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Systemic Lupus Erythematosus: HELP
Articles by Joab Chapman
Based on 7 articles published since 2008
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Between 2008 and 2019, J. Chapman wrote the following 7 articles about Lupus Erythematosus, Systemic.
 
+ Citations + Abstracts
1 Review Neuropsychiatric SLE: from animal model to human. 2017

Pikman, R / Kivity, S / Levy, Y / Arango, M-T / Chapman, J / Yonath, H / Shoenfeld, Y / Gofrit, S G. ·1 Israel Defense Forces Medical Corps, Ramat Gan, Israel. · 2 Department of Medicine A, Sheba Medical Center, Tel-Hashomer, Israel. · 3 The Zabludovicz Center for Autoimmune Diseases. · 4 The Dr Pinchas Borenstein Talpiot Medical Leadership Program 2013; and Sheba Medical Center, Tel-Hashomer, Israel. · 5 Sackler Faculty of Medicine, Tel Aviv University, Ramat-Aviv, Israel. · 6 Department of Medicine E, Meir Medical Center, Kfar Saba, Israel; affiliated with the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. · 7 Doctoral Program in Biomedical Sciences, Universidad del Rosario, Bogotá-Colombia. · 8 Department of Neurology, Sagol Neuroscience Center, Sheba Medical Center, Tel-Hashomer, Israel. · 9 The Danek Gartner Institute of Human Genetics, Sheba Medical Center, Tel-Hashomer, Israel. · 10 Incumbent of the Laura Schwarz-Kip Chair for Research of Autoimmune Diseases, Sackler Faculty of Medicine, Tel Aviv University, Israel. ·Lupus · Pubmed #28394237.

ABSTRACT: Animal models are a key element in disease research and treatment. In the field of neuropsychiatric lupus research, inbred, transgenic and disease-induced mice provide an opportunity to study the pathogenic routes of this multifactorial illness. In addition to achieving a better understanding of the immune mechanisms underlying the disease onset, supplementary metabolic and endocrine influences have been discovered and investigated. The ever-expanding knowledge about the pathologic events that occur at disease inception enables us to explore new drugs and therapeutic approaches further and to test them using the same animal models. Discovery of the molecular targets that constitute the pathogenic basis of the disease along with scientific advancements allow us to target these molecules with monoclonal antibodies and other specific approaches directly. This novel therapy, termed "targeted biological medication" is a promising endeavor towards producing drugs that are more effective and less toxic. Further work to discover additional molecular targets in lupus' pathogenic mechanism and to produce drugs that neutralize their activity is needed to provide patients with safe and efficient methods of controlling and treating the disease.

2 Review Pharmacologic management of neuropsychiatric lupus. 2016

Kivity, Shaye / Baker, Britain / Arango, Maria-Teresa / Chapman, Joab / Shoenfeld, Yehuda. ·a The Zabludowicz Center for Autoimmune Diseases , The Chaim Sheba Medical Center, Tel-Hashomer , Ramat-Gan , Israel. · b Rheumatology Unit, The Chaim Sheba Medical Center , Tel Hashomer , Ramat-Gan , Israel. · c Department of Medicine 'A', The Chaim Sheba Medical Center , Tel Hashomer , Ramat-Gan , Israel. · d The Dr. Pinchas Borenstein Talpiot Medical Leadership Program 2013, The Chaim Sheba Medical Center , Tel Hashomer , Ramat-Gan , Israel. · e St Georges University of London/Nicosia Medical School , University of Nicosia , Egkomi , Cyprus. · f Doctorate Program of Universidad del Rosario , Bogotá , Colombia. · g Department of Neurology , Sagol Neuroscience Center, Sheba Medical Center, Tel-Hashomer , Ramat Gan , Israel. · h Sackler Faculty of Medicine , Tel-Aviv University , Tel-Aviv , Israel. · i Incumbent of the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases , Tel-Aviv University , Tel-Aviv , Israel. ·Expert Rev Clin Pharmacol · Pubmed #26559084.

