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Systemic Lupus Erythematosus: HELP
Articles from Long Island towns
Based on 173 articles published since 2008
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These are the 173 published articles about Lupus Erythematosus, Systemic that originated from Long Island towns during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7
1 Editorial Remission in SLE: closing in on the target. 2015

van Vollenhoven, Ronald F / Voskuyl, Alexandre / Morand, Eric / Aranow, Cynthia. ·Department of Medicine, The Karolinska Institute, Stockholm, Sweden. · Department of Rheumatology, Amsterdam Rheumatology and Immunology Center ARC, Amsterdam, The Netherlands. · School of Clinical Sciences, Monash University, Clayton, Victoria, Australia. · Center for Autoimmune and Musculoskeletal, The Feinstein Institute for Medical Research, Manhasset, New York, USA. ·Ann Rheum Dis · Pubmed #26511997.

ABSTRACT: -- No abstract --

2 Editorial Editorial: autoimmunity to vimentin and lupus nephritis. 2014

Davidson, Anne. ·Feinstein Institute for Medical Research, Manhasset, New York. ·Arthritis Rheumatol · Pubmed #25250522.

ABSTRACT: -- No abstract --

3 Editorial Editorial: the power of a modular approach to transcriptional analysis. 2014

Gregersen, Peter K / Oswald, Michaela. ·Feinstein Institute for Medical Research, Manhasset, New York. ·Arthritis Rheumatol · Pubmed #24644035.

ABSTRACT: -- No abstract --

4 Review Point-of-Care Ultrasound to Identify the Source of Dyspnea in a Patient With Systemic Lupus Erythematosus. 2019

Lee, Horton J / Budhathoki, Rasmita. ·From the Pediatric Emergency Medicine, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York and Elmhurst Hospital, NYC Health + Hospitals, Elmhurst, NY. ·Pediatr Emerg Care · Pubmed #30747789.

ABSTRACT: Point-of-care ultrasound can be used to help identify the source of dyspnea in patients presenting to the emergency department. We present a case of an adolescent girl with a history of systemic lupus erythematosus presenting to the emergency department with chest pain and dyspnea and found to have both pleural and pericardial effusions on point-of-care ultrasound.

5 Review The gut microbiome and elevated cardiovascular risk in obesity and autoimmunity. 2018

Kasselman, Lora J / Vernice, Nicholas A / DeLeon, Joshua / Reiss, Allison B. ·Winthrop Research Institute and Department of Medicine, NYU Winthrop Hospital, Mineola, NY, USA. Electronic address: lkasselman@nyuwinthrop.org. · Winthrop Research Institute and Department of Medicine, NYU Winthrop Hospital, Mineola, NY, USA. ·Atherosclerosis · Pubmed #29524863.

ABSTRACT: Cardiovascular disease associated with obesity and autoimmunity is the leading cause of death in these populations and significant residual risk remains despite current treatment approaches. Obesity, type 1 diabetes mellitus (T1DM), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE) are linked to chronic inflammation, and subjects with these disorders have characteristic shifts in their gut microbiome composition. Recent data suggest that alterations in gut microbial and metabolic composition may be responsible, in part, for induction of chronic inflammation, thus promoting cardiovascular disease. Common microbiome changes observed in obesity, T1DM, RA, and SLE include a decrease in the ratio of bacteria, such as Gram-positive Firmicutes to Gram-negative Bacteroidetes, as well as an overabundance or depletion of certain species, including Prevotella copri. The consequent effects of these shifts include alterations in the metabolic composition of the gut, hyper-activation of toll-like receptor 4 (TLR-4), upregulation of inflammatory pathways, e.g. c-Jun N-terminal kinase and nuclear factor-kappa B (NFκB), increased intestinal permeability, increased C-reactive protein, and increased levels of trimethylamine N-oxide (TMAO). Differential microbiome compositions may also explain sex differences observed in autoimmunity, where a male gut microbiome promotes anti-inflammatory processes as compared to a female pro-inflammatory gut microbiome. Intervention at the level of the microbiota appears to attenuate symptoms in these inflammatory syndromes with probiotic treatment, such as Lactobacilli, playing a uniquely beneficial role in restoring intestinal health, decreasing inflammation, and reducing cardiovascular disease. This review will discuss obesity, T1DM, RA, and SLE in the context of how each unique microbiome profile contributes to elevated cardiovascular risk.

6 Review Lessons learned from bone marrow failure in systemic lupus erythematosus: Case reports and review of the literature. 2018

Anderson, Erik / Shah, Bhakti / Davidson, Anne / Furie, Richard. ·Division of Rheumatology, Northwell Health, Great Neck, NY. Electronic address: eanderson22@northwell.edu. · Division of Rheumatology, Northwell Health, Great Neck, NY. ·Semin Arthritis Rheum · Pubmed #29395255.

