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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiphospholipid antibody syndrome (APS) is defined by widespread arterial and venous thromboses associated with elevated plasma levels of antiphospholipid antibodies (APLA). The primary antiphospholipid antibody syndrome (PAPS) appear to be a fairly homogeneous disease, and HLA, family and other studies provide new insights into this cause of thrombosis and vascular disease. We describe two patients with PAPS (lupus anticoagulant positive), whose family members were analyzed for clinical and laboratory abnormalities associated with APS. Familial screening seems to be important, in order to prevent the thrombotic events. Low dose aspirin is the first line treatment in asymptomatic subjects with APLA, previous or present thrombosis requiring long-term, possibly life-long anticoagulation.
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PMID:Familial lupus anticoagulant. 1184 63

Vascular disease and atherosclerosis are significant clinical features of systemic lupus erythematosus and antiphospholipid syndrome. Oxidation is one of the major factors responsible for atheroma development in this context. Anticardiolipin antibodies seem to play an important role by inducing nitric oxide and superoxide production, resulting in enhanced levels of plasma peroxynitrite, which is a powerful pro-oxidant substance. Furthermore, direct interference of these antibodies with paraoxonase activity, a high-density lipoprotein-related anti-oxidant enzyme, would contribute to the oxidative stress found in these conditions. The accelerated process of atherogenesis found in these diseases can represent a useful model for the study of atherosclerosis in the general population.
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PMID:Oxidative stress in systemic lupus erythematosus and antiphospholipid syndrome: a gateway to atherosclerosis. 1296 25

Over a 5-year period, we investigated 77 consecutive patients (36 males, 41 females, mean age 40.9 years) referred to our hospital with the diagnosis of CNS vasculitis. Extensive workup including MRI, echocardiography, laboratory tests, angiography ( n=53), and biopsies at appropriate sites ( n=26) was performed based on individual history and symptoms. Prominent symptoms were stroke ( n=61), encephalopathy ( n=14), and headaches ( n=2). Vasculitis was finally diagnosed in 13 patients (17%) including isolated angiitis of the CNS ( n=3), giant cell arteritis ( n=4), and septic arteritis ( n=3). Thirty-two patients (42%) presented noninflammatory vasculopathies including moyamoya ( n=6), Sneddon's syndrome ( n=5), dissection ( n=4), CADASIL ( n=2), and collagen vascular disease ( n=9). Coagulopathy was found in 14 cases (18%) including antiphospholipid syndrome ( n=8) and APC resistance ( n=4). Other causes were cardiogenic embolism ( n=8), multiple sclerosis ( n=5), and migraine stroke ( n=3). Only a minority of patients referred for evaluation of suspected CNS vasculitis actually present with inflammatory vascular disease. Main differential diagnosis includes noninflammatory vasculopathies, coagulopathies, and cardiac disease. Since septic processes may be responsible for the symptoms, "blind" treatment with immunosuppressive agents should be strictly avoided.
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PMID:[Diagnosis and differential cerebral vasculitis diagnosis]. 1477 Feb 79

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by disturbances in innate and adaptive immune mechanisms. Multiple systems and organs may be involved. Tissue damage and dysfunction are mediated by autoantibodies and immune complex formation. The lungs are among the organ systems commonly involved. The pulmonary manifestations usually occur in patients with multisystem disease and include: pleural involvement, parenchymal disease, pulmonary vascular disease and diaphragmatic dysfunction. Manifestations may range from sub-clinical abnormalities to life threatening disorders. Many of the pulmonary manifestations characteristic of SLE are seen in the antiphospholipid syndrome (APS) as well, in both the primary and secondary syndrome. In this review the diverse pulmonary manifestations are described as well as the diagnostic modalities available, including the use of induced sputum evaluation for early diagnosis and follow up. New treatment modalities are referred to.
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PMID:Pulmonary disease in systemic lupus erythematosus and the antiphospholpid syndrome. 1487 52

Stroke in young adults has been related to mechanisms different to those found in older individuals. Cardiogenic embolism, arteritis, atherosclerosis, fibromuscular dysplasia, pregnancy-related angiopathy, migrainous stroke, anaemia, antiphospholipid syndrome, arterial dissection, the consumption of toxic substances and head trauma have been described. We present a young man with a case history of tobacco and cocaine abuse who suffered a mild head trauma, with normal neurological examination, and a computed tomography scan image of a right anterior cerebral infarction. Serum biochemistry showed no alterations according to the diagnosis protocol for stroke in young patients. Various mechanisms have been involved, such as vasospasm, increasing arterial pressure and embolism. Considering the cocaine abuse and the mild head trauma, in our patient vasospasm was thought to be the mechanism involved in the cerebral infarction, which proved a challenge to diagnose in the emergency room.
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PMID:Stroke in young patients: a diagnostic challenge in the emergency room. 1516 83

