Relevant bibliographies by topics / Systemic lupus erythematosus/etiology

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Systemic lupus erythematosus/etiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Systemic lupus erythematosus/etiology"

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Adhami, Eftim. "Calculating the etiology of systemic lupus erythematosus." Medical Hypotheses 62, no. 2 (2004): 237–46. http://dx.doi.org/10.1016/s0306-9877(03)00340-2.

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Burlingame, Mark B., and Jeffrey C. Delafuente. "Treatment of Systemic Lupus Erythematosus." Drug Intelligence & Clinical Pharmacy 22, no. 4 (1988): 283–89. http://dx.doi.org/10.1177/106002808802200401.

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Systemic lupus erythematosus (SLE) is an autoimmune disease with clinical manifestations involving a multitude of tissue sites. This article describes the pathophysiology, etiology, clinical manifestations, and therapy of SLE, and focuses mainly on drugs used in SLE treatment. The reader will be able to identify which pharmacologic agents are used in SLE and list the drugs that are useful for specific clinical manifestations. The reader will also be able to describe the common adverse drug reactions seen from SLE treatment and the potential risks involved with these therapies. Information on expected outcomes from drug therapy that will aid in monitoring patients receiving treatment for SLE is provided.
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Perry, Daniel, Allison Sang, Yiming Yin, Ying-Yi Zheng, and Laurence Morel. "Murine Models of Systemic Lupus Erythematosus." Journal of Biomedicine and Biotechnology 2011 (2011): 1–19. http://dx.doi.org/10.1155/2011/271694.

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Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disorder. The study of diverse mouse models of lupus has provided clues to the etiology of SLE. Spontaneous mouse models of lupus have led to identification of numerous susceptibility loci from which several candidate genes have emerged. Meanwhile, induced models of lupus have provided insight into the role of environmental factors in lupus pathogenesis as well as provided a better understanding of cellular mechanisms involved in the onset and progression of disease. The SLE-like phenotypes present in these models have also served to screen numerous potential SLE therapies. Due to the complex nature of SLE, it is necessary to understand the effect specific targeted therapies have on immune homeostasis. Furthermore, knowledge gained from mouse models will provide novel therapy targets for the treatment of SLE.
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Niewold, Timothy B., Daniel N. Clark, Rafah Salloum, and Brian D. Poole. "Interferon Alpha in Systemic Lupus Erythematosus." Journal of Biomedicine and Biotechnology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/948364.

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The pleiotropic cytokine interferon alpha is involved in multiple aspects of lupus etiology and pathogenesis. Interferon alpha is important under normal circumstances for antiviral responses and immune activation. However, heightened levels of serum interferon alpha and expression of interferon response genes are common in lupus patients. Lupus-associated autoantibodies can drive the production of interferon alpha and heightened levels of interferon interfere with immune regulation. Several genes in the pathways leading to interferon production or signaling are associated with risk for lupus. Clinical and cellular manifestations of excess interferon alpha in lupus combined with the genetic risk factors associated with interferon make this cytokine a rare bridge between genetic risk and phenotypic effects. Interferon alpha influences the clinical picture of lupus and may represent a therapeutic target. This paper provides an overview of the cellular, genetic, and clinical aspects of interferon alpha in lupus.
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Teplyuk, N. P., O. V. Grabovskaya, and Polina A. Razhev. "Clinical case of lupus erythematosus panniculitis." Russian Journal of Skin and Venereal Diseases 23, no. 5 (2020): 334–40. http://dx.doi.org/10.17816/dv60811.

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BACKGROUND: This clinical case is interesting because of extreme rarity of lupus panniculitis in the population, as well as the possible risk of developing systemic lupus erythematosus.
 CASE REPORT: The article presents a clinical observation of a rare skin disorder lupus erythematosus panniculitis and the results of a successful combined treatment of the disease with systemic glucocorticoids (prednisolone), and an antimalarial agent (hydroxychloroquine). A review of the literature on the etiology, pathogenesis, and diagnosis of lupus panniculitis has been conducted.
 CONCLUSION. Early detection of lupus erythematosus panniculitis (LEP) makes systemic steroid therapy and quinoline drugs more effective in achieving remission. That is why dynamic monitoring of patients with LEP is important to identify new or progressive symptoms.
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Gökalp, C., G. Aygun, A. F. Dogan, U. Usta, I. Kurultak, and S. Ustundag. "Idiopathic membranous nephropathy preceding membranous lupus nephritis: a case report." Lupus 29, no. 3 (2020): 340–43. http://dx.doi.org/10.1177/0961203319899998.