ABSTRACT: OBJECTIVE: In the present review, four new cases of bone marrow failure are presented and the potential contribution of systemic lupus erythematosus (SLE) is discussed. Furthermore, a comprehensive literature review of cases of autoimmune myelofibrosis (AIMF), aplastic anemia (AA), and paroxysmal nocturnal hemoglobinuria (PNH) with concurrent SLE aims to allow their direct comparison. Based on a clearer characterization of reported cases and our own experience, diagnostic and therapeutic strategies of these disorders in SLE are proposed based on lessons learned from the present and previous cases. METHODS: A literature search was done in PubMed, accessed via the National Library of Medicine PubMed interface (http://www.ncbi.nlm.nih.gov/pubmed). Using PubMed, a Boolean search of the literature was performed by crossing the keywords "systemic lupus erythematosus," AND ["bone marrow fibrosis" or "bone marrow failure" or "myelofibrosis" or "aplastic anemia" or "paroxysmal nocturnal hemoglobinuria"]. RESULTS: After a stringent selection of previous cases with a clear diagnosis of SLE, we summarized in the present review 31 cases of AIMF, 26 cases of AA, and 3 cases of PNH. In addition, four new cases illustrate the problem of attribution of bone marrow failure to SLE. CONCLUSIONS: The attribution of SLE to bone marrow failure is challenging due to a lack of biomarkers, which complicates treatment decisions. Autoimmune myelofibrosis is likely underreported, but corticosteroids and intravenous immunoglobulin appear to be effective immediate therapies. In AA attributable to SLE, a serum inhibitor of bone marrow precursors should be tested, since plasma exchange has been universally successful in these cases, and a PNH clone should be tested for in the setting of ongoing hemolysis, as complement inhibition may be effective. Further research is warranted to elucidate pathophysiological mechanisms of bone marrow failure in SLE.

7 Review Renal Macrophages and Dendritic Cells in SLE Nephritis. 2017

Maria, Naomi I / Davidson, Anne. ·Center for Autoimmunity and Musculoskeletal Diseases, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York, NY, 11030, USA. · Center for Autoimmunity and Musculoskeletal Diseases, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York, NY, 11030, USA. adavidson1@northwell.edu. ·Curr Rheumatol Rep · Pubmed #29119288.

ABSTRACT: PURPOSE OF REVIEW: The purpose of the study was to review the characteristics of renal macrophages and dendritic cells during homeostasis and disease, with a particular focus on lupus nephritis. RECENT FINDINGS: Resident renal macrophages derive from embryonic sources and are long-lived and self-renewing; they are also replaced from the bone marrow with age. The unique characteristics of macrophages in each tissue are imposed by the microenvironment and reinforced by epigenetic modifications. In acute renal injury, inflammatory macrophages are rapidly recruited and then replaced by those with a wound healing/resolution phenotype. In lupus nephritis, dendritic cells infiltrate the kidneys and function to present antigen and organize tertiary lymphoid structures that amplify inflammation. In addition, both infiltrating and resident macrophages contribute to ongoing injury. These cells have a mixed inflammatory and alternatively activated phenotype that may reflect failed resolution, potentially leading to tissue fibrosis and irreversible damage. A further understanding of the renal inflammatory cells that mediate tissue injury and fibrosis should lead to new therapies to help preserve renal function in patients with lupus nephritis.

8 Review A framework for remission in SLE: consensus findings from a large international task force on definitions of remission in SLE (DORIS). 2017

