Relevant bibliographies by topics / Autoimmune systemic diseases

Contents

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

Academic literature on the topic 'Autoimmune systemic diseases'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Autoimmune systemic diseases"

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Shi, Guixiu, Jianying Zhang, Zhixin (Jason) Zhang, and Xuan Zhang. "Systemic Autoimmune Diseases." Clinical and Developmental Immunology 2013 (2013): 1–2. http://dx.doi.org/10.1155/2013/728574.

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Ripoll, E., E. Ripoll, M. Goma, N. Bolanos, I. Herrero, O. Bestard, J. M. Cruzado, et al. "Autoimmune systemic diseases." Nephrology Dialysis Transplantation 27, suppl 2 (May 1, 2012): ii61—ii62. http://dx.doi.org/10.1093/ndt/gfs205.

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Delgadillo, Xavier, Adrián E. Ortega, and Alejandro Moreira Greco. "Systemic and Autoimmune Diseases." Clinics in Colon and Rectal Surgery 32, no. 05 (September 2019): 372–76. http://dx.doi.org/10.1055/s-0039-1687833.

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Shi, Guixiu, Jianying Zhang, Zhixin (Jason) Zhang, and Xuan Zhang. "Systemic Autoimmune Diseases 2014." Journal of Immunology Research 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/183591.

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Cavestro, Cinzia, and Marcella Ferrero. "Migraine in Systemic Autoimmune Diseases." Endocrine, Metabolic & Immune Disorders - Drug Targets 18, no. 2 (February 13, 2018): 124–34. http://dx.doi.org/10.2174/1871530317666171124124340.

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Royer, Mathieu, and Xavier Puéchal. "Mucormycosis in systemic autoimmune diseases." Joint Bone Spine 81, no. 4 (July 2014): 303–7. http://dx.doi.org/10.1016/j.jbspin.2014.01.002.

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Kallenberg, Cees G. M. "Etiopathogenesis of systemic autoimmune diseases." Current Opinion in Rheumatology 25, no. 2 (March 2013): 223–24. http://dx.doi.org/10.1097/bor.0b013e32835cf2d1.

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Wang, Chrong-Reen, and Hung-Wen Tsai. "Autoimmune liver diseases in systemic rheumatic diseases." World Journal of Gastroenterology 28, no. 23 (June 21, 2022): 2527–45. http://dx.doi.org/10.3748/wjg.v28.i23.2527.

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Terzin, Viktória. "Association between autoimmune pancreatitis and systemic autoimmune diseases." World Journal of Gastroenterology 18, no. 21 (2012): 2649. http://dx.doi.org/10.3748/wjg.v18.i21.2649.

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Ralli, Massimo, Vittorio D’Aguanno, Arianna Di Stadio, Armando De Virgilio, Adelchi Croce, Lucia Longo, Antonio Greco, and Marco de Vincentiis. "Audiovestibular Symptoms in Systemic Autoimmune Diseases." Journal of Immunology Research 2018 (August 19, 2018): 1–14. http://dx.doi.org/10.1155/2018/5798103.

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Immune-mediated inner ear disease can be primary, when the autoimmune response is against the inner ear, or secondary. The latter is characterized by the involvement of the ear in the presence of systemic autoimmune conditions. Sensorineural hearing loss is the most common audiovestibular symptom associated with systemic autoimmune diseases, although conductive hearing impairment may also be present. Hearing loss may present in a sudden, slowly, rapidly progressive or fluctuating form, and is mostly bilateral and asymmetric. Hearing loss shows a good response to corticosteroid therapy that may lead to near-complete hearing restoration. Vestibular symptoms, tinnitus, and aural fullness can be found in patients with systemic autoimmune diseases; they often mimic primary inner ear disorders such as Menière’s disease and mainly affect both ears simultaneously. Awareness of inner ear involvement in systemic autoimmune diseases is essential for the good response shown to appropriate treatment. However, it is often misdiagnosed due to variable clinical presentation, limited knowledge, sparse evidence, and lack of specific diagnostic tests. The aim of this review is to analyse available evidence, often only reported in the form of case reports due to the rarity of some of these conditions, of the different clinical presentations of audiological and vestibular symptoms in systemic autoimmune diseases.
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Dissertations / Theses on the topic "Autoimmune systemic diseases"

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Leeuw, Karina de. "Premature atherosclerosis in systemic autoimmune diseases." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn/.