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Membranous nephropathy is one of the most common causes of nephrotic syndrome in the adult population. According to the underlying etiology, membranous nephropathy is classified as either primary or secondary. Systemic lupus erythematosus is an autoimmune disease that can affect the kidneys in 50% of patients in the course of the disease. Renal disease may be the first manifestation of systemic lupus erythematosus and the development of systemic findings may be delayed for about 1–5 years following the diagnosis of lupus nephritis. We present a 59-year-old male patient who had a diagnosis of idiopathic membranous nephropathy since 2007 and developed membranous lupus nephritis during the 12-year follow-up without any extrarenal systemic lupus erythematosus findings.
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Heyneman, Catherine A. "Systemic Lupus Erythematosus: A Therapeutic Update." Journal of Pharmacy Practice 22, no. 1 (2008): 29–52. http://dx.doi.org/10.1177/0897190008322246.

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Systemic lupus erythematosus (SLE) is a complex autoimmune disease with variable clinical manifestations that is characterized by flares and periods of relative quiescence. The disease occurs approximately 10 times more frequently in women and is more prevalent among certain ethnic groups. The etiology is complex and dependent upon an interaction of genetic, hormonal, and environmental factors. Corticosteroids and immunosuppressive agents have transformed the outlook for patients with lupus. Unfortunately, the increased lifespan unmasked an accelerated process of atherosclerosis and cardiovascular disease. Early mortality is usually attributable to active lupus, but deaths late in the disease process are often secondary to thrombotic events. Advancements in the understanding of molecular and cellular mechanisms involved in the pathogenesis have resulted in development of novel therapies. Immunomodulatory drugs developed for other diseases are being investigated for use in specific manifestations of lupus. Individualization of treatment and lifelong monitoring are required in most patients.
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Young, K. A., M. E. Munroe, J. M. Guthridge, et al. "Screening characteristics for enrichment of individuals at higher risk for transitioning to classified SLE." Lupus 28, no. 5 (2019): 597–606. http://dx.doi.org/10.1177/0961203319834675.

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Objective Further prospective study is needed to elucidate the etiology and natural history of systemic lupus erythematosus development. The clinical complexity of this heterogeneous disease makes study design challenging. Our objective was to ascertain useful screening factors for identifying at-risk individuals for follow-up rheumatologic assessment or inclusion in prospective studies. Methods We attempted to re-contact 3823 subjects with a family history of systemic lupus erythematosus, who did not meet American College of Rheumatology systemic lupus erythematosus classification at a baseline study visit; 436 agreed to follow-up participation an average of 6.3 years after baseline. In total, 56 of these individuals had transitioned to classified systemic lupus erythematosus (≥ 4 cumulative American College of Rheumatology criteria, verified by medical record review) by the time of follow up. Generalized estimating equations assessed associations between our dichotomous outcome of transitioning to systemic lupus erythematosus with baseline characteristics, including ANA positivity, Connective Tissue Disease Screening questionnaire systemic lupus erythematosus score, and number of American College of Rheumatology criteria. We analyzed predictive accuracy of characteristics on transitioning. Results ANA positivity, Connective Tissue Disease Screening questionnaire systemic lupus erythematosus score categorization of possible or probable systemic lupus erythematosus, and greater number of American College of Rheumatology criteria at baseline were each associated with transitioning to systemic lupus erythematosus classification. Being ANA positive and having confirmed immunologic criteria at baseline had the highest positive predictive value and specificity for transitioning to systemic lupus erythematosus. American College of Rheumatology Connective Tissue Disease Screening questionnaire systemic lupus erythematosus score categorization of possible or probable systemic lupus erythematosus had a better positive predictive value, negative predictive value, sensitivity, and specificity than ANA positivity. Conclusion Given limited resources, identifying individuals for follow up based on the systemic lupus erythematosus portion of the Connective Tissue Disease Screening questionnaire could be an efficient way to identify family members at highest risk of disease transition.
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Khurana, Dheeraj, Anu Gupta, Vishal Jogi, ManojKumar Goyal, and Manish Modi. "Chronic meningitis in systemic lupus erythematosus: An unusual etiology." Annals of Indian Academy of Neurology 17, no. 4 (2014): 426. http://dx.doi.org/10.4103/0972-2327.144019.