van Vollenhoven, Ronald / Voskuyl, Alexandre / Bertsias, George / Aranow, Cynthia / Aringer, Martin / Arnaud, Laurent / Askanase, Anca / Balážová, Petra / Bonfa, Eloisa / Bootsma, Hendrika / Boumpas, Dimitrios / Bruce, Ian / Cervera, Ricard / Clarke, Ann / Coney, Cindy / Costedoat-Chalumeau, Nathalie / Czirják, László / Derksen, Ronald / Doria, Andrea / Dörner, Thomas / Fischer-Betz, Rebecca / Fritsch-Stork, Ruth / Gordon, Caroline / Graninger, Winfried / Györi, Noémi / Houssiau, Frédéric / Isenberg, David / Jacobsen, Soren / Jayne, David / Kuhn, Annegret / Le Guern, Veronique / Lerstrøm, Kirsten / Levy, Roger / Machado-Ribeiro, Francinne / Mariette, Xavier / Missaykeh, Jamil / Morand, Eric / Mosca, Marta / Inanc, Murat / Navarra, Sandra / Neumann, Irmgard / Olesinska, Marzena / Petri, Michelle / Rahman, Anisur / Rekvig, Ole Petter / Rovensky, Jozef / Shoenfeld, Yehuda / Smolen, Josef / Tincani, Angela / Urowitz, Murray / van Leeuw, Bernadette / Vasconcelos, Carlos / Voss, Anne / Werth, Victoria P / Zakharova, Helena / Zoma, Asad / Schneider, Matthias / Ward, Michael. ·Department of Medicine, Unit for Clinical Therapy Research, Inflammatory Diseases (ClinTRID), Karolinska Institutet, D1:00 Karolinska University Hospital, Solna, Stockholm, Sweden. · Amsterdam Rheumatology and Immunology Center, VU University Medical Center, Amsterdam, The Netherlands. · Department of Rheumatology, Clinical Immunology and Allergy, University of Crete School of Medicine, Iraklion, Greece. · Feinstein Institute for Medical Research, Manhasset, New York, USA. · Department of Medicine III, University Medical Center TU Dresden, Dresden, Germany. · New York University, New York, USA. · LPRe SR-Klub Motýlik, Bratislava, Slovakia. · Rheumatology Division, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil. · Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. · Department of Medicine and Joint Academic Rheumatology Program Medical School, National and Kapodestrian University of Athens, Athens, Greece. · NIHR Manchester Biomedical Research Unit, The University of Manchester and Central Manchester Foundation Trust, Manchester, UK. · Department of Autoimmune Diseases, Hospital Clinic, Barcelona, Catalonia, Spain. · Division of Rheumatology, The Arthritis Society Chair in Rheumatic Diseases Cumming School of Medicine University of Calgary, Calgary, Alberta, Canada. · Lupus Foundation of America, Washington DC, USA. · Université Paris-Decartes, Paris, France. · AP-HP, Hôpital Cochin, service de médecine interne, centre de reference maladies auto-immunes et systémiques rares, Paris, France. · Department of Rheumatology and Immunology, Institute of Bioanalysis, Institute of Family Medicine, University of Pécs, Pécs, Hungary. · Third Department of Internal Medicine, Semmelweis University, Budapest, Hungary. · Department Rheumatology and Clinical Immunology, University Medical Center, Utrecht, The Netherlands. · Rheumatology Unit, Department of Medicine, University of Padova, Padova, Italy. · Department Medicine/Rheumatology and Clinical Immunology, Charite Universitätsmedizin Berlin, Berlin, Germany. · Polyclinic of Rheumatology, Hiller Research Unit, University Clinic Duesseldorf, Heinrich-Heine-University, Duesseldorf, Germany. · Rheumatology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK. · Division of Rheumatology, Medical University of Graz, Graz, Austria. · Service de Rhumatologie, Cliniques universitaires Saint-Luc, Pôle de pathologies rhumatismales inflammatoires et systémiques, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Bruxelles, Belgium. · Department of Medicine, The Centre for Rheumatology, University College London, UK. · Copenhagen Lupus and Vasculitis Clinic, Center for Rheumatology and Spine Diseases, Copenhagen, Denmark. · Department of Medicine, University of Cambridge, Cambridge, UK. · Interdisciplinary Center for Clinical Trials (IZKS), University Medical Center Mainz, Mainz, Germany. · LUPUS EUROPE, co-opted trustee for research, Essex UK. · Rheumatology Department, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. · Université Paris-Sud; Assistance Publique-Hôpitaux de Paris, Hôpitaux Universitaires Paris-sud; INSERM U1184, Le Kremlin Bicêtre, France. · Bone Densitometry Unit, Monla Hospital, Tripoli, Lebanon. · Monash University, Faculty of Medicine, Nursing & Health Sciences, Monash Medical Centre, Clayton, Australia. · Rheumatology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. · Department of Internal Medicine, Division of Rheumatology, Istanbul University, Istanbul Medical Faculty, Istanbul, Turkey. · University of Santo Tomas, Manila, Philippines. · Vasculitis.at, Vienna, Austria. · Department of Connective Tissues Diseases, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland. · Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. · RNA and Molecular Pathology Research Group, Institute of Medical Biology, Health Science Faculty, University of Tromsø, Tromsø, Norway. · National Institute for Rheumatic Diseases, Piešťany, Slovak Republic. · Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center (Affiliated to Tel-Aviv University), Tel-Aviv, Israel. · Division of Rheumatology, Department of Medicine 3, Medical University of Vienna, Vienna, Austria. · 2nd Department of Medicine, Hietzing Hospital, Vienna, Austria. · Dipartimento di Scienze Cliniche e Sperimentali, Università degli Studi di Brescia, U.O. Reumatologia e Immunolgia Clinica, Spedali Civili di Brescia, Brescia, Italy. · Centre for Prognosis Studies in the Rheumatic Diseases, Senior Scientist Krembil Research Institute, Professor Medicine, University of Toronto, Toronto Western Hospital EW 1-409, Toronto, Canada. · Unidade de Imunologia Clínica, Hospital Santo António, Centro Hospitalar do Porto, UMIB, Instituto de Ciencias Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal. · Department of Rheumatology, Odense University Hospital, University of Southern Denmark, Denmark. · Corporal Michael J. Crescenz VA Medical Center (Philadelphia), Philadelphia, Philadelphia, USA. · Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA. · Nephrology Unit, City Clinical Hospital n.a. S.P. Botkin, Moscow, Russia. · Lanarkshire Centre for Rheumatology, Hairmyres Hospital, Scotland, UK. · National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA. ·Ann Rheum Dis · Pubmed #27884822.