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Lövgren, Tanja. "Endogenous type I interferon inducers in systemic autoimmune diseases /." Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7181.

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Lövgren, Tanja. "Endogenous Type I Interferon Inducers in Systemic Autoimmune Diseases." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7181.

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Patients with systemic lupus erythematosus (SLE) have elevated levels of interferon (IFN)-α in blood and IFN-α-producing cells in tissues. In the present thesis, we investigate the mechanisms behind the upregulated IFN-α-production in SLE and also show that the IFN-α system is activated in primary Sjögren’s syndrome (pSS), with IFN-α-producing cells in the major affected organ, the salivary glands. The IFN-α is a type I IFN, a family of cytokines counteracting especially viral infections, by acting directly on infected cells, and via many immunomodulatory effects. The latter may also contribute to autoimmune processes.

The type I IFNs are usually produced upon recognition of microbial structures. In SLE, however, DNA-containing immune complexes (ICs) that induce IFN-α production are found. Many autoantibodies in SLE and pSS are directed to nucleic acids or to DNA/RNA-binding proteins. We show that also RNA in complex with autoantibodies from SLE or pSS patients (RNA-IC) induces IFN-α-production. The RNA could be either in the form of RNA-containing material released from apoptotic or necrotic cells or as a pure RNA-containing autoantigen, the U1 small nuclear ribonucleoprotein particle.

The IFN-α-production induced by RNA-IC occurred in plasmacytoid dendritic cells (PDCs), also termed natural IFN-producing cells (NIPCs), via binding to Fcγ-receptor IIa, endocytosis and triggering of Toll-like receptors (TLRs), probably TLR7 and TLR9. The RNA-IC may also have other effects, and we found that they induce prostaglandin E2 (PGE2) production in monocytes and tumor necrosis factor (TNF)-α in both monocytes and NIPC/PDC. The PGE2 downregulated the IFN-α induction in NIPC/PDC, and the IFN-α induction was increased in monocyte-depleted cell cultures.

The findings presented in this thesis aids in the understanding of the mechanisms behind the activated IFN-α system in SLE and other autoimmune diseases, and shows that also pSS is one of these diseases.

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Dumoitier, Nicolas. "Analysis of B lymphocytes in systemic autoimmune vascular diseases." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC304.