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Uva, Luís, Diana Miguel, Catarina Pinheiro, João Pedro Freitas, Manuel Marques Gomes, and Paulo Filipe. "Cutaneous Manifestations of Systemic Lupus Erythematosus." Autoimmune Diseases 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/834291.

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Systemic lupus erythematosus (SLE) is a multiorgan autoimmune disease of unknown etiology with many clinical manifestations. The skin is one of the target organs most variably affected by the disease. The American College of Rheumatology (ACR) established 11 criteria as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. Cutaneous lesions account for four of these 11 revised criteria of SLE. Skin lesions in patients with lupus may be specific or nonspecific. This paper covers the SLE-specific cutaneous changes: malar rash, discoid rash, photosensitivity, and oral mucosal lesions as well as SLE nonspecific skin manifestations, their pathophysiology, and management. A deeper thorough understanding of the cutaneous manifestations of SLE is essential for diagnosis, prognosis, and efficient management. Thus, dermatologists should cooperate with other specialties to provide optimal care of SLE patient.
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Dissertations / Theses on the topic "Systemic lupus erythematosus/etiology"

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Maier, Shannon Marie. "Murine models in the investigation of lupus etiology." Oklahoma City : [s.n.], 2006.

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Capelas, Maria Pacheco. "Lupus eritematoso sistémico: terapias atuais e novas abordagens." Master's thesis, [s.n.], 2015. http://hdl.handle.net/10284/5303.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas<br>O Lupus Eritematoso Sistémico (LES) é uma doença crónica inflamatória de etiologia desconhecida que pode afetar múltiplos órgãos. A doença caracteriza-se por períodos de exacerbação e de remissão e atinge particularmente as mulheres. A produção de autoanticorpos anti-nucleares tem um papel determinante no curso da doença, sendo responsável pelas principais manifestações clínicas que podem envolver o sistema nervoso central, pele, músculos, articulações e rins. As terapêuticas atuais do LES passam pelo uso de corticosteróides sistémicos que suprimem a ativação do sistema imunitário, pelo uso de agentes citotóxicos como a ciclosporina e a azatriopina (AZA), e pela imunoterapia com anticorpos. A terapêutica no LES deve ser individualizada e irá depender do grau de comprometimento do órgão ou sistema, sendo adaptada consoante o paciente responde ou não ao tratamento convencional. Neste ultimo caso de pacientes, sem dúvida, a imunoterapia assume-se como a ultima linha de tratamento. As complicações inerentes à própria doença e aos tratamentos usados tornam a pesquisa por novas terapêuticas, decisivas, de maneira a aumentar a qualidade de vida dos doentes.<br>Systemic Lupus Erythematosus (SLE) is an unknown infflammatory chronicle disease. This disease is characterized bu aggravation and relaxing and affects mainly the woman. The production of anti-nuclear antibodies as an important role on the disease course, being responsible for several clinical manifestations which may involve the central nervous system, skin, muscles, articulations and kidneys. The current therapies of SLE are mainly the application of systemic corticosteroids which supress the activation of the immune system, the use of cytotoxic agents like cyclosporine and azathioprine (AZA) and immune therapy with antibodies. SLE therapy must be individualized and will depende of the severity of the lesions in the organs and systems, and will be adapted if the patient doesn`t respond to conventional treatments. In this last case, without a doubt, immunotherapy assumes itself has the last line of treatment. The inherent complications to the particular disease and of the treatments used make the search of new therapies decisive in order to increase the quality of life of these patients.
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Teh, Lee-Suan. "Neuropsychiatric systemic lupus erythematosus." Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240703.