ABSTRACT: OBJECTIVES: Treat-to-target recommendations have identified 'remission' as a target in systemic lupus erythematosus (SLE), but recognise that there is no universally accepted definition for this. Therefore, we initiated a process to achieve consensus on potential definitions for remission in SLE. METHODS: An international task force of 60 specialists and patient representatives participated in preparatory exercises, a face-to-face meeting and follow-up electronic voting. The level for agreement was set at 90%. RESULTS: The task force agreed on eight key statements regarding remission in SLE and three principles to guide the further development of remission definitions:1. Definitions of remission will be worded as follows: CONCLUSIONS: The work of this international task force provides a framework for testing different definitions of remission against long-term outcomes.

9 Review A systems approach to renal inflammation in SLE. 2017

Berthier, Celine C / Kretzler, Matthias / Davidson, Anne. ·Internal Medicine, Department of Nephrology, University of Michigan, Ann Arbor, MI, USA. · Feinstein Institute, Center for Autoimmunity and Musculoskeletal Diseases, Manhasset, NY, USA 11030. Electronic address: adavidson1@nshs.edu. ·Clin Immunol · Pubmed #27534926.

ABSTRACT: Lupus disease and its complications including lupus nephritis (LN) are very disabling and significantly impact the quality of life and longevity of patients. Broadly immunosuppressive treatments do not always provide the expected clinical benefits and have significant side effects that contribute to patient morbidity. In the era of systems biology, new strategies are being deployed integrating diverse sources of information (molecular and clinical) so as to identify individual disease specificities and select less aggressive treatments. In this review, we summarize integrative approaches linking molecular disease profiles (mainly tissue transcriptomics) and clinical phenotypes. The main goals are to better understand the pathogenesis of lupus nephritis, to identify the risk factors for renal flare and to find the predictors of both short and long-term clinical outcome. Identification of common key drivers and additional patient-specific key drivers can open the door to improved and individualized therapy to prevent and treat LN.

10 Review DNA-reactive B cells in lupus. 2016

Suurmond, Jolien / Calise, Justine / Malkiel, Susan / Diamond, Betty. ·Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, 350 Community Drive, Manhasset, NY 11030, USA. · Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, 350 Community Drive, Manhasset, NY 11030, USA; PhD Program in Molecular Medicine, Hofstra-Northwell School of Medicine, 500 Hofstra Blvd, Hempstead, NY 11549, USA. · Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, 350 Community Drive, Manhasset, NY 11030, USA. Electronic address: bdiamond@northwell.edu. ·Curr Opin Immunol · Pubmed #27504587.

ABSTRACT: IgG anti-DNA antibodies are both diagnostic and pathogenic for systemic lupus erythematosus (SLE). They contribute to tissue inflammation through direct tissue binding and to systemic inflammation through activation of Toll-like receptors by nucleic acid-containing immune complexes. IgG DNA-reactive antibodies originate when B cell tolerance mechanisms are impaired. The heterogeneous immune perturbations in SLE lead to the survival and activation of DNA-reactive B cells in various B cell subsets at distinct stages of B cell maturation and differentiation. We propose that the spectrum of B cell alterations and failed tolerance mechanisms for DNA-reactive B cells in lupus patients is best understood by studying genetic risk alleles. This implies that the B cells producing IgG anti-DNA antibodies and the failed tolerance mechanisms(s) will differ across patients. A better understanding of these differences should lead to better patient stratification, improved outcomes of clinical trials, and the identification of novel therapeutic targets.

11 Review Targeted B cell therapies in the treatment of adult and pediatric systemic lupus erythematosus. 2016

Hui-Yuen, J S / Nguyen, S C / Askanase, A D. ·Division of Pediatric Rheumatology, Steven and Alexandra Cohen Children Medical Center, Hofstra Northwell School of Medicine, USA. · Division of Rheumatology, New York-Presbyterian Hospital/Columbia University Medical Center, USA. · Division of Rheumatology, New York-Presbyterian Hospital/Columbia University Medical Center, USA ada20@cumc.columbia.edu. ·Lupus · Pubmed #27497253.