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Différents mécanismes de tolérance centraux et périphériques permettent la sélection négative des lymphocytes B auto-réactifs tout en préservant la sélection positive et la différenciation en plasmocytes producteurs d’anticorps de haute affinité. Ces mécanismes de tolérance sont altérés dans les pathologies auto-immunes et ces altérations conduisent à la production d’auto-anticorps. Ainsi, un ciblage thérapeutique des lymphocytes B autoréactifs, notamment avec les anticorps monoclonaux anti-CD20, donne des résultats prometteurs dans différentes pathologies auto-immunes. Si ces traitements ont démontré leur efficacité dans les vascularites associées aux anticorps anti-protéines cytoplasmiques des polynucléaires neutrophiles (ANCA) (VAA), d’autres maladies auto-immunes à composante vasculaire, dont la sclérodermie systémique (ScS) ou l’hypertension artérielle pulmonaire idiopathique (iHTAP), restent insensibles à ce ciblage. D’autre part, la caractérisation des sous-populations lymphocytaires B pathologiques porte essentiellement sur la détection des cellules exprimant ces auto-anticorps. Ce projet a ainsi eu pour objectif une caractérisation phénotypique et fonctionnelle comparative des sous-populations lymphocytaires B impliquées dans ces différentes pathologies auto-immunes vasculaires.Les patients atteints de granulomatose avec polyangéite présentent une activation importante de l’immunité innée mais aussi une production augmentée d’IL6 par les lymphocytes B en lien avec une activation importante des lymphocytes T. Des modifications phénotypiques des lymphocytes B sont observées chez les patients atteints de VAA, notamment la polyangéite microscopique suggérant pour cette vascularite une composante auto-immune. Ainsi, le CD69, le CD95 et le récepteur à l’IL-6 permettent de discriminer les différentes formes de la maladie. Dans la ScS et plus particulièrement dans les formes les plus sévères, diffuses, et dans l’HTAP associée, une activation basale des lymphocytes B est observée avec une sécrétion importante d’IL-6 et de TGF-ß. Ce dernier contribue, in vitro, à la prolifération des fibroblastes et à la sécrétion de collagène, responsables des mécanismes fibrosants observés dans la pathologie. Enfin, les basophiles présents dans la ScS semblent également activés et participer à l’activation des lymphocytes B et des fibroblastes malades. Ces résultats montrent que le lymphocyte B, en plus de son rôle dans la production d’anticorps, peut intervenir en physiopathologie par la sécrétion de cytokines pro-inflammatoires ou pro-fibrosantes comme l’IL-6 et le TGF-ß, toutes deux impliquées dans les processus d’activation vasculaire
Tolerance mechanisms allow the negative selection of auto-reactive B lymphocytes while protecting the positive selection and differentiation of plasmocytes that produce high affinity antibodies. Tolerance mechanisms are altered in various auto-immune diseases and allow the production of auto-antibodies. Indeed, therapeutic targeting of autoreactive B lymphocytes, notably using anti-CD20 monoclonal antibodies, gives promising results in several auto-immune pathologies. While these treatments show a relative efficacy in anti-neutrophil cytoplasmic antibodies associated vasculitis (ANCA) (AAV), other autoimmune diseases with vascular components, among which systemic sclerosis (SSc) or idiopathic high blood pressure (iPAH), remain resistant to the targeting. Previous studies have essentially addressed the characterization of auto-antibodies producing B cells sub-populations. Therefore, this thesis project aimed at delineating phenotypic and functional characterization of the lymphocytic B cells sub-populations involved in these various vascular autoimmune diseases.Patients affected by Granulomatosis with polyangiitis presented with important activation of innate immune system altogether with an increased production of IL6 by B lymphocytes correlated with T lymphocytes activation. Phenotypic alterations of B lymphocytes were observed for AAV patients, notably with MPA, suggesting an autoimmune component. Expression of CD69, CD95 and IL-6- receptor allowed discrimination between the various forms of the disease. In SSc, with particular emphasis in the most severe, diffuse forms, and in the associated PAH, a basal activation of the B cells was observed, allowing an important secretion of IL-6 and TGF-ß1. The latter contributed to the proliferation of fibroblasts and to the secretion of collagen, responsible for fibrosis induction as observed in the pathology. Finally, presence of activated basophils in SSc also participates in the activation of B cells and fibroblasts. These results place B lymphocytes, besides their role in antibody production, as important pathophysiological players through the secretion of pro-inflammatory and pro-fibrotic cytokines such as IL-6 and TGF-ß which are both implicated in endothelial cells activation in autoimmune vascular diseases
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Imgenberg-Kreuz, Juliana. "Epigenetic and Gene Expression Signatures in Systemic Inflammatory Autoimmune Diseases." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-310388.

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Autoimmune diseases are clinical manifestations of a loss-of-tolerance of the immune system against the body’s own substances and healthy tissues. Primary Sjögren’s syndrome (pSS) and systemic lupus erythematosus (SLE) are two chronic inflammatory autoimmune diseases characterized by autoantibody production and an activated type I interferon system. Although the precise mechanisms leading to autoimmune processes are not well defined, recent studies suggest that aberrant DNA methylation and gene expression patterns may play a central role in the pathogenesis of these disorders. The aim of this thesis was to investigate DNA methylation and gene expression in pSS and SLE on a genome-wide scale to advance our understanding of how these factors contribute to the diseases and to identify potential biomarkers and novel treatment targets. In study I, differential DNA methylation was analyzed in multiple tissues from pSS patients and healthy controls. We identified thousands of CpG sites with perturbed methylation; the most prominent finding was a profound hypomethylation at regulatory regions of type I interferon induced genes in pSS. In study II, a cases-case study comparing DNA methylation in pSS patients with high fatigue to patients with low fatigue, we found methylation patterns associated to the degree of fatigue. In study III, RNA-sequencing was applied to investigate the transcriptome of B cells in pSS in comparison to controls. Increased expression of type I and type II interferon regulated genes in pSS was observed, indicating ongoing immune activation in B cells. In study IV, the impact of DNA methylation on disease susceptibility and phenotypic variability in SLE was investigated. We identified DNA methylation patterns associated to disease susceptibility, SLE manifestations and different treatments. In addition, we mapped methylation quantitative trait loci and observed evidence for genetic regulation of DNA methylation in SLE.   In conclusion, the results presented in this thesis provide new insights into the molecular mechanisms underlying autoimmunity in pSS and SLE. The studies confirm the central role of the interferon system in pSS and SLE and further suggest novel genes and mechanisms to be involved in the pathogenesis these autoimmune diseases.
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Atta, Mustafa S. "Investigation of the humoral and cellular features of autoimmune diseases." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281586.

