Relevant bibliographies by topics / Endocardite de Libman-Sacks

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Endocardite de Libman-Sacks'

Author: Grafiati
Published: 10 September 2021
Last updated: 1 February 2022

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Journal articles on the topic "Endocardite de Libman-Sacks"

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Cunha, O. S., A. S. Silva, D. P. D. Bosco, B. M. B. Souza, S. L. E. Ribeiro, and H. L. A. Pereira. "SÍNDROME ANTIFOSFOLÍPIDE PRIMÁRIA E ENDOCARDITE DE LIBMAN SACKS." Revista Brasileira de Reumatologia 57 (2017): S369. http://dx.doi.org/10.1016/j.rbr.2017.07.516.

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Marques, Raul Amorim, Carolina Salim Gonçalves Freitas, Romeo Ceccon, and Sandra Gofinet Pasotto. "Endocardite de Libman-Sacks, anticorpos antifosfolípides e trombose arterial no lúpus ertitematoso sistêmico: relato de caso." Revista Brasileira de Reumatologia 50, no. 6 (December 2010): 716–19. http://dx.doi.org/10.1590/s0482-50042010000600010.

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Wagner, R., A. Cardoso, M. Bandeira, C. F. Pelajo, I. H. R. Grein, and A. C. Dourado. "LÚPUS ERITEMATOSO SISTÊMICO JUVENIL, RELATO DE DIAGNÓSTICO EM CRIANÇA DE DOIS ANOS COM ENDOCARDITE DE LIBMAN‐SACKS." Revista Brasileira de Reumatologia 57 (2017): S326—S327. http://dx.doi.org/10.1016/j.rbr.2017.07.442.

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Ghule, Aishwarya, Shilpa Abhay Gaidhane, Sourya Acharya, Charan Bagga, and Anil Wanjari. "Libman-Sacks Endocarditis Involving Tricuspid Valve in Systemic Lupus Erythematosus - A Case Report." Journal of Evolution of Medical and Dental Sciences 10, no. 16 (April 19, 2021): 1179–81. http://dx.doi.org/10.14260/jemds/2021/251.

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Libman-Sacks endocarditis is non-infectious thrombotic involvement of cardiac valves seen in systemic lupus erythematosus.1,2 Mitral valve followed by aortic valve are involved in systemic lupus erythematosus. However, involvement of tricuspid valve is rare.3 A case of a 36-year-old woman with systemic lupus erythematosus with isolated tricuspid valve endocarditis has been reported here. Within the background of the relevant medical literature, this is a rare event. In systemic lupus erythematosus (SLE) patients, mostly the aortic and mitral valves are affected.4 Echo shows evidence of vegetation in tip and septa of tricuspid valve which is suggestive of Libman-Sacks endocarditis. In our case we have discussed Libman-Sacks endocarditis involving tricuspid valve.
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Roldan, Carlos A., Wilmer L. Sibbitt, Ernest R. Greene, Clifford R. Qualls, and Rex E. Jung. "Libman-Sacks endocarditis and associated cerebrovascular disease: The role of medical therapy." PLOS ONE 16, no. 2 (February 16, 2021): e0247052. http://dx.doi.org/10.1371/journal.pone.0247052.

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Background Libman-Sacks endocarditis in patients with systemic lupus erythematosus (SLE) is commonly complicated with embolic cerebrovascular disease (CVD) or valve dysfunction for which high-risk valve surgery is frequently performed. However, the role of medical therapy alone for Libman-Sacks endocarditis and associated acute CVD remains undefined. Objective To determine in this cross-sectional and longitudinal study if conventional anti-inflammatory and anti-thrombotic therapy may be an effective therapy in SLE patients with Libman-Sacks endocarditis and associated acute CVD. Methods and materials 17 SLE patients with Libman-Sacks endocarditis detected by two-and-three-dimensional transesophageal echocardiography (TEE) and complicated with acute CVD [stroke/TIA, focal brain injury on MRI, or cognitive dysfunction] were treated with conventional anti-inflammatory and anti-thrombotic therapy for a median of 6 months and then underwent repeat TEE, transcranial Doppler, brain MRI, and neurocognitive testing for re-assessment of Libman-Sacks endocarditis and CVD. Results Valve vegetations decreased in number, diameter, and area (all p ≤0.01); associated valve regurgitation significantly improved (p = 0.04), and valve thickening did not progress (p = 0.56). In 13 (76%) patients, valve vegetations or valve regurgitation resolved or improved in number and size or by ≥1 degree, respectively, as compared to 4 (24%) patients in whom vegetations or valve regurgitation persisted unchanged or increased in size or by ≥1 degree (p = 0.03). Also, cerebromicroembolism, lobar and global gray and white matter cerebral perfusion, ischemic brain lesion load, and neurocognitive dysfunction resolved or significantly improved (all p ≤0.04). Conclusion These preliminary data suggest that combined conventional anti-inflammatory and antithrombotic therapy may be an effective treatment for Libman-Sacks endocarditis and its associated CVD and may obviate the need for high-risk valve surgery.
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Sharma, Jayendra, Zoran Lasic, Abraham Bornstein, Rubin Cooper, and Jonathan Chen. "Libman–Sacks endocarditis as the first manifestation of systemic lupus erythematosus in an adolescent, with a review of the literature." Cardiology in the Young 23, no. 1 (July 18, 2012): 1–6. http://dx.doi.org/10.1017/s1047951112001023.