ABSTRACT: Belimumab (Benlysta) is a fully-humanized monoclonal antibody that inhibits B-lymphocyte stimulator (also known as B cell activating factor) and was approved by the U.S. Federal Drug Administration and European Medicines Evaluation Agency for treatment in adults with autoantibody-positive systemic lupus erythematosus (SLE). Rituximab (Rituxan) is a chimeric anti-CD20 monoclonal antibody targeting B lymphocytes. This review discusses the key findings of the phase III trials in adults with SLE and of real-world use of belimumab and rituximab in the care of both adult and pediatric SLE patients. It highlights the safety profile of belimumab and rituximab and gives insight into the consideration of these therapies for specific SLE disease states. It concludes with a discussion of the current clinical trials investigating B cell therapies in specific SLE disease states and a look to the future, with ongoing clinical trials.

12 Review T-cell-directed therapies in systemic lupus erythematosus. 2016

Nandkumar, P / Furie, R. ·Division of Rheumatology, Northwell Health, Great Neck, NY, USA pnandkumar@northwell.edu. · Division of Rheumatology, Northwell Health, Great Neck, NY, USA. ·Lupus · Pubmed #27497252.

ABSTRACT: Drug development for the treatment of systemic lupus erythematosus (SLE) has largely focused on B-cell therapies. A greater understanding of the immunopathogenesis of SLE coupled with advanced bioengineering has allowed for clinical trials centered on other targets for SLE therapy. The authors discuss the benefits and shortcomings of focusing on T-cell-directed therapies in SLE and lupus nephritis clinical trials.

13 Review Update on clinical trials in systemic lupus erythematosus. 2016

Narain, Sonali / Furie, Richard. ·Division of Rheumatology Northwell Health, Hofstra Northwell School of Medicine and the Program in Novel Therapeutics, Great Neck, New York, USA. ·Curr Opin Rheumatol · Pubmed #27314466.

ABSTRACT: PURPOSE OF REVIEW: With advancement in our understanding of pathogenic mechanisms in systemic lupus erythematosus (SLE), there is tremendous enthusiasm in examining drugs, old and new, to improve outcomes. This review highlights recent trials' successes and impasses that have come to fore. RECENT FINDINGS: Among B-cell therapies, belimumab continues its run of successes with sustained safety and tolerability documented in a long-term extension as well as the likely approval of a subcutaneous formulation in the near future. With greater antibody-dependent cytotoxicity and less immunogenicity, there is hope for obinituzumab to succeed where its anti-CD 20 predecessors have failed. Drugs targeting type I interferons - sifalimumab and anifrolumab - have been efficacious albeit with an increase in incidence of Herpes zoster infections. There is also renewed interest in evaluating the efficacy of calcineurin inhibitors, specifically tacrolimus in the induction and maintenance of lupus nephritis. Introspection into clinical trial designs have highlighted the effects of entry criteria, end points, background medications and geographical differences on study outcomes. SUMMARY: There are at least 50 drugs and targets being evaluated in SLE. In addition to developing new drugs to treat lupus, future trials have to focus on more effective study designs to improve chances of trial success.

14 Review Arthrodesis of the Metacarpophalangeal and Interphalangeal Joints of the Hand: Current Concepts. 2016

Beldner, Steven / Polatsch, Daniel B. ·From the New York Hand and Wrist Center, Lenox Hill Hospital, New York, NY. ·J Am Acad Orthop Surg · Pubmed #27097126.

ABSTRACT: Metacarpophalangeal arthrodesis and interphalangeal arthrodesis are excellent tools in the surgeon's armamentarium to restore function of the disabled hand. Typical indications for these procedures are pain, deformity, and/or stiffness. Arthrodesis is generally considered a salvage procedure to be used when other reconstructive procedures, such as arthroplasty, are not possible or would be associated with a high rate of complication or failure. To determine the most functional position for arthrodesis in each patient, the surgeon should preoperatively evaluate the compromised joint in the context of the disease process, determine the initial cause of the joint pathology, and assess the condition of the surrounding joints. Current methods of achieving fusion of metacarpophalangeal and interphalangeal joints include options for incisions, bone preparation techniques, and surgical implants; each has advantages and associated risks.

15 Review A link: Allergic rhinitis, Asthma & Systemic Lupus Erythematosus. 2016

Sin, Eric / Anand, Prachi / Frieri, Marianne. ·Nassau University Medical Center, Department of Medicine, 2201 Hempstead Turnpike. East Meadow, N.Y, 11554. · Nassau University Medical Center, Department of Medicine, 2201 Hempstead Turnpike. East Meadow, N.Y, 11554. Electronic address: mfrieri@numc.edu. ·Autoimmun Rev · Pubmed #26851551.