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Wang, Chuan. "DNA Sequence Variants in Human Autoimmune Diseases." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-179189.

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Human autoimmune diseases are hallmarked by inappropriate loss-of-tolerance and self-attacking response of the immune system. Studies included in this thesis are focusing on the implication and functional impact of genetic factors in three autoimmune diseases rheumatoid arthritis (RA), asthma, and systemic lupus erythematosus (SLE). Using genetic association studies, we found in study I and II that sequence variants of the interferon regulatory factor 5 (IRF5) gene were associated with RA and asthma, and the associations were more pronounced in certain disease subtypes. Distinct association patterns or risk alleles of the IRF5 gene variants were revealed in different diseases, indicating that IRF5 contributes to disease manifestations in a dose-dependent manner. In study III, we found that seven out of eight genetic risk loci for SLE, which were originally identified in East Asian populations, also conferred disease risk with the same risk alleles and comparable magnitudes of effect sizes in Caucasians. Remarkable differences in risk allele frequencies were observed for all associated loci across ethnicities, which seems to be the major source of genetic heterogeneity for SLE. In study IV we explored an exhaustive spectrum of sequence variants in the genes inhibitor of kappa light polypeptide gene enhancer in B-cells kinase epsilon (IKBKE) and interferon induced with helicase C domain 1 (IFIH1) by gene resequencing, and identified nine variants in IKBKE and three variants in IFIH1 as genetic risk factors for SLE. One of the associated variants may influence splicing of IKBKE mRNA. In study V we provided genome-wide transcriptional regulatory profiles for IRF5 and signal transducer and activator of transcription 4 (STAT4) using chromatin immunoprecipitation-sequencing (ChIP-seq). The target genes of IRF5 and STAT4 were found to play active roles in pathways related with inflammatory response, and their expression patterns were characteristic for SLE patients. We also identified potential cooperative transcription factors for IRF5 and STAT4, and disease-associated sequence variants which may affect the regulatory function of IRF5 and STAT4. In conclusion, this thesis illuminates the contribution of several genetic risk factors to susceptibility of human autoimmune diseases, which facilitates our understanding of the genetic basis of their pathogenesis.
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McCormick, Natalie. "The health resource utilization and economic burden of systemic autoimmune rheumatic diseases." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42149.

