatory receptors involved in negative regulation of IFNα secretion. These receptors use the γ‐chain of high‐affinity Fc receptor (FcR) for IgE, FcɛRI. We undertook this study to test our hypothesis that IgE engagement of FcɛRI on PDCs may impact IFNα production in SLE patients.


British Journal of Dermatology | 2018

Efficacy and safety of autologous haematopoietic stem cell transplantation in systemic sclerosis: A systematic review of literature

A. Eyraud; L. Scouppe; T. Barnetche; E. Forcade; E. Lazaro; P. Duffau; Christophe Richez; Julien Seneschal; Marie-Elise Truchetet

We aimed to assess the efficacy of autologous haematopoietic stem cell transplantation (HSCT) for skin sclerosis (SSc) and lung function in SSc. We performed a systematic literature review in the PubMed and Scopus databases from the earliest records to March 2016. We assessed study quality using the Cochrane tool for randomized studies, the Newcastle–Ottawa Scale for controlled cohort studies and an 18‐item quality‐appraisal checklist for case series. The primary outcome was the improvement of skin thickening using the modified Rodnan Skin Score (mRSS). The secondary outcome was efficacy on lung function, using diffusing capacity of the lungs for carbon monoxide and forced vital capacity (FVC). The safety of the procedure was evaluated. The literature search identified 431 citations. There were 38 studies involving a total of 344 patients who fulfilled our inclusion criteria. No meta‐analysis was performed due to a high heterogeneity. There was a significant improvement in mRSS in the majority of the reports (P < 0·05), and the results were sustained for up to 8 years after autologous HSCT. The randomized studies and the four cohort studies each showed a slight but statistically significant improvement in FVC at 1 or 2 years. The treatment‐related mortality calculated by pooling patients of 35 studies (336 patients with a follow‐up up to 146 months) was 8·3% after autologous HSCT and 1% in cyclophosphamide‐treated groups. Despite heterogeneity among the studies, we determined that autologous HSCT significantly improved cutaneous fibrosis and slightly improved FVC. Safety of autologous HSCT is acceptable given the severity of the disease. This systematic review was registered on PROSPERO, number CRD42016027951.


Current Rheumatology Reports | 2017

New Insights on Platelets and Platelet-Derived Microparticles in Systemic Lupus Erythematosus

Marc Scherlinger; Vanja Sisirak; Christophe Richez; E. Lazaro; P. Duffau; Patrick Blanco

Purpose of reviewCurrent knowledge on the role of platelets and platelet-derived microparticles (PMPs) on the immune system has been fast-growing. Systemic lupus erythematosus (SLE) is a systemic auto-immune disorder characterized by a loss of tolerance toward nuclear auto-antigens. Although recent studies allowed a better understanding of SLE pathogenesis, there is an urgent need for the development of new treatments and the identification of new biomarkers to assess the disease activity. We describe here the state-of-the-art knowledge linking platelets and PMPs to SLE.Recent findingsPlatelet system activation is a key event in the pathogenesis of SLE. Circulating immune complexes, anti-phospholipid antibodies, and infectious agents such as virus are the main activators of platelets in SLE. Platelet activation can be monitored through different ways such as P-selectin expression, mean platelet volume, or circulating PMP levels, suggesting their potential use as biomarkers. Upon activation, platelets promote type I interferon production, NETosis, dendritic cell activation, and T and B lymphocyte activation, all essential events contributing to the development of SLE. Of interest, platelets also play a fundamental role in SLE organ disease such as the development of cardiovascular, thrombotic, and renal diseases. Finally, we review current knowledge on drugs targeting platelet activation and their potential impact on SLE pathogenesis.SummaryPlatelets play a major role in SLE pathogenesis and organ disease and represent a great potential for novel biomarkers and drug development.