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Neuropsychiatric (NP) symptoms are relatively common in patients with SLE. The diverse and dramatic clinical presentations, the unclear pathogenesis, the lack of diagnostic test/s and uncertainties about the optimal management are some problems facing a clinician. When serum anti P antibodies were claimed to be highly correlated to lupus psychosis, this needed confirmation. An ELISA for measuring anti P antibodies was developed and validated. The prevalence of anti P antibodies was determined in different patient groups in a large retrospective study. Although anti P antibodies were highly specific for SLE, there was no correlation between the presence of these antibodies and lupus psychosis or other NP symptoms. Two prospective studies were carried out to eliminate any bias in our retrospective study. In one, none of the patients developed psychosis and these antibodies were not found to be specific for lupus depression or anxiety. In the other, anti P antibodies were measured in Malaysian Chinese SLE patients. No correlation was found between these antibodies and NP-SLE but a high prevalence of these antibodies was demonstrated in this group. Genetic studies showed that there was an increase in HLA-Dr2w16X subtype allele in anti P-positive patients but this did not reach significance. The usefulness of measuring antineuronal antibodies in helping to diagnose NP-SLE was examined but these antibodies were not better indicators of NP-SLE. Although the clinical correlations of anti P antibodies remain controversial, anti P antibodies were found to selectively bind to neuroblastoma cell surfaces <i>in vitro</i> but the nature of the surface antigen was not determined. Finally, sera from patients with lupus psychosis were found to significantly influence the response of neuroblastoma cells to agonist-induced stimulation and if confirmed, would offer an explanation for the reversible changes in cell function associated with psychiatric lupus.
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Peixoto, Tatiana Vasconcelos. "Aumento de células T CD4+CD69+ e redução de células T reguladoras CD4+CD25+FoxP3+ em camundongos com Lúpus Eritematoso Sistêmico (LES) induzido por pristane." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-14122015-152214/.