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Background: SARDs (Systemic Autoimmune Rheumatic Diseases) are a group of rare, chronic conditions (systemic vasculitis, systemic lupus erythematosus, scleroderma, Sjogren's disease, and poly/dermatomyositis) associated with high health resource consumption. However, estimates of their healthcare burden are sparse, with most determined at tertiary centres over short periods. Studying them separately has also limited research progress. Here we grouped the SARDs, for the first time ever, to quantify their collective, longitudinal (twelve-year) burden at the population-level. Methods: A population-based cohort of SARDs cases was identified from the administrative database of BC’s single-payer health system (PopDataBC). A detailed algorithm, with time and specialist parameters, was used to enhance diagnostic specificity. From PopDataBC, all provincially-funded health services, and all prescriptions (regardless of funding source), consumed from 1996 -2007 were captured. Costs for outpatient services and prescriptions were summed directly from paid claims; case-mix methodology was used for most hospitalizations. To quantify their net burden, costs were summed for claims attributable (under broad and narrow definitions) to SARDs. Costs are reported in 2007 Canadian dollars. Results: 18,741 SARDs cases were identified, contributing 82,140 patient-years(PY). After inflation adjustments, the annual mean per-PY direct medical costs of SARDs averaged $6,954/PY, with $1,882/PY(27%) from outpatient, $3,551/PY(51%) from hospital, and $1,521/PY(22%) from prescriptions. Over twelve years, annual costs decreased by 32%, from $8,901/PY in 1996 to $6,087/PY in 2007. Outpatient costs and encounters decreased by 26% ($2,205-$1,641/PY) and 19% (34-27/PY), respectively. Mean annual hospital costs decreased by half ($5,579-$2,776/PY), and admissions by 46% (0.89-0.48/PY). Despite these decreases, the annual mean number of dispensed prescriptions increased by 49% (23-34/PY), and their costs by 50% ($1,117-$1,670/PY). The annual net per-PY costs of SARDs, mainly from hospitalizations(18-43% of costs) and prescriptions(48-76%), averaged $2,011-$3,202/PY. Conclusions: SARDs impart a substantial healthcare burden at the population level, and in 2007 were directly responsible for ≥44% of cases’ gross mean annual healthcare costs ($6,087/PY). Most costs have decreased over twelve years; however, medication costs are rising (by 4% annually, on-average), which suggests comorbidity burdens are too. As demand grows for expensive but potentially-better SARDs therapies, research to assess their impact on long-term comorbidity risk is needed.
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Duffy, Emeir. "An investigation of the influence of dietary supplementation of n-3 fish oil and/or copper on systemic lupus erythematosus." Thesis, University of Ulster, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273795.

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Esfandiari, Ehsanollah. "Role of Th1 and Th2 cytokines in the pathogenesis of systemic autoimmune diseases." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366255.

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Books on the topic "Autoimmune systemic diseases"

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Rolando, Cimaz, and Lehman Thomas J. A, eds. Pediatrics in systemic autoimmune diseases. Amsterdam: Elsevier, 2008.

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U, Wells A., and Denton C. P, eds. Pulmonary involvement in systemic autoimmune diseases. Amsterdam: Elsevier, 2004.

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service), ScienceDirect (Online, ed. Digestive involvement in systemic autoimmune diseases. Amsterdam: Elsevier, 2008.

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service), ScienceDirect (Online, ed. Antiphospholipid syndrome in systemic autoimmune diseases. Amsterdam: Elsevier, 2009.

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Piercarlo, Sarzi-Puttini, ed. The skin in systemic autoimmune diseases. Amsterdam: Elsevier, 2006.

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A, Doria, and Pauletto Paolo 1947-, eds. The heart in systemic autoimmune diseases. Amsterdam: Elsevier, 2004.

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Walker, Sara, and Luis J. Jara. Endocrine manifestations of systemic autoimmune diseases. Amsterdam: Elsevier Science, 2008.

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A, Asherson Ronald, ed. Vascular manifestations of systemic autoimmune diseases. Boca Raton: CRC Press, 2001.

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1937-, Cruse J. M., and Lewis R. E. 1947-, eds. Autoimmunity: Basis concepts , systemic and selectedorgan-specific diseases. Basel: Karger, 1985.

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1937-, Cruse Julius M., and Lewis R. E. 1947-, eds. Autoimmunity: Basis concepts : systemic and selected organ-specific diseases. Basel: Karger, 1985.

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Book chapters on the topic "Autoimmune systemic diseases"

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Townsend, Henry B., Anthony M. Turkiewicz, and Xena A. Whittier. "Systemic Corticosteroids." In Autoimmune Bullous Diseases, 233–41. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26728-9_13.

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Petri, Michelle. "Life-Threatening Complications of Systemic Lupus Erythematosus." In Autoimmune Diseases, 9–17. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-358-9_2.

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Quillinan, Niamh P., and Christopher P. Denton. "Systemic Sclerosis: Severe Involvement of Internal Organs." In Autoimmune Diseases, 67–88. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-358-9_6.

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Jonkman, Marcel F., and J. M. Meijer. "Bullous Systemic Lupus Erythematosus." In Autoimmune Bullous Diseases, 137–41. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-91557-5_17.

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Jonkman, Marcel F. "Bullous Systemic Lupus Erythematosus." In Autoimmune Bullous Diseases, 151–56. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-23754-1_17.