ABSTRACT: Neuropsychiatric lupus affects above 50% of patients with systemic lupus erythematosus and may span from mild symptoms to acute devastating life-threatening ones. Owing to the clinical variability, most pharmacological data rely on small, uncontrolled trials and case reports. The mainstay of therapy relies on immune-suppression by glucocorticoids, in adjunction with cyclophosphamide or anti-B-cell therapy, in moderate to severe cases. In selected scenarios (e.g., chorea) intravenous immunoglobulin or plasmapheresis may be effective. Anticoagulation is warranted if anti-phospholipid antibodies are present. In parallel there may be a need for symptomatic treatment such as anti-epileptic or anti-depressive treatments, etc. In the future, more studies addressed to assess pathogenesis and preferred treatments of specific manifestations are needed in order to personalize treatments.

3 Review Neuropsychiatric lupus: a mosaic of clinical presentations. 2015

Kivity, Shaye / Agmon-Levin, Nancy / Zandman-Goddard, Gisele / Chapman, Joab / Shoenfeld, Yehuda. · ·BMC Med · Pubmed #25858312.

ABSTRACT: Neuropsychiatric symptoms affect nearly half of the patients with systemic lupus erythematosus; however, the effect on disease severity, quality of life, and prognosis is tremendous. Symptoms of neuropsychiatric systemic lupus erythematosus may range from mild diffuse ones, to acute life threatening events. Although the underlying mechanisms are still largely unraveled, several pathogenic pathways are identified, such as antibody-mediated neurotoxicity, vasculopathy due to anti-phospholipid antibodies and other mechanisms, and cytokine-induced neurotoxicity. In the current review, we describe the old and the new regarding epidemiology, pathophysiology, diagnosis, and management of neuropsychiatric systemic lupus erythematosus. The possible link between neuropsychiatric symptoms and specific mechanisms may help to facilitate our understanding of the disease in the future, thus allowing for better treatment strategies.

4 Article Immunization with hepatitis B vaccine accelerates SLE-like disease in a murine model. 2014

Agmon-Levin, Nancy / Arango, María-Teresa / Kivity, Shaye / Katzav, Aviva / Gilburd, Boris / Blank, Miri / Tomer, Nir / Volkov, Alex / Barshack, Iris / Chapman, Joab / Shoenfeld, Yehuda. ·Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer 52621, Israel; Sackler Medical School, Tel Aviv University, Israel. · Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer 52621, Israel; Doctoral Program in Biomedical Sciences Universidad del Rosario, Bogota 111221, Colombia; Center for Autoimmune Diseases Research - CREA, Universidad del Rosario, Bogota 111221, Colombia. · Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer 52621, Israel; Sackler Medical School, Tel Aviv University, Israel; The Dr. Pinchas Borenstein Talpiot Medical Leadership Program 2013, Sheba Medical Center, Tel-Hashomer 52621, Israel. · Department of Neurology and Sagol Neuroscience Center, Sheba Medical Center, Tel-Hashomer 52621, Israel. · Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer 52621, Israel. · Institute of Pathology, Sheba Medical Center, Tel Hashomer 52621, Israel. · Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer 52621, Israel; Incumbent of the Laura Schwarz-Kip Chair for Autoimmunity, Tel-Aviv University, Israel. Electronic address: shoenfel@post.tau.ac.il. ·J Autoimmun · Pubmed #25042822.

ABSTRACT: Hepatitis-B vaccine (HBVv) can prevent HBV-infection and associated liver diseases. However, concerns regarding its safety, particularly among patients with autoimmune diseases (i.e. SLE) were raised. Moreover, the aluminum adjuvant in HBVv was related to immune mediated adverse events. Therefore, we examined the effects of immunization with HBVv or alum on SLE-like disease in a murine model. NZBWF1 mice were immunized with HBVv (Engerix), or aluminum hydroxide (alum) or phosphate buffered saline (PBS) at 8 and 12 weeks of age. Mice were followed for weight, autoantibodies titers, blood counts, proteinuria, kidney histology, neurocognitive functions (novel object recognition, staircase, Y-maze and the forced swimming tests) and brain histology. Immunization with HBVv induced acceleration of kidney disease manifested by high anti-dsDNA antibodies (p < 0.01), early onset of proteinuria (p < 0.05), histological damage and deposition of HBs antigen in the kidney. Mice immunized with HBVv and/or alum had decreased cells counts mainly of the red cell lineage (p < 0.001), memory deficits (p < 0.01), and increased activated microglia in different areas of the brain compare with mice immunized with PBS. Anxiety-like behavior was more pronounced among mice immunized with alum. In conclusion, herein we report that immunization with the HBVv aggravated kidney disease in an animal model of SLE. Immunization with either HBVv or alum affected blood counts, neurocognitive functions and brain gliosis. Our data support the concept that different component of vaccines may be linked with immune and autoimmune mediated adverse events.