ABSTRACT: This review has discussed a link between allergic rhinitis, asthma and systemic lupus erythematosus (SLE) and a case report in this area. A clear link with symptoms of allergic rhinitis, asthma and SLE exists. Several articles found on pubmed in the literature are listed on allergic rhinitis and allergy, Th1-immune responses, mast cells in autoimmunity, total immunoglobulin E levels in lupus, atopic diseases and SLE are reviewed. In addition, risks and correlations, genetic predisposition, environmental factors, immune regulation, elevated serum IgE levels, regulatory B cells for both allergic and autoimmune diseases are mentioned, Asthma and the vascular endothelial cell growth factor, asthma and autoimmune diseases, allergy and autoimmunity, neutrophils, innate and adaptive immunity in the development of SLE, the (Tim) gene family, complement activation in SLE and immunomodulation, hypersensitivity reactions in autoimmunity are discussed.

16 Review SLE-associated risk factors affect DC function. 2016

Son, Myoungsun / Kim, Sun Jung / Diamond, Betty. ·The Feinstein Institute for Medical Research, Center for Autoimmune and Musculoskeletal Diseases, Manhasset, NY, USA. ·Immunol Rev · Pubmed #26683148.

ABSTRACT: Numerous risk alleles for systemic lupus erythematosus (SLE) have now been identified. Analysis of the expression of genes with risk alleles in cells of hematopoietic origin demonstrates them to be most abundantly expressed in B cells and dendritic cells (DCs), suggesting that these cell types may be the drivers of the inflammatory changes seen in SLE. DCs are of particular interest as they act to connect the innate and the adaptive immune response. Thus, DCs can transform inflammation into autoimmunity, and autoantibodies are the hallmark of SLE. In this review, we focus on mechanisms of tolerance that maintain DCs in a non-activated, non-immunogenic state. We demonstrate, using examples from our own studies, how alterations in DC function stemming from either DC-intrinsic abnormalities or DC-extrinsic regulators of function can predispose to autoimmunity.

17 Review What is damaging the kidney in lupus nephritis? 2016

Davidson, Anne. ·Centre for Autoimmunity &Musculoskeletal Diseases, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA. ·Nat Rev Rheumatol · Pubmed #26581344.

ABSTRACT: Despite marked improvements in the survival of patients with severe lupus nephritis over the past 50 years, the rate of complete clinical remission after immune suppression therapy is <50% and renal impairment still occurs in 40% of affected patients. An appreciation of the factors that lead to the development of chronic kidney disease following acute or subacute renal injury in patients with systemic lupus erythematosus is beginning to emerge. Processes that contribute to end-stage renal injury include continuing inflammation, activation of intrinsic renal cells, cell stress and hypoxia, metabolic abnormalities, aberrant tissue repair and tissue fibrosis. A deeper understanding of these processes is leading to the development of novel or adjunctive therapies that could protect the kidney from the secondary non-immune consequences of acute injury. Approaches based on a molecular-proteomic-lipidomic classification of disease should yield new information about the functional basis of disease heterogeneity so that the most effective and least toxic treatment regimens can be formulated for individual patients.

18 Review Systemic lupus erythematosus and atherosclerosis: Review of the literature. 2016

Frieri, Marianne / Stampfl, Heather. ·Division of Allergy Immunology, Nassau University Medical Center, East Meadow, NY, United States; Department of Medicine, Nassau University Medical Center, East Meadow, NY, United States. Electronic address: mfrieri@numc.edu. · Department of Medicine, Nassau University Medical Center, East Meadow, NY, United States. ·Autoimmun Rev · Pubmed #26299985.

ABSTRACT: The purpose of this manuscript is to extensively review the literature related to systemic lupus erythematosus and atherosclerosis. The conclusion of this review has covered accelerated atherosclerosis in systemic lupus erythematosus, the role of complement, interferon in premature atherosclerosis, inflammatory mediators such as cytokines, leukocytes, innate and adaptive immunity, hydrolytic enzymes, reactive oxygen species, vascular endothelial growth factor, toll receptors in lupus nephritis, several specific anti-inflammatory pharmacological therapies, and potential prevention strategies for atherothrombotic events, interferons and the inflammasome. It is important for allergist-immunologists, rheumatologists both in academic institutions and in practice to understand this important disorder.

19 Review Lessons Learned From the Clinical Trials of Novel Biologics and Small Molecules in Lupus Nephritis. 2015

Furie, Richard / Toder, Kiley / Zapantis, Ekaterini. ·Division of Rheumatology, North Shore-Long Island Jewish Health System, Great Neck, NY; Hofstra North Shore-Long Island Jewish School of Medicine, Great Neck, NY. Electronic address: rfurie@nshs.edu. · Division of Rheumatology, North Shore-Long Island Jewish Health System, Great Neck, NY. ·Semin Nephrol · Pubmed #26573553.