Arthritis & Rheumatism | 2016

IgE inhibits TLR‐7 and ‐9 mediated expression of interferon‐alpha by plasmacytoid dendritic cells in systemic lupus patients

Liliane Khoryati; Jean‐François Augusto; Emilie Shipley; Cécile Contin-Bordes; Isabelle Douchet; Stéphane Mitrovic; Marie-Elise Truchetet; E. Lazaro; P. Duffau; Lionel Couzi; Clément Jacquemin; Thomas Barnetche; Pierre Vacher; Thierry Schaeverbeke; Patrick Blanco; Christophe Richez

Plasmacytoid dendritic cells (PDCs) play a central role in pathogenesis of systemic lupus erythematosus (SLE) through their unique ability to produce large amounts of type I interferon (IFN) upon Toll‐like receptor 7 (TLR‐7) and TLR‐9 triggering. PDCs express specific surface regulatory receptors involved in negative regulation of IFNα secretion. These receptors use the γ‐chain of high‐affinity Fc receptor (FcR) for IgE, FcɛRI. We undertook this study to test our hypothesis that IgE engagement of FcɛRI on PDCs may impact IFNα production in SLE patients.


Arthritis Research & Therapy | 2017

Predictive biological markers of systemic lupus erythematosus flares: a systematic literature review

Noémie Gensous; Aurélie Marti; Thomas Barnetche; Patrick Blanco; E. Lazaro; Julien Seneschal; Marie-Elise Truchetet; P. Duffau; Christophe Richez

BackgroundThe aim of this study was to identify the most reliable biomarkers in the literature that could be used as flare predictors in systemic lupus erythematosus (SLE).MethodsA systematic review of the literature was performed using two databases (MEDLINE and EMBASE) through April 2015 and congress abstracts from the American College of Rheumatology and the European League Against Rheumatism were reviewed from 2010 to 2014. Two independent reviewers screened titles and abstracts and analysed selected papers in detail, using a specific questionnaire. Reports addressing the relationships between one or more defined biological test(s) and the occurrence of disease exacerbation were included in the systematic review.ResultsFrom all of the databases, 4668 records were retrieved, of which 69 studies or congress abstracts were selected for the systematic review. The performance of seven types of biomarkers performed routinely in clinical practice and nine types of novel biological markers was evaluated. Despite some encouraging results for anti-double-stranded DNA antibodies, anti-C1q antibodies, B-lymphocyte stimulator and tumour necrosis factor-like weak inducer of apoptosis, none of the biomarkers stood out from the others as a potential gold standard for flare prediction. The results were heterogeneous, and a lack of standardized data prevented us from identifying a powerful biomarker.ConclusionsNo powerful conclusions could be drawn from this systematic review due to a lack of standardized data. Efforts should be undertaken to optimize future research on potential SLE biomarkers to develop validated candidates. Thus, we propose a standardized pattern for future studies.


Revue de Médecine Interne | 2009

Lupus érythémateux systémique : de la physiopathologie au traitement

Cécile Contin-Bordes; E. Lazaro; J.L. Pellegrin; J.-F. Viallard; Jean-François Moreau; Patrick Blanco

Resume Le lupus erythemateux systemique (LES) est une maladie auto-immune systemique non specifique d’organe, caracterisee par une reponse immunitaire anormalement dirigee contre du materiel nucleaire. L’expression de la maladie est tres variable d’un patient a un autre et evolue par poussee. Bien que des anomalies touchant les mecanismes impliques dans l’elimination du materiel nucleaire circulant, des complexes immuns ou encore l’activation lymphocytaire aient ete decrites, la physiopathologie de la maladie reste largement meconnue puisque resultant de l’association de facteurs genetiques, epigenetiques et environnementaux (tels que les infections virales). L’immunite innee joue un role central dans la physiopathologie de la maladie au travers de l’activation du reseau des cellules dendritiques et de la production incontrolee de quantite anormalement elevee d’IFN-alpha. Ces dernieres sont capables de capturer de grandes quantites de materiel nucleaire et d’activer secondairement lymphocytes T et lymphocytes B auto-reactifs et ainsi induire la production d’auto-anticorps diriges contre des composants d’origine nucleaire. Bien que le role du depot de complexes immuns ait ete clairement demontre dans la genese des lesions tissulaires et l’inflammation, des etudes recentes tendent a montrer que d’autres effecteurs, tels que les lymphocytes T CD8 cytotoxiques peuvent participer, de part leur capacite a migrer vers les tissus inflammatoires, a l’entretien des lesions. L’objet de cette revue n’est pas de proposer une analyse exhaustive de la physiopathologie du lupus mais plutot de decrire « les grandes lignes qui sous-tendent les mecanismes immunologiques » impliques dans cette maladie et les outils therapeutiques dont on dispose ou disposera pour les contrer. Bien qu’ayant fait l’objet de decouvertes de tout premier ordre recemment, les aspects genetiques de la maladie ne seront pas abordes ici.