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Ruiz-Irastorza, Guillermo, and Munther A. Khamashta. "Complicated Pregnancies in Patients with Autoimmune Systemic Diseases." In Autoimmune Diseases, 331–44. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-358-9_20.

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Walker, Jennifer G., and Marvin J. Fritzler. "Systemic Sclerosis." In Diagnostic Criteria in Autoimmune Diseases, 31–36. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_6.

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López-Isac, Elena, Marialbert Acosta-Herrera, and Javier Martín. "Systemic Sclerosis." In Genetics of Rare Autoimmune Diseases, 19–35. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03934-9_2.

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Laskaris, George, and Crispian Scully. "Autoimmune Diseases." In Periodontal Manifestations of Local and Systemic Diseases, 245–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55596-1_23.

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Bertolaccini, Maria Laura, Graham R. V. Hughes, and Munther A. Khamashta. "Systemic Lupus Erythematosus." In Diagnostic Criteria in Autoimmune Diseases, 3–8. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_1.

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Conference papers on the topic "Autoimmune systemic diseases"

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KCHIR, hela, Dhouha Cherif, Dhilel Issaoui, Maha Mtir, Dhia Kaffel, Faten Limaiem, and Nadia Maamouri. "SAT0195 SYSTEMIC DISEASES ASSOCIATED WITH AUTOIMMUNE LIVER DISEASES." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8246.

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Feijoo, ML Velloso, N. Plaza Aulestia, S. Rodriguez Montero, and JL Marenco de la Fuente. "AB0459 Treatment of systemic autoimmune diseases with rituximab: safety data." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3890.

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Ginosyan, K., A. Beglaryan, and V. Vardanyan. "AB0983 Mefv mutations in armenian patients with systemic autoimmune diseases." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5109.

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Priori, R., F. Conti, E. Cassarà, E. Medda, MA Stazi, R. Gerli, A. Manfredi, F. Franceschini, MG Danieli, and G. Valesini. "THU0248 Familial clustering of systemic lupus erythematosus with other autoimmune diseases." 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-2001.792.

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Vilariño Seijas, A., A. Morales Triadó, L. Carabias Ané, G. Cardona Peitx, E. Valls Sánchez, C. Codina Jiménez, and C. Quiñones Ribas. "5PSQ-053 Off-label use of rituximab in systemic autoimmune diseases." In 25th EAHP Congress, 25th–27th March 2020, Gothenburg, Sweden. British Medical Journal Publishing Group, 2020. http://dx.doi.org/10.1136/ejhpharm-2020-eahpconf.370.

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Feijoo, ML Velloso, S. Rodriguez Montero, N. Plaza Aulestia, and JL Marenco de la Fuente. "AB0458 B cells depletion for the treatment of systemic autoimmune diseases." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6402.

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Barturen, Guillermo, Sepideh Babaei, Francesc Català-Moll, Manuel Martínez-Bueno, Zuzanna Makowska, Jordi Martorell-Marugán, Pedro Carmona-Sáez, et al. "O31 Integrative analysis reveals a molecular stratification of systemic autoimmune diseases." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.42.

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Pelegrin, L., J. Hernández-Rodríguez, J. Torras, G. Espinosa, A. Adán, and M. T. Sainz. "AB0678 Peripheral ulcerative keratitis associated to autoimmune systemic diseases: visual prognosis and occurrence while systemic disease in remission." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4334.

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Ling, JES, M. Ter Wee, W. Lems, M. Nurmohamed, and H. Raterman. "SAT0695 No association between vitamin d levels and cardiovascular diseases in inflammatory joint diseases and systemic autoimmune diseases – a systematic review." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4302.

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Acosta-Herrera, M., M. Kerick, D. Gonzalez-Serna, C. Wijmenga, A. Franke, L. Padyukov, T. Vyse, et al. "OP0283 Cross-disease meta-analysis in four systemic autoimmune diseases to identify shared genetic etiologies." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2876.

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Reports on the topic "Autoimmune systemic diseases"

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Li, Mingqiang, Juan Wan, and Zhenhong Xu. The association between Parkinson’s disease and autoimmune diseases: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0088.

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Gong, Boshen, Fanrui Meng, and Yang Yang. Association Between Gut Microbiota and Autoimmune Thyroid Disease: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0135.