5 Article Antiphospholipid antibodies and the brain: a consensus report. 2011

Brey, R L / Muscal, E / Chapman, J. ·University of Texas Health Science Center at San Antonio, Department of Neurology, San Antonio, TX 78229, USA. brey@uthscsa.edu ·Lupus · Pubmed #21303831.

ABSTRACT: This report discusses the difference between antiphospholipid antibodies (aPL) as a predictor for first and recurrent ischemic stroke, whether or not concomitant systemic lupus erythematosus (SLE) increases aPL-associated risk, and the association of aPL with other neurological manifestations. The neurological manifestations covered in this report were selected because they are among the most common, including cognitive dysfunction, headache, multiple sclerosis and seizures/epilepsy. Recommendations are made regarding further research that is needed to clarify remaining uncertainties.

6 Article Abnormal olfactory function demonstrated by manganese-enhanced MRI in mice with experimental neuropsychiatric lupus. 2010

Kivity, Shaye / Tsarfaty, Galia / Agmon-Levin, Nancy / Blank, Miri / Manor, David / Konen, Eli / Chapman, Joab / Reichlin, Morris / Wasson, Craig / Shoenfeld, Yehuda / Kushnir, Tammar. ·Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Israel. ·Ann N Y Acad Sci · Pubmed #20398010.

ABSTRACT: Mice with experimental neuropsychiatric lupus (NPSLE), induced by anti-ribosomal-P antibodies, developed depression-like behavior and a diminished sense of smell. Manganese-enhanced MRI (MEMRI) allows in vivo mapping of functional neuronal connections in the brain, including the olfactory tract. The aim of this study was to analyze and describe, via the MEMRI technique, the effect of the anti-ribosomal-P injection on the olfactory pathway. Twenty mice were intra-cerebra-ventricular injected to the right hemisphere: 10 with human anti-ribosomal-P antibodies and 10 with human IgG antibodies (control). Depression was addressed by forced swimming test and smell function was evaluated by smelling different concentrations of menthol. MEMRI was used to investigate the olfactory system in these mice. Passive transfer of anti-ribosomal-P to mice resulted in a depression-like behavior, accompanied with a significant deficit in olfactory function. MEMRI of these mice demonstrated significant reduction (P < 0.001) in normalized manganese enhancement ratios of olfactory structures, compared to control mice. We concluded that an impaired olfactory neuronal function in mice with experimental depression, mediated by passive transfer of human-anti-ribosomal-P, can be demonstrated by MEMRI.

7 Article Anti-P ribosomal antibodies induce defect in smell capability in a model of CNS -SLE (depression). 2008

Katzav, Aviva / Ben-Ziv, Tal / Chapman, Joab / Blank, Miri / Reichlin, Morris / Shoenfeld, Yehuda. ·Department of Neurology, Sagol Neuroscience Center, Sheba Medical Center, Tel-Hashomer, Israel. ·J Autoimmun · Pubmed #18947972.

ABSTRACT: METHODS: Mice were injected intracerebroventricularily (ICV) with affinity-purified human anti-P antibodies or normal commercial IgG as control. Mice were examined for depression by the forced swimming test (FST) and for olfactory function by the smell threshold test. Treatments included the antidepressant drug fluoxetine or aroma therapy by exposure to lemon or cinnamon odor. RESULTS: Mice injected with anti-P developed depression-like behavior, which improved significantly upon treatment with fluoxetine. Depressed mice had a significant deficit in olfactory function which was not reversed by fluoxetine. Exposure of anti-P-injected mice to lemon odor was associated with some improvement of the immobility time, a measure of depression. CONCLUSIONS: ICV injection of anti-P induces both depression-like behavior and impaired olfactory function in mice. Fluoxetine and possibly lemon odor exposure improve depressive behavior in these mice.