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Introdução: O Lúpus Eritematoso Sistêmico (LES) é uma doença autoimune multissistêmica de etiologia complexa que envolve fatores ambientais, genéticos e hormonais. É caracterizada pela produção de autoanticorpos e mediadores inflamatórios, ativação e proliferação de células T autorreativas e perda da autotolerância imunológica. Em pacientes com LES, a expressão do receptor primário de ativação CD69 é aumentada e a de células T supressoras/reguladoras (Treg) CD4+CD25+FoxP3+ é reduzida. O CD69 é essencial para ativação de células T CD4 autorreativas enquanto que as células Treg são importantes na manutenção da autotolerância. Desta forma, células T tem um papel central na patogênese do LES, mas os mecanismos implicados na falência da autotolerância ainda não são elucidados, destacando a importância de estudos em modelos experimentais da doença, como o de LES-induzido por pristane. Objetivo: Quantificar células T CD4+CD69+ ativadas e Treg CD4+CD25+FoxP3+ no sangue, baço e LP de camundongos Balb/c LESinduzido por pristane no sentido de avaliar a falência de autotolerância neste modelo. Métodos: Analisamos 84 camundongos Balb/c fêmeas: 52 receberam por via intraperitoneal uma dose única de 0,5 ml de pristane e 32 a mesma dose de salina. Amostras de sangue, baço e LP dos camundongos eutanasiados foram coletadas 90, 120, 180 e 300 (T90, T120, T180 e T300) dias após a inoculação de pristane ou salina. Células mononucleares do sangue periférico (CMSP), do LP (CMLP) e esplenócitos foram obtidos por lise das hemácias seguida de lavagens com RPMI medium 1640 e centrifugação, e posteriormente criopreservadas até a avaliação por citometria de fluxo usando o aparelho Guava EasyCyteTM HT (Millipore). Para esta etapa, as células foram descongeladas, lavadas com RPMI medium 1640 e incubadas com anticorpos monoclonais dirigidos contra CD3, CD4, CD25, CD28, CD69, CTLA-4, FoxP3, CD14 e Ly6C (BD PharmingenTM). Os resultados foram expressos como média ± DP e teste de Mann-Whitney foi utilizado para análises estatísticas, sendo p<0,05 considerado significante. Resultados: Comparados aos animais controles, animais com LES-induzido por pristane apresentaram aumento de células T CD4+CD69+ no sangue nos T90, T120 e T180 (p < 0,022, p=0,008 e p=0,010, respectivamente) e no baço no T120 (p=0,049), enquanto que, no LP, houve redução destas células nos T120, T180 e T300 (p=0,001, p=0,001 e p < 0,001, respectivamente). A porcentagem de células Treg CD4+CD25+FoxP3+ foi menor no sangue nos T90, T120 e T180 (p=0,018, p=0,012, p < 0,046, respectivamente), no baço, nos T120 e T180 (p=0,018 e p=0,013), e no LP nos T90 e T300 (p=0,008 e p=0,005). Conclusão: Aumento da expressão de células T CD4+CD69+ e redução da expressão de Treg CD4+CD25+FoxP3+ sugerem células T CD4 ativadas e perda da autotolerância periférica em camundongos com LES-induzido por pristane. Estas alterações são semelhantes às observadas no lúpus humano, de modo que demonstramos que este modelo também pode ser útil na avaliação de mecanismos de ativação celular, tolerância periférica desequilíbrio imune homeostático envolvidos no LES<br>Introduction: Systemic Lupus Erythematosus (SLE) is multisystemic autoimmune disease with complex etiology that involves environmental, genetic and hormonal factors. Is characterized by auto-antibodies and inflammatory mediators production, autoreactive T cells activation and proliferation and loss of immunogenic autotolerance. In patients with SLE, expression of CD69 activation primary receptor is increased and the CD4+CD25+FoxP3+ suppressor/regulatory T cell (Treg) is reduced. CD69 is essential for activation of autoreactive CD4 T cells while Treg cells are important in autotolerance maintenance. In this way, T cells have a central role in the pathogenesis of SLE however, the mechanisms implied in the autotolerance failure are still not elucidated, highlighting the importance of studies in this disease\'s experimental models, such as pristane-induced SLE. Objective: Quantify activated CD4+CD69+ T cells and CD4+CD25+FoxP3+ Treg in blood, spleen and peritoneal lavage (PL) of Balb/c mice with pristane-induced SLE in order to evaluate autotolerance failure in this model. Methods: 84 female Balb/c mice were analyzed: 52 received a single intraperitoneal 0,5 ml dose of pristane and 32 the same dose of saline. Euthanized mice samples of blood, spleen and peritoneal lavage were collected 90, 120, 180 and 300 (T90, T120, T180 and T300) days after inoculation of pristane or saline. Mononuclear cells from peripheral blood (PBMC), PL (PLMC) and splenocytes were obtained by lysis of erythrocytes followed by washings with RPMI medium 1640 and centrifugation, subsequently criopreserved until evaluation by flow cytometry using the appliance GuavaEasyCyteTM HT (Millipore). For this step, cells were unfrozen, washed with RPMI medium 1640 and incubated with monoclonal antibodies against CD3, CD4, CD25, CD28, CD69, CTLA-4, FoxP3, CD14 and Ly6C (BD PharmingenTM). The results were expressed as mean ± SD and Mann-Whitney 11 test was used for statistical analysis, being considered significant p < 0,05. Results: Compared to control animals, SLE pristane-induced animals presented increase of CD4+CD69+ T cells in blood on T90, T120 and T180 (p=0.022, p=0.008 and p=0.010, respectively) and in spleen on T120 (p=0.049), while, in PL, there was reduction of these cells on T120, T180 and T300 (p=0.001, p=0.001 and p < 0.001, respectively). The porcentage of Treg CD4+CD25+FoxP3+ was smaller in blood on T90, T120 and T180 (p=0.018, p=0.012 and p < 0.046, respectively), in spleen on T120 and T180 (p=0.018 and p=0.013), and in PL on T90 and T300 (p=0.008 and p=0.005). Conclusion: Increase of CD4+CD69+ T cell and reduction of CD4+CD25+FoxP3+ Treg expression suggests activated T CD4 cells and loss of peripheral autotolerance in pristane-induced SLE mice. These alterations are similar to observed in human lupus, in order we showed that this model can also be useful in evaluating the mechanisms of cellular activation, peripheral tolerance and homeostatic immune imbalance involved in the LES
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Bernatsky, Sasha. "Malignancy in systemic lupus erythematosus." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32761.

