Multiple aortic aneurysms complicated by a rupture in the systemic lupus erythematosus: A case report

Sato, Junichiro; Kawakami, Tomohiro; Nakabayashi, Kimimasa; Fukuoka, Kazuhito; Hirano, Kazuhiko; Terado, Yuichi; Yokoyama, Kenichi; Ohtsuka, Takako; Ohkura, Yasuo; Fujioka, Yasunori; Kurata, Atsushi

doi:10.1016/j.prp.2008.05.009

Cited by 17 publications

(16 citation statements)

References 23 publications

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“…Several case reports with pathology, in persons of any age, describe aPL syndrome associated with widespread (multi-organ) microvascular thrombotic injury, and in the brain specifically, with brain infarcts or hemorrhages, and no evidence for inflammation. 6,9,21,22 Few case series are available, almost all with less than 10 subjects with aPL and brain pathology data available. These series describe thrombo-occlusive disease in the brain, small but also some large infarcts, and no inflammation or vasculitis.…”

Section: Discussionmentioning

confidence: 99%

Relation of Antiphospholipid Antibodies to Postmortem Brain Infarcts in Older People

et al. 2015

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Background-There are few data on the relationship of antiphospholipid antibodies (aPLs) to pathologically proven brain infarcts. We tested the hypothesis that aPLs are associated with a higher odds of brain infarcts among older, communitydwelling individuals who came to autopsy. Methods and Results-Specimens and clinical and pathological data were derived from 607 deceased subjects (mean age at death, 89 years; 66% women) who were participating in 1 of 2 cohort studies of aging (Rush Memory and Aging Project and Religious Orders Study) and had agreed to brain autopsy. Brain infarcts were identified on gross and microscopic examinations, and severity of cerebral vessel disease (atherosclerosis, arteriolosclerosis) was graded. Four clinically used aPLs were measured longitudinally: 3 in serum (anticardiolipin antibodies, β 2-glycoprotein I, and anti-phosphatidylserine) and 1 in plasma (lupus anticoagulant). A quarter of subjects (142 of 607, 23%) had at least 1 aPL present at baseline (median time interval from baseline to death, 4.6 years), and three quarters of these subjects had persistently positive measures over time. In a logistic regression analysis, baseline aPL positivity did not increase the odds of brain infarcts (odds ratio=1.08; 95% confidence interval, 0.74-1.58; P=0.19) or of gross or microscopic infarcts separately. Findings were essentially unchanged when considering number of baseline aPLs, aPLs proximate to death, and persistence of aPLs. Associations did not differ among subjects with increased severity of vessel disease. Conclusion-Overall, we did not find evidence that aPLs increase the odds of pathological brain infarcts in older people. (Circulation. 2015;131:182-189.

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Section: Discussionmentioning

confidence: 99%

Relation of Antiphospholipid Antibodies to Postmortem Brain Infarcts in Older People

et al. 2015

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“…Transforming growth factor-â and CD56 were both detcted in the atherosclerosis area and in the CMN lesion without atheromatous deposit in the aortic aneurysms, respectively. There were more transforming growth factor-â-positive cells in the atherosclerostic region, while rarely were the cells seen in the CMN [46]. SUMMARY CMN may develop in the aortic tissues of patients with various aortopathies, such as Marfan's syndrome, aortic aneurysm, aortic dissection, atheroslerotic disease, congenital heart disease and even healthy individuals.…”

Section: Molecular Findingsmentioning

confidence: 99%

“…the development of CMN by heralding connective tissue defects [44], as in the patient with acromegaly [45], or with systemic lupus erythematosus [46], or in drug addict [47]. Growth hormone excess can be associated with excess mucopolysaccharide deposition characteristic by both CMN and extensive myxomatous degeneration, which even invading all four cardiac valves [44].…”

Section: Fig 5 -Histology Of the Ascending Aorta Of A 59-year-old Mamentioning

confidence: 99%

Cystic medial necrosis: pathological findings and clinical implications

Yuan¹,

Hua²

2011

Rev Bras Cir Cardiovasc

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Artigo recebido em 1 de novembro de 2010 Artigo aprovado em 11 de janeiro de 2011 ResumoA necrose cística da média (NCM) é uma desordem das grandes artérias, em particular a aorta, caracterizada por acúmulo de substância basofílica na camada média com lesões císticas-símile. É sabido que a NCM ocorre em certas doenças do tecido conjuntivo tal como síndrome de Marfan, síndrome de Ehlers-Danlos, e ectasia ânulo-aórtica, que normalmente resulta de mudanças degenerativas na parede aórtica. A relação entre NCM e defeitos congênitos do coração, assim como outras desordens, tem sido evidenciada. Os mecanismos são ainda controversos, embora muitos estudos moleculares tenham sido conduzidos. O objetivo do presente artigo é fornecer uma visão geral da NCM em termos de características patológicas, implicações clínicas e etiologia baseada em resultados de pesquisa molecular. Descritores

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“…Thus, other factors in addition to atherosclerosis are presumed to contribute to aneurysm formation in SLE patients. Several lines of accumulating evidence suggest that mucoid degeneration, vasculitic damage, hypertension, atherosclerosis, and steroid treatment are associated with aneurysm formation in SLE patients (10). Long-term steroid therapy leads to connective tissue weakness by suppressing the formation of granulation tissue and chondroitin sulfate, eventually leading to aneurysm formation (10,11,18).…”

Section: A B Cmentioning

confidence: 99%

“…TGF-β is crucially involved in extracellular matrix production. In SLE patients, TGF-β production is impaired because of dysfunctional NK cells (10). Thus, an immunological disorder is presumed to contribute to aneurysm formation in SLE patients.…”

Section: A B Cmentioning

confidence: 99%

Aortic Aneurysm with Severe Aortic Regurgitation in a Patient with Systemic Lupus Erythematosus

et al. 2010

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A 37-year-old man was admitted to our hospital for precordial chest pain. He had taken prednisolone (5 mg/day) for systemic lupus erythematosus (SLE) and had been symptom free for the past 12 years. Echocardiography and contrast-enhanced CT of chest showed an enlarged ascending aortic aneurysm, which is rarely seen in SLE. Severe aortic regurgitation was also present, and surgical replacement of the ascending aorta and aortic valve was successfully accomplished by the Bentall procedure. Medial cystic necrosis in the ascending aorta, which is rarely seen in SLE angiopathy, was confirmed by histology. There were no significant histopathological findings in the aortic valve.

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Multiple aortic aneurysms complicated by a rupture in the systemic lupus erythematosus: A case report

Cited by 17 publications

References 23 publications

Relation of Antiphospholipid Antibodies to Postmortem Brain Infarcts in Older People

Relation of Antiphospholipid Antibodies to Postmortem Brain Infarcts in Older People

Cystic medial necrosis: pathological findings and clinical implications

Aortic Aneurysm with Severe Aortic Regurgitation in a Patient with Systemic Lupus Erythematosus

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