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AbstractLibman–Sacks endocarditis is rare in children and adolescents, more so as a first manifestation of systemic lupus erythematosus. Currently, sterile verrucous lesions of Libman–Sacks endocarditis are recognised as a cardiac manifestation of both systemic lupus erythematosus and antiphospholipid syndrome. They are clinically silent in a majority of the cases. The presence of antiphospholipid antibodies in systemic lupus erythematosus is associated with three times higher prevalence of mitral valve nodules and significant mitral regurgitation. We present the case of isolated mitral regurgitation with abnormal looking mitral valve, detected in early childhood, which deteriorated to a severe degree in the next decade and was diagnosed as Libman–Sacks endocarditis after surgical repair from histopathology. The full-blown clinical spectrum of systemic lupus erythematosus with antiphospholipid antibodies was observed several weeks after cardiac surgery. We discuss the atypical course of Libman–Sacks endocarditis with follow-up for 10 years, along with a review of the literature.
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Saldarriaga, Carolina, Ana G. Múnera, and Mauricio Duque. "Endocarditis de Libman-Sacks." Revista Colombiana de Cardiología 22, no. 3 (May 2015): 144–48. http://dx.doi.org/10.1016/j.rccar.2015.03.010.

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8

Porubčinová, Ingrid, Michal Hulman, and Jana Jevčáková. "Libman-Sacks endocarditis versus infectious endocarditis." Cor et Vasa 48, no. 7-8 (July 1, 2006): 281–84. http://dx.doi.org/10.33678/cor.2006.087.

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Azeem, Amir, Myrna E. Alexander-Nickens, Vikas Majithia, and Michael Hall. "IS IT LIBMAN-SACKS ENDOCARDITIS?" Journal of the American College of Cardiology 67, no. 13 (April 2016): 1193. http://dx.doi.org/10.1016/s0735-1097(16)31194-9.

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Mraz-Gernhard, Serena M., Thomas M. Bush, and Jerome B. Riebman. "Clinical images: Libman-Sacks endocarditis." Arthritis & Rheumatism 44, no. 9 (2001): 2111. http://dx.doi.org/10.1002/1529-0131(200109)44:9<2111::aid-art362>3.0.co;2-n.

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Dissertations / Theses on the topic "Endocardite de Libman-Sacks"

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Portecop, Patrick. "Endocardite de Libman-Sacks, à propos d'un cas." Bordeaux 2, 1998. http://www.theses.fr/1998BOR2M023.

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Bourges, Monique. "Endocardites de Libman-Sacks : à propos d'un cas - revue de la littérature." Bordeaux 2, 1992. http://www.theses.fr/1992BOR2M114.

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ABOULKER, NAHON DANIELE. "L'endocardite de libman sacks au cours du lupus erythemateux dissemine ; a propos d'une observation." Amiens, 1990. http://www.theses.fr/1990AMIEM096.

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4

Schrader, Lauran N. "Does ANA-positive SLE human serum promote development of Libman-Sacks endocarditis in the NP-SLE Lewis rat model?" Muncie, IN : Ball State University, 2009. http://cardinalscholar.bsu.edu/675.

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Ferreira, Alexandra Cristina Joaquim. "Acidente vascular cerebral associado a endocardite de Libman-Sacks no contexto de sindrome antifosfolipídico e lúpus eritematoso sistémico." Master's thesis, 2016. http://hdl.handle.net/10451/25865.

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Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2016
A Endocardite de Libman-Sacks refere-se a um espetro de lesões valvulares caracterizada pela presença de vegetações nas válvulas cardíacas não secundária à ação de agentes infeciosos. É uma patologia incomum que se associa a doenças como Síndrome Antifosfolipídico ou Lúpus Eritematoso Sistémico. A válvula mitral é a mais frequentemente afetada e estima-se que estas lesões sejam um forte fator de risco independente para AVC/AIT. Neste trabalho apresenta-se o caso clínico de uma doente com 24 anos com diagnóstico prévio de Síndrome Antifosfolipídico no contexto de dois AVCs isquémicos, que recorre ao serviço de urgência por um quadro de afasia não fluente. A investigação subsequente levou ao diagnostico de AVC isquémico e demonstrou a presença de uma massa no folheto posterior da válvula mitral compatível com Endocardite de Libman-Sacks. Pretende-se neste contexto, rever e resumir informação recente relacionada com esta patologia.
Libman-Sacks endocarditis refers to valvular lesions characterized by the presence of vegetations on heart valves without an infectious agent. It is uncommon, and is associated with diseases such as antiphospholipid syndrome or systemic lupus erythematosus. The mitral valve is the most frequently affected and it is estimated that these injuries are a strong independent risk factor for stroke/TIA. This paper presents the case of a female patient with 24 years old, previously diagnosed with antiphospholipid syndrome in the context of two ischemic strokes, who goes to the emergency department with non-fluent aphasia. The subsequent investigation led to the diagnosis of ischemic stroke and demonstrated the presence of a mass in the posterior leaflet of the mitral valve compatible with Libman-Sacks endocarditis. In this context, this work pretends to review and summarize recent information about this disease.
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Books on the topic "Endocardite de Libman-Sacks"