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Objectives. (1) To estimate cancer incidence in systemic lupus erythematosus (SLE) as compared to the general population. (2) To estimate the sensitivity and specificity of methods of cancer ascertainment. (3) To determine the prevalence of malignancy risk factors in SLE. Methods. (1) We determined the incidence of malignancy in the Montreal General Hospital (MGH) lupus cohort, through linkage with the Quebec tumor registry. Standardized incidence ratios (SIRS) were generated, using Quebec population rates. In addition, a meta-analysis was performed by pooling data from eight cohort studies of malignancy in SLE. (2) We administered a postal survey to cohort members to determine risk factors for cancer and self-report of cancer occurrence. For dead or lost-to-follow-up patients, data was abstracted from charts. We calculated the sensitivity and specificity of self-report and chart review for cancer ascertainment, compared to registry linkage results. (3) Using the data collected on self-report and chart review, we compared risk factor prevalence within the MGH cohort to that of the Quebec population. Results. (1) Observed cancers in our cohort were greater than what would be expected; for all cancers, the SIR was 1.8 (95% Confidence Interval 1.2--2.6). The meta-analysis SIR (for all malignancies) was 1.67 (1.42--1.94). Postal survey and chart review methods demonstrated high specificity. Sensitivity was imperfect, but did not greatly effect estimation of the SIR estimate. (2) Our lupus cohort had a distinct profile of risk factors for malignancy compared to the general population; differences included more prevalent nulliparity, obesity, and use of hormone replacement therapy. Conclusions. The risk of malignancy in SLE patients is increased. Risk factor profiles could influence the incidence of certain malignancies in SLE.
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Clarke, Alexander James. "Autophagy in Systemic Lupus Erythematosus." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/autophagy-in-systemic-lupus-erythematosus(1e5a4a5e-99f7-456e-bcb4-634a4e3fd986).html.

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Autophagy has emerged as a critical homeostatic mechanism in lymphocytes, influencing proliferation and differentiation. I sought to explore the role of autophagy in the pathogenesis of human and murine lupus, a disease in which B cells are critical effectors of pathology. Autophagy was assessed using multiple techniques in NZB/W and control mice, and in patients with SLE compared to healthy controls. I evaluated the phenotype of the B cell compartment in Vav-Atg7-/- mice in vivo, and examined human and murine plasmablast formation following inhibition of autophagy. I found activation of autophagy in early developmental stages of B cell development in a lupus mouse model even before disease-onset, and which progressively increased with age. In human disease, again autophagy was activated compared with healthy controls, principally in naïve B cells. B cells isolated from Vav-Atg7-/- mice failed to effectively differentiate into plasma cells following stimulation in vitro. Similarly, human B cells stimulated in the presence of autophagy inhibition did not differentiate into plasmablasts. My data suggest activation of autophagy is a mechanism for survival of autoreactive B cells, and also demonstrate that it is required for plasmablast differentiation, processes that induce significant cellular stress. The implication of autophagy in two major pathogenic pathways in SLE suggests the potential to use inhibition of autophagy as a novel treatment target.
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Carvalho, Jozélio Freire de. ""Antilipoproteína lipase (LPL): um novo componente no complexo processo aterosclerótico do lúpus eritematoso sistêmico?"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5145/tde-27092005-130705/.

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Dislipidemia é implicada no processo aterosclerótico do LES. A descrição de aLPL no LES associado a hipertrigliceridemia levou-nos a analisar esse anticorpo no contexto da inflamação envolvida na aterogênese. aLPL foi encontrado em 38% dos pacientes com LES com altos níveis de triglicérides. Correlação positiva significante foi observada entre aLPL e PCR, VHS, SLEDAI, anti-DNA, anti-cardiolipina e CH100 baixo. Análise de regressão múltipla confirmou a forte associação entre aLPL e PCR. Esses dados dão suporte à associação entre inflamação, resposta imune e dislipidemia, introduzindo o aLPL como um novo componente nos complexos eventos da aterogênese do LES<br>Dyslipidemia is implicated in the atherosclerosis process of SLE. The description of aLPL in SLE associated with hypertrigliceridemia prompted us to analyze this antibody in the context of the inflammation involved in the atherogenesis. aLPL was found in 38 por cento of SLE patients with high levels of triglycerides. Significant positive correlation was observed between aLPL and CRP, ESR, SLEDAI, anti-DNA, anti-cardiolipin and low CH100. Multiple regression analysis confirmed the strong association between aLPL and CRP. These data support the link between inflammation, immune response and dyslipidemia, introducing anti-LPL as new player in the complex events of atherogenesis in SLE
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Peschken, Christine A. "Systemic lupus erythematosus in Manitoba Aboriginals." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0019/MQ55086.pdf.

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Svenungsson, Elisabet. "Cardiovascular disease in systemic lupus erythematosus /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-501-8.

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Russell, Andrew Ian. "Genetic predisposition to systemic lupus erythematosus." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406513.