We report an 80-year-old woman who had rheumatoid arthritis and antiphospholipid syndrome. She was treated for rheumatoid arthritis since her thirties. At 76 years of age, she was diagnosed antiphospholipid syndrome serologically. She felt It. limb weakness and dysarthria and was admitted to the hospital on July 18, 2003. The brain MRI showed T2 hyperintensity signal on the rt. pre-central lobe. She was treated by the argatroban, edaravone, glycerol, and aspirin. However, she became bedridden and fed by NG-tube because her symptoms progressed in spite of the therapy. Progression of stroke stopped by adding heparin at last. After that, she repeated pneumonia. She was found dead on the bed August 2, 2003. The patient was discussed in a CPC. The chief discussant arrived at a conclusion that the cause of infarction was angitis due to rheumatoid arthritis. Other possibilities were multiple thrombus due to antiphospholipid syndrome, amyloid angiopathy, and atherosclerotic infarction. Post-mortem study revealed sputum obstruction in her bronchus, string deposition in her organs. The brain showed infarction on the rt. pre-central lobe. There were multiple thrombus in the leptomeningeal artery, but few atherosclerotic changes of the small arteries. Amyloid didn't deposit in the brain artery and the parenchyma. Pathologist concluded that her infarction was induced with multiple thrombus due to antiphospholipid syndrome.
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PMID:[An 80-year-old woman with progressive stroke, who had rheumatoid arthritis and antiphospholipid syndrome]. 1651 17

Antiphospholipid antibodies are associated with a hypercoagulable state leading to a wide variety of systemic manifestations and obstetric complications. The different pathologic manifestations can be a result of arterial and venous thrombosis, microthrombotic angiopathy, embolization, obstetric disease, and non-thrombotic phenomenon. Presently, the treatment centers on anticoagulation. Two randomized prospective studies in patients with antiphospholipid syndrome with initial thromboembolic event support the target international normalized ratio of 2.0 to 3.0 for the prevention of future thrombotic events. With pregnancy, the combination of aspirin and heparin is still the standard of care. In addition, non-thrombotic features and any associated autoimmune disease may need to be treated. Underlying risk factors precipitating the thromboembolic phenomenon need to be addressed as well.
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PMID:Management of the antiphospholipid syndrome. 1656 70

Chorea is a hyperkinetic movement disorder characterised by excessive spontaneous movements that are irregularly timed, randomly distributed and abrupt. In this article, the authors discuss the causes of chorea, particularly Huntington's disease and the genetic syndromes that may resemble it, including HDL1-3, inherited prion disease, spinocerebellar ataxias 1, 3 and 17, neuroacanthocytosis, dentatorubro-pallidoluysian atrophy (DRPLA), brain iron accumulation disorders, Wilson's disease, benign hereditary chorea, Friedreich's ataxia and mitochondrial disease. Acquired causes of chorea include vascular disease, post-infective autoimmune central nervous system disorders (PANDAS), drugs, systemic lupus erythematosus, antiphospholipid syndrome, thyrotoxicosis, AIDS, chorea gravidarum, and polycythaemia rubra vera. The authors suggest an approach to the clinical assessment of chorea, the value of investigations, including genetic tests (for which they offer a structured framework highlighting the importance of prior counselling), and finally briefly discuss symptomatic drug treatment of chorea.
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PMID:The differential diagnosis of chorea. 1802 76

The issue of atherosclerosis in the antiphospholipid syndrome (APS) is receiving considerable attention within and without the autoimmune setting. Measurement of arterial intima media thickness (IMT) of is an easy and surrogate means of detecting subclinical atherosclerosis. This technique has been applied to patients with systemic lupus erythematosus (SLE) nand primary APS in the attempt to unravel a possible association between antiphospholipid antibodies and premature atherosclerosis. The available data is reviewed in the light of the most recent atherogenic pathways that may differentially account for premature vascular disease in SLE and primary APS.
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PMID:Antiphospholipid antibodies and atherosclerosis: insights from systemic lupus erythematosus and primary antiphospholipid syndrome. 1898 84

Pregnancy and the puerperium have been recognized to increase the risk of stroke, particularly from late pregnancy and through the puerperium. The reported incidences of stroke during pregnancy and the puerperium varied widely, ranging from 5 to 67 per 100,000 deliveries or pregnancies. Important causes of stroke during pregnancy and the puerperium include preeclampsia and eclampsia, cardioembolism, rupture of cerebral vascular anomaly, peripartum or postpartum cerebral angiopathy and cerebral venous thrombosis. Management of patients with pregnancy-related stroke is largely the same as that of nonpregnant patients, with more consideration on maternal and fetal risks. Low-dose aspirin reduces the occurrence of perinatal deaths and preeclampsia in women with historical risk factors for preeclampsia. Anticoagulation during pregnancy is indicated for current arterial or venous thromboembolism, prior venous thromboembolism on long-term anticoagulation, antiphospholipid syndrome with prior venous thromboembolism and patients with a mechanical heart valve. Data from thrombolytic therapy for pregnant women with acute ischemic stroke are limited. It is critical that the risks and benefits of thrombolytic therapy for pregnant women and fetuses are considered cautiously.
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PMID:Management of stroke in pregnancy and the puerperium. 2013 77


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