ABSTRACT: Systemic lupus erythematosus (SLE) is a ripe area for drug development. There are great unmet needs, especially for those with lupus nephritis, in which good responses occur only in the minority of treated patients. An expanded understanding of immunopathogenesis of SLE coupled with the availability of sophisticated bioengineering technologies has resulted in the ability to supply the lupus community with the reagents needed to perform clinical trials. However, drug development in SLE has proven to be particularly challenging. Only one drug, belimumab, has been approved for patients with SLE through the traditional route of randomized controlled trials. The basis for our failures is unknown, but most assuredly relates to trial design issues, confounding by background medicines, and the multiplicity of active biologic pathways in this disease. Off-label use of failed trial drugs such as mycophenolate mofetil and rituximab paradoxically has become routine in many parts of the world. Despite the obstacles, there currently is unprecedented clinical trial activity in lupus nephritis, which most likely will lead to at least one drug approval in years to come.

20 Review Lupus brain fog: a biologic perspective on cognitive impairment, depression, and fatigue in systemic lupus erythematosus. 2015

Mackay, Meggan. ·Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA. mmackay@NSHS.edu. ·Immunol Res · Pubmed #26481913.

ABSTRACT: Cognitive disturbances, mood disorders and fatigue are common in SLE patients with substantial adverse effects on function and quality of life. Attribution of these clinical findings to immune-mediated disturbances associated with SLE remains difficult and has compromised research efforts in these areas. Improved understanding of the role of the immune system in neurologic processes essential for cognition including synaptic plasticity, long term potentiation and adult neurogenesis suggests multiple potential mechanisms for altered central nervous system function associated with a chronic inflammatory illness such as SLE. This review will focus on the biology of cognition and neuroinflammation in normal circumstances and potential biologic mechanisms for cognitive impairment, depression and fatigue attributable to SLE.

21 Review Integrative neuroscience approach to neuropsychiatric lupus. 2015

Huerta, Patricio T / Gibson, Elizabeth L / Rey, Carson / Huerta, Tomás S. ·Laboratory of Immune and Neural Networks, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA. pato.huerta@gmail.com. · Department of Molecular Medicine, Hofstra North Shore LIJ Medical School, Hempstead, NY, USA. pato.huerta@gmail.com. · Laboratory of Immune and Neural Networks, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA. ·Immunol Res · Pubmed #26467973.

ABSTRACT: We present a succinct review of our approach to study the interactions between the DNA-reactive antibodies that cross-react with the GluN2A and GluN2B subunits of the N-methyl-D-aspartate receptor, denoted DNRABs, and their brain targets in subjects with neuropsychiatric systemic lupus erythematosus (NPSLE). We have analyzed the DNRAB-based brain symptomatology in mouse models of NPSLE by using an integrative neuroscience approach, which includes behavioral assessment coupled with electrophysiological studies of neural networks and synaptic connections in target brain regions, such as the CA1 region of the hippocampus. Our results suggest a framework for understanding the interactions between immune factors and neural networks.

22 Review Molecular studies of lupus nephritis kidneys. 2015

Davidson, Anne / Bethunaickan, Ramalingam / Berthier, Celine / Sahu, Ranjit / Zhang, Weijia / Kretzler, Matthias. ·Center for Autoimmunity and Musculoskeletal Diseases, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York, NY, 11030, USA. adavidson1@nshs.edu. · Center for Autoimmunity and Musculoskeletal Diseases, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York, NY, 11030, USA. · Department of Internal Medicine, Nephrology, University of Michigan, Ann Arbor, MI, 48109, USA. · Department of Medicine, Mount Sinai Medical Center, New York, NY, 10029, USA. ·Immunol Res · Pubmed #26376897.

ABSTRACT: Lupus nephritis is a devastating complication of systemic lupus erythematosus (SLE) for which current therapies are insufficiently effective. Histologic evaluation of renal biopsies is a poor predictor of therapeutic response or outcome. Integrated immunologic, genomic and proteomic approaches may yield new insights into disease pathogenesis and thereby improve therapeutic strategies for lupus nephritis. Given the lack of sequential biopsies from humans, it also remains essential to study informative animal models of disease. Cross-species analyses can identify cells or pathways that are relevant to human disease and can be further studied in mouse models. Using a systems biology approach in which we compare molecular data from kidneys of three different mouse models of lupus nephritis with data from human lupus biopsies, we have found that inflammatory events escalate rapidly around the time of proteinuria onset. This is followed by hypoxia and metabolic stress, and by tubular and endothelial dysfunction. The failure of complete reversal of these abnormalities may increase the sensitivity of the kidney to further insult. We further found that renal macrophages and dendritic cells are key players in lupus nephritis both in mouse models and humans and that macrophages display a hybrid molecular profile that reflects incomplete resolution of inflammation and excessive tissue remodeling. Finally, our studies have suggested several new biomarkers for disease stage that can now be tested longitudinally in human SLE patients.