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Books on the topic "Systemic lupus erythematosus/etiology"

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Guggenheim, Alena. Underlying hormonal and neurotransmitter abnormalities in systemic lupus erythematous [sic]: Evidence for novel treatments in management of disease. NCNM, 2007.

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Systemic lupus erythematosus. 5th ed. Elsevier Academic Press, 2011.

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Eggleton, Paul, and Frank J. Ward, eds. Systemic Lupus Erythematosus. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0326-9.

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Miescher, Peter A., ed. Systemic Lupus Erythematosus. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79622-7.

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Smolen, Josef S., and Christoph C. Zielinski. Systemic Lupus Erythematosus. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71642-3.

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Hirohata, Shunsei, ed. Neuropsychiatric Systemic Lupus Erythematosus. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-76496-2.

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A, Sessa, Meroni Mietta, and Battini Graziana, eds. Systemic lupus erythematosus: Renal vasculitis. Karger, 1992.

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1917-, Aladjem Henrietta, ed. Understanding lupus. Scribner, 1985.

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Systemic lupus erythematosus: Methods and protocols. Humana Press, 2014.

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Arnaud, Laurent, and Ronald van Vollenhoven. Advanced Handbook of Systemic Lupus Erythematosus. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-43035-5.

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Book chapters on the topic "Systemic lupus erythematosus/etiology"

1

Graninger, W., C. C. Zielinski, and J. S. Smolen. "Etiologic and Pathogenetic Aspects of Systemic Lupus Erythematosus: A Critical Approach." In Systemic Lupus Erythematosus. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71642-3_2.

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Lockshin, Michael D. "Lupus pregnancies and neonatal lupus." In Systemic Lupus Erythematosus. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79622-7_8.

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Bertolaccini, Maria Laura, Graham R. V. Hughes, and Munther A. Khamashta. "Systemic Lupus Erythematosus." In Diagnostic Criteria in Autoimmune Diseases. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_1.

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Fassbender, Hans G. "Systemic Lupus Erythematosus." In Pathology and Pathobiology of Rheumatic Diseases. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04819-1_9.

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Treadwell, Patricia. "Systemic Lupus Erythematosus." In Atlas of Adolescent Dermatology. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58634-8_15.

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Nagaratnam, Nages, Kujan Nagaratnam, and Gary Cheuk. "Systemic Lupus Erythematosus." In Geriatric Diseases. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-33434-9_63.

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Laxer, Ronald M., David D. Sherry, and Philip J. Hashkes. "Systemic Lupus Erythematosus." In Pediatric Rheumatology in Clinical Practice. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-13099-6_4.

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Sharma, Aman, Shankar Naidu, Manish Rathi, and Ritambhra Nada. "Systemic Lupus Erythematosus." In The Uveitis Atlas. Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2506-5_77-1.

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Sharma, Aman, Shankar Naidu, Manish Rathi, and Ritambhra Nada. "Systemic Lupus Erythematosus." In The Uveitis Atlas. Springer India, 2019. http://dx.doi.org/10.1007/978-81-322-2410-5_77.

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Wren, Katherine, Shirley Lee, and Lori B. Siegel. "Systemic Lupus Erythematosus." In Encyclopedia of Women’s Health. Springer US, 2004. http://dx.doi.org/10.1007/978-0-306-48113-0_426.

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Conference papers on the topic "Systemic lupus erythematosus/etiology"

1

DUARTE, ANNA BEATRIZ GOMES SOUZA, ELISA GUIMARÃES MOTTA, ADIB CHICRE MANSUR, GUILHERME SALLES DE ESCOBAR GONÇAVES, LARISSA BARROS DE OLIVEIRA, and GABRIELLEN VITIELLO. "FEVER IN SYSTEMIC LUPUS ERYTHEMATOSUS." In 36º Congresso Brasileiro de Reumatologia. Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-102.

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Greene, E. R., K. R. Lanphere, J. Sharrar, and C. A. Roldan. "Arterial distensibility in systemic lupus erythematosus." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334459.

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Egeli, Bugra, Asli Ece Soykut, and Serdal Ugurlu. "226 Comorbidity in systemic lupus erythematosus." In 13th International Congress on Systemic Lupus Erythematosus (LUPUS 2019), San Francisco, California, USA, April 5–8, 2019, Abstract Presentations. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-lsm.226.