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Turc, Guillaume, David Calvet, and Jean-Louis Mas. Cardiac aetiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0005.

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Cardiac aetiology accounts for approximately 20% of strokes in young adults. Although atrial fibrillation is a leading cause of stroke in the general population, it is uncommon in young adults. In such patients, more diverse causes of ischaemic stroke are observed, including valvular heart diseases, infective endocarditis, Libman–Sacks endocarditis, dilated cardiomyopathies, congenital heart diseases, myocardial infarction, and intracardiac tumours. Patent foramen ovale is commonly observed in young adults with ischaemic stroke, but this association may be incidental in a sizeable proportion of patients. Young adults who are the most likely to have a stroke-related patent foramen ovale are also those with the lowest recurrence risk.
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Book chapters on the topic "Endocardite de Libman-Sacks"

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Melzer, Mark. "Pyrexia of Unknown Origin (PUO)." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0033.

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Petersdorf and Beeson defined pyrexia of unknown origin (PUO) in 1961. It is defined as an illness more than three weeks’ duration, with a fever > 38.3°C on several occasions and failure to reach a diagnosis after one week of in-patient investigation. Additional categories have now been added. These include: ● Nosocomial PUO in hospital patients: This is defined as fever of 38.3°C on several occasions caused by a process not present or incubating on admission, where initial cultures are negative and diagnosis remains unknown after three days of investigations. Fever is often related to hospital factors such as surgery, use of biomedical devices (e.g. intravascular devices/urinary catheters), C. difficile infection, and decubitus ulcers related to immobilization. ● HIV- associated PUO: This is defined as fever (as in Nosocomial PUO) for four weeks as an outpatient or three days as an in- patient. The commonest causes of fever are typical and atypical mycobacterial infections, cryptococcosis, and Cytomegalovirus (CMV). Lymphoma may cause fever in up to 25% of cases. ● Neutropenic PUO: This includes patients with a fever (as in Nosocomial PUO) with neutrophils < 1.0 x 109/L, with initial negative cultures and an uncertain diagnosis after three days. Bacterial infection is the commonest cause and should be treated empirically. The causes of a PUO can be categorized as infection (30–40%), neoplasia (20–30%), collagen-vascular and autoimmune diseases (10–20%), and miscellaneous (10–20%). The commonest causes of localized bacterial infections causing PUO are infective endocarditis, intra- abdominal or pelvic infections, oral cavity infections, osteomyelitis, and infected peripheral vessels. These conditions include: ● Infective endocarditis (IE): ■ Organisms associated with indolent onset (e.g. Streptococcus viridans, Enterococcus species, coagulase- negative staphylococci). ■ HACEK organisms (e.g. Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella). ■ Culture-negative endocarditis (e.g. Chlamydia, Coxiella, or Bartonella). ■ Non- infective endocarditis: ● Marantic endocarditis, associated with malignancy. ● Libman Sacks endocarditis, associated with systemic lupus erythematosus (SLE). ● Intra-abdominal infections. ■ Abscesses: ● Hepatic (GI tract or biliary in origin). ● Splenic (associated with IE). ● Sub-phrenic (associated with previous surgery). ● Pancreatic (post-pancreatitis).
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Conference papers on the topic "Endocardite de Libman-Sacks"

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CARDOSO, CAIO RUSTICHELLI, JUAREZ ROBERTO DE OLIVEIRA VASCONCELOS, ARTHUR CARVALHO DE MACEDO, ARNOLD JASON BENAVIDES PENA, and GELVANA FLAVIO BARRETO REIS. "LIBMAN-SACKS ENDOCARDITIS AND ALVEOLAR HEMORRHAGE IN SYSTEMIC LUPUS ERYTEMATOSUS: A CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-154.

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Cassol Silva, Olga, Gladys Lentz Martins, and Alessandra Laitart. "ISCHEMIC STROKE AS THE INITIAL MANIFESTATION OF ANTIPHOSPHOLIPID SYNDROME ASSOCIATED WITH LIBMAN SACKS ENDOCARDITIS." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17340.

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