Autoimmunity Reviews | 2018

Systemic lupus erythematosus and systemic sclerosis: All roads lead to platelets

Marc Scherlinger; Vivien Guillotin; Marie-Elise Truchetet; Cécile Contin-Bordes; Vanja Sisirak; P. Duffau; E. Lazaro; Christophe Richez; Patrick Blanco

Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are two phenotypically distincts inflammatory systemic diseases. However, SLE and SSc share pathogenic features such as interferon signature, loss of tolerance against self-nuclear antigens and increased tissue damage such as fibrosis. Recently, platelets have emerged as a major actor in immunity including auto-immune diseases. Both SLE and SSc are characterized by strong platelet system activation, which is likely to be both the witness and culprit in their pathogenesis. Platelet activation pathways are multiple and sometimes redundant. They include immune complexes, Toll-like receptors activation, antiphospholipid antibodies and ischemia-reperfusion associated with Raynaud phenomenon. Once activated, platelet promote immune dysregulation by priming interferon production by immune cells, providing CD40L supporting B lymphocyte functions and providing a source of autoantigens. Platelets are actively implicated in SLE and SSc end-organ damage such as cardiovascular and renal disease and in the promotion of tissue fibrosis. Finally, after understanding the main pathogenic implications of platelet activation in both diseases, we discuss potential therapeutics targeting platelets.


Rheumatology | 2017

Neutrophil-derived mitochondrial DNA promotes receptor activator of nuclear factor κB and its ligand signalling in rheumatoid arthritis

Anne Contis; Stéphane Mitrovic; Julie Lavie; Isabelle Douchet; E. Lazaro; Marie-Elise Truchetet; Cyril Goizet; Cécile Contin-Bordes; Thierry Schaeverbeke; Patrick Blanco; Rodrigue Rossignol; Benjamin Faustin; Christophe Richez; P. Duffau

Objectives Mitochondrial DNA (mtDNA) contains sequestered damage-associated molecular patterns that might be involved in osteoimmunological pathogenesis of RA. Here, we aimed to investigate the cellular source of mtDNA and its role in RANK ligand (RANKL) expression by RA SF neutrophils. Methods The gene expression signature of SF neutrophils was examined by proteomic quantitative analysis. Levels of mtDNA in circulating and SF neutrophils from RA patients and OA control subjects were assessed by real-time PCR. Purified neutrophils were challenged in vitro with Toll-like receptor agonists as well as mtDNA. RANKL expression by neutrophils was studied by flow cytometry. Results SF neutrophils from RA patients displayed a gene expression signature of oxidative stress. This stress signature was associated with the release of mtDNA in SF as observed by a significant increase of mtDNA in the SF of RA patients compared with OA patients. mtDNA in RA SF was correlated with systemic inflammation as assessed by CRP concentrations. We also showed that mtDNA drives neutrophil RANKL expression to the same extent as Toll-like receptor agonists. Conclusion Our data identify SF neutrophils as a cellular source of mtDNA that leads to a subsequent expression of RANKL. This highlights the important role of neutrophils in RA osteoimmunology.

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P. Duffau

University of Bordeaux

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P. Blanco

Centre national de la recherche scientifique

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C. Richez

Centre national de la recherche scientifique

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Jean-François Moreau

Centre national de la recherche scientifique

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