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ZAMBONI, SHERON, JEAN PAULO VERONESE DE SOUZA, CAMILA DE DAVID CRUZ, et al. "SEVERE ENTERITIS IN SYSTEMIC LUPUS ERYTHEMATOSUS." In 36º Congresso Brasileiro de Reumatologia. Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-245.

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TANAKA, ELOISE AKEMI, HARYMY BARROS, JULIANA DELFINO, THIAGO ALBERTO FERNANDES GOMES DOS SANTOS, JOSÉ FERNANDO POLANSKI, and THELMA LAROCA SKARE. "HEARING LOSS IN SYSTEMIC LUPUS ERYTHEMATOSUS." In 36º Congresso Brasileiro de Reumatologia. Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-464.

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Barboza, Flavio, Tassia Caroline Beckert Viana, Eduarda Judith Dias Jacome Silva, et al. "Systemic Lupus Erythematosus mimicking Hodgkin's lymphoma." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.16937.

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Souza da Paz, Adriane, Gustavo Luiz Behrens Pinto, and Mittermayer Barreto Santiago. "COLLAPSING GLOMERULOPATHY IN SYSTEMIC LUPUS ERYTHEMATOSUS." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17616.

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dos Santos Cavalcante, Anauá Fernanda, Sabrina Longo, Lucas P. G., et al. "DRY EYE IN SYSTEMIC LUPUS ERYTHEMATOSUS." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17297.

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Voulgari, PV, P. Katsimbri, Y. Alamanos, and AA Drosos. "FRI0115 Systemic lupus erythematosus in men." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.150.

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Moszkorzova, L., C. Dostal, J. Marek, Z. Lacinova, and L. Musilova. "FRI0137 Prolactin in systemic lupus erythematosus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.172.

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Reports on the topic "Systemic lupus erythematosus/etiology"

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Harley, John. Genome-Wide Association Study in African-Americans with Systemic Lupus Erythematosus. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada592038.

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Harley, John. Genome-Wide Association Study in African-Americans With Systemic Lupus Erythematosus. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada554417.

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Harley, John. Genome-Wide Association Study in African-Americans with Systemic Lupus Erythematosus. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada574794.

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Gontar, I. P., O. A. Rusanova, O. I. Emelyanova, S. S. Khortieva, and E. G. Cherkesova. AUTOIMMUNITY ISSUES IN PATIENTS WITH SYSTEMIC SCLERODERMA AND SYSTEMIC LUPUS ERYTHEMATOSUS WITH PREDOMINANT PULMONARY INVOLVEMENT. "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-73-81.

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Pfeifer, Maria. Self-help Support Groups: Choices in Participation Among Women Facing Systemic Lupus Erythematosus (SLE). Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.6685.

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Gontar, I. P., O. A. Rusanova, O. I. Emelyanova, and O. V. Paramonova. CLINICLA FEATURES OF SYSTEMIC LUPUS ERYTHEMATOSUS ASSOCIATED WITH CHANGES IN ANTIBODIES TO THYROXIN AND TRIIODOTHYRONINE. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxv-96-100.

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Luo, Shuaihantian, Ying Zhou, and Guiying Zhang. Association between complement 4 copy number variation and systemic lupus erythematosus: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.8.0076.

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Aleksandrov, A. V., I. Y. Alekhina, V. A. Aleksandrov, and N. V. Aleksandrova. The role of antibodies to xanthine oxidase in the development of immunopathological reactions in the rheumatoid arthritis and systemic lupus erythematosus. ООО ИМА-Пресс, 2018. http://dx.doi.org/10.18411/1995-4484-2018-56-3(2)-11.

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Aleksandrova, N. V., E. V. Benedickaya, I. Yu Alekhina, and A. V. Aleksandrov. ROLE OF ANTIBODIES TO PURINE NUCLEOSIDE PHOSPHORYLASE IN THE DIAGNOSIS OF INFECTIOUS DISEASES IN PATIENTS WITH RHEUMATOID ARTHRITIS AND SYSTEMIC LUPUS ERYTHEMATOSUS. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxv-23-27.

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Yuan, Qihang. Circulating Leptin Level, Soluble Leptin Receptor Level and Their Gene Polymorphism in Patients with Systemic Lupus Erythematosus: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.4.0137.

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