23 Review Systematic Review of Diffuse Alveolar Hemorrhage in Systemic Lupus Erythematosus: Focus on Outcome and Therapy. 2015

Ednalino, Christina / Yip, Julie / Carsons, Steven E. ·From the Division of Rheumatology, Allergy & Immunology, Winthrop-University Hospital, Clinical Campus of Stony Brook University School of Medicine, Mineola, New York. ·J Clin Rheumatol · Pubmed #26308350.

ABSTRACT: BACKGROUND: Diffuse alveolar hemorrhage (DAH) is an uncommon but potentially life-threatening manifestation of systemic lupus erythematosus (SLE) associated with high mortality. Although survival and its associated clinical, laboratory, and therapeutic features have been reported for case reports and series, they have not been systematically reviewed. OBJECTIVES: The purpose of this systematic review was to assess survival of episodes of DAH in SLE over 3 decades and to categorize trends in therapies, commonly utilized to treat this disorder. RESULTS: Overall, SLE patients survived 61% of 174 DAH episodes representing 140 patients. Episode survival was 67% in the time period from 2000 to 2013. Corticosteroids were nearly universally used therapeutically, and cyclophosphamide was used in 55%. Plasmapheresis was used in 31% and did not appear to be associated with survival. CONCLUSIONS: Diffuse alveolar hemorrhage in SLE still carries a high risk of mortality; however, survival trends appear to demonstrate an increase from approximately 25% in the 1980s to 67% in the current decade. Increased use of cyclophosphamide appears to be associated with better survival, whereas plasmapheresis does not appear to influence outcome. Although these results need to be interpreted with caution because they are not derived from randomized controlled trials, we believe this represents the largest reported compilation of survival data in DAH associated with SLE.

24 Review Therapeutics to block autoantibody initiation and propagation in systemic lupus erythematosus and rheumatoid arthritis. 2015

Suurmond, Jolien / Zou, Yong Rui / Kim, Sun Jung / Diamond, Betty. ·Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, Manhasset, NY 11030, USA. · Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, Manhasset, NY 11030, USA. bdiamond@nshs.edu. ·Sci Transl Med · Pubmed #25810309.

ABSTRACT: Most current therapies for the autoimmune diseases systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), as well as many of the drugs in the therapeutic pipeline, reduce the autoimmune inflammatory process but lead to a general immunosuppression. The goal of the next generation of therapies should be to reduce autoimmunity while at the same time better maintain immunocompetence. We propose three approaches for accomplishing this goal: (i) modulate antigen presentation to the adaptive immune system, (ii) alter B cell selection in the germinal center, and (iii) use decoy antigens to prevent the formation of proinflammatory immune complexes. These approaches are based on recent advances in the field: We now appreciate the role of dendritic cell function in autoimmune disease and the importance of citrullinated proteins as neoantigens in RA. There is also new recognition that most pathogenic autoantibodies are produced by B cells that have matured within the germinal center and that immune complexes in both diseases contain ligands for Toll-like receptors. We propose that treatments that target these newly revealed aspects of RA and SLE will decrease systemic inflammation with less immunocompromise.

25 Review Common presentations of pediatric rheumatologic diseases: a generalist's guide. 2013

Reyhan, Iris / Goldberg, Baruch R / Gottlieb, Beth S. ·The Steven and Alexandra Cohen Children's Medical Center of New York, The Hofstra North Shore-LIJ School of Medicine, Hempstead, New York, USA. ·Curr Opin Pediatr · Pubmed #23652686.

ABSTRACT: PURPOSE OF REVIEW: To present a case-based approach of three common scenarios which often present to the primary care physician. The approach to these cases and the differential diagnosis are discussed for these common rheumatologic diseases. RECENT FINDINGS: Numerous healthy children and adolescents are referred to pediatric rheumatologists for the evaluation of suspected rheumatologic diseases. Often, general rheumatologic laboratory tests are sent which are not necessarily specific to the clinical situation. There is a high false-positive rate associated with many of these tests and undue anxiety and referrals result from these. Directed laboratory studies based on history and exam findings are more prudent and useful in the evaluation of these children. Routine antinuclear antibody testing, for example, is not recommended without supportive symptoms or signs. SUMMARY: A practical approach for primary care physicians is described for the evaluation of patients suspected of having some of the more common pediatric rheumatologic symptoms and diseases.

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