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Räber, Miro E., Dilara Sahin, Ufuk Karakus, and Onur Boyman. A systematic review of interleukin-2-based immunotherapies in clinical trials for cancer and autoimmune diseases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0086.

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Liu, Miao, Hongan Wang, Jing Lu, Zhiyue Zhu, Chaoqun Song, Ye Tian, Xinzhi Chen, et al. Vitamin D supplementation in the treatment of Myasthenia Gravis A protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0129.

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Review question / Objective: The patients should meet the internationally recognized diagnostic criteria for myasthenia gravis and be definitely diagnosed as myasthenia gravis, excluding MG patients caused by congenital, drug and other factors, as well as patients with serious primary diseases, autoimmune diseases or mental diseases. Patients are not restricted by race, region, gender, age, background, course of disease and other factors. We will focus on trials using vitamin D as an intervention at any dose and in any regimen (eg daily/weekly/monthly intake). The control group was routinely given western medicine, including cholinesterase inhibitors, glucocorticoids, immunosuppressants, alone or in combination, or placebo. The intervention group was treated with vitamin D on the basis of western medicine treatment in the control group. The specific dosage form and dose were not limited, and the shortest course of treatment should be 4 weeks. Main outcome measures: (1) Quantitative score of myasthenia gravis (QMG); (2) Recurrence rate; (3) Effective. Secondary outcome measures: (1) The level of serum acetylcholine receptor antibody (AchRab); (2) The levels of inflammatory factors such as IL-6 and IL-10; (3) Clinical absolute score; (4) TCM syndrome score scale; (5) Quality of life score (QOL); (6) Incidence rate of adverse events. All randomized controlled trials (RCT) literatures from the establishment to September 2022 were retrieved and classified.
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Timm, Eliane, Julia Vieregg, and Ursula Wolf. Movement based mindfulness therapies in patients with multiple sclerosis – a systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0102.

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Review question / Objective: The aim is to review the clinical benefits of mindful moving techniques for persons with multiple sclerosis. Condition being studied: Multiple sclerosis. Multiple sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system (Gholamzad et al., 2019; Oh, Vidal-Jordana, & Montalban, 2018). It has shown to be increasing since 2013, and as of 2020 the estimated number of people with MS is 2.8 million worldwide (Walton et al., 2020). Due accumulation of relapses or gradual progression, disability from MS is worsening over time (Cameron & Nilsagard, 2018), which results in common symptoms like pain, imbalance, weakness, motor disorders, fatigue, depression, and more (Cameron & Nilsagard, 2018; Guicciardi et al., 2019).
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Zhang, Yingrong, Sanchun Tan, Jieyu Wang, Yanji Zhang, Mengyuan Huang, Hongjie Xia, Yaxin Hu, Yinyue Rao, and Zhongyu Zhou. A scoping review protocol of systematic reviews and meta-analyses to acupuncture for the treatment of peripheral facial paralysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0084.

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Review question / Objective: To conduct a systematic comprehensive review for Acupuncture treatment of peripheral facial paralysis and to evaluate the efficacy and safety of acupuncture therapy for peripheral facial paralysis. Condition being studied: Peripheral facial paralysis, known as peripheral facial never palsy, includes Bell’s palsy and Ramsay Hunt syndrome.Any medical conditions such as infection, malignancy and autoimmune issues can result it. Idiopathic Bell's palsy is the most common disease causing peripheral facial nerve palsy, which clinical features include unilateral weakness of the facial nerve, hyperacusis, dysgeusia, dry eye or uncontrollable tears, but the etiology of it is unclear. Ramsay Hunt syndrome, less common than Bell’s palsy, is often caused by herpes zoster virus, which clinical features are unilateral weakness of face with ear herpes, tinnitus and dizziness. Facial paralysis patients with ear herpes can be diagnosed with Ramsay Hunt syndrome. Peripheral facial paralysis not only result the dyskinesia of facial muscles but also affect the quality of patient’s life.There are lot of evidence shows that Acupuncture can be used in any period and any kind of peripheral facial paralysis.However, we still lack systematic reviews to assess the efficacy and safety of acupuncture therapy. As a result, we conduct a scoping review of systematic reviews and meta-analyses to address this gap.
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