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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary artery aneurysms are uncommon and the prevalence in patients undergoing coronary artery angiography is 1.5-4.9%. The most common cause of coronary artery aneurysm is arteriosclerosis, followed by Kawasaki disease, periarteritis nodosa, systemic lupus erythematosus, syphilis, rheumatic fever, congenital heart disease and trauma. Most coronary aneurysms remain asymptomatic. Patients may present symptoms of angina or myocardial infarction due to thrombosis within the aneurysm. This would lead to occlusion of the coronary artery or to distal thromboembolisms. There is no consensus on how to manage coronary artery aneurysms. Medical therapies include aspirin as well as warfarin. Surgery may be performed in patients with a large aneurysm, i.e. when the risk of rupture or thrombosis is high. We present a 60-year-old female patient with symptoms of a transient ischaemic attack followed by a period of fever, nausea, vomiting and ecchymoses on the lower extremity. Transthoracic and transoesophageal echocardiography was suggestive of a tumour located at the basis of the lateral wall of the right atrium. Heart surgery revealed, however, a large right coronary aneurysm and an atrial septum defect of the secundum type.
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PMID:[A 60-year-old woman with asthenia and dyspnoea]. 1576 62

Thirty-seven patients with systemic lupus erythematosus underwent complete clinical and laboratory evaluations, including antiphospholipid antibodies and lupus anticoagulant, magnetic resonance imaging of the brain, and transesophageal echocardiography. Cerebrovascular disease manifested as stroke, transient ischemic attack, or cerebral infarcts in patients with nonfocal neurologic deficits was detected in 19 patients (51%), and significant left-sided valvular heart disease in 25 (68%). Valve vegetations, valve thickening, valve regurgitation, and lupus anticoagulant antibody occurred 2 to 3 times more often in patients with than without cerebrovascular disease (all p < or =0.04) and were the only independent predictors of cerebrovascular disease (odd ratios 5.3 to 10.6, all p < or =0.03). Thus, valvular heart disease probably exacerbated by hypercoagulability appears to be a source of embolic ischemic brain injury and cerebrovascular disease.
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PMID:Valvular heart disease as a cause of cerebrovascular disease in patients with systemic lupus erythematosus. 1595 May 67

The study was undertaken to determine a possible association of retinal vascular lesion in systemic lupus erythematosus (SLE) with the antiphospholipid syndrome (APS). A hundred and ninety-four patients (160 females and 34 males, whose mean age was 30.7+/-8.9 years) with verified SLE were examined. Group I comprised 67 patients with retinal vascular lesions (Subgroup la (n = 13) with retinal vascular occlusions and Subgroup 1b (n = 54) without occlusions). Group 2 included 127 patients without retinal vascular lesions. APS was detected in 86 patients. Retinal vascular occlusions more frequently occurred in patients with APS (13.9%) than in those without APS (0.9%) (p = 0.0009) and more frequently in patients with APS and thrombocytopenia (24.3%) than in those with APS without thrombocytopenia (6.1%) (p = 0.0359). Extraocular thromboses were more frequently encountered in Subgroup 1a (69.2%) than in Subgroup 1b (33.3%) (p = 0.0399) and in Group 2 (22.8%), (p = 0.0010). Cerebral circulatory disorder (CCD) was observed in 30.7% in Subgroup la, in 14.8% in Subgroup 1b, and in 7.9% in Group 2 (p = 0.0268). Transient ischemic attack (TIA) occurred in 46.2% in Subgroup la, in 24.1% in Subgroup 2a, and in 14.9% in Group 2 (p = 0.0129). Thrombocytopenia was identified in 69.2% in Subgroup 1a, in 22.2% in Subgroup 2a (p = 0.0021), and in 12.6% in Group 2 (p < 0.0000). The frequency of elevated IgG of anticadiolipin (aCL) in Subgroup 1a (80%) exceeded that in Subgroup 1b (37.9%) (p = 0.0309) and Group 2 (30.7%) (p = 0.0096). Another isotype of aCL (IgM 80%) was observed in patients with retinal vascular occlusions, but the differences in this index were insignificant in the groups and subgroups. The association of pathological changes in retinal vessels in the presence of lupus anticoagulant (LA) was particularly noticeable (91.7 and 52% in Subgroup la and Subgroup 1b, respectively (p = 0.0191) and 47.1% in Group 2 (p = 0.0088). There was an association of amaurosis fugax with eyeground occlusions (p < 0.004), CCD and TIA (p < 0.0002), APS (p < 0.0003), and essential hypertension (p < 0.05). Thus, occlusive lesions in the fundus of the eye are a common manifestation of thrombogenesis in SLE in the presence of APS. The frequency of concomitance of retinal vascular occlusions with cerebral circulatory disorders should be referred to as severe manifestations of SLE. Amaurosis fugas is a manifestation of retinal vascular lesion and associated with the presence of APS and elevated blood pressure in patients with SLE. There is an association of an occlusive process in the fundus of the eye with different symptoms of APS and primarily with IgG of aCL, LA, and thrombocytopenia.
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PMID:[Retinal vascular lesions in systemic lupus erythematosus and secondary antiphospholipid syndrome]. 1627 63

Antiphospholipid syndrome is characterized by arterial or venous thrombosis, and the presence of antiphospholipid antibodies (aPL). APL are considered to be a cause of an acquired hypercoagulable state leading to stroke and transient ischemic attack (TIA). We examined the causes in 50 young patients with ischemic stroke. The most prevalent cause was atherosclerosis and the incidence of APS was 12.5%. APL comprise a heterogeneous group of autoantibodies, such as beta2-glycoprotein I dependent anticardiolipin antibody (beta2-GPIaCL), lupus anticoagulant (LA), and other antiphospholid-protein antibodies. We examined the incidence and the pathogenic role of antiphospholipid protein antibodies. The subjects comprised 250 patients (155 male, 95 females) with ischemic stroke, aged 26 to 92 years (mean 72 years). We measured beta2-GPI aCL, IgG aCL, LA, phosphatidyserine dependent antiprothrtombin antibody (PS-PT), antiphosphatidyl-serine antibody (PS), antiphosphatidyl-inositol antibody (PI) in each patient. The incidence of beta2-GPI aCL, IgG aCL, LA, phosphatidyserine, PS-PT, PS, and PI was 2.8%, 12%, 9.2%, 7.2%, 9.6%, and 8.8%, respectively. The incidence of young stroke patients under 50 years was 5.2%. Among 13 young stroke patients, 5 had SLE. Among 23 patients with LA., 18 (78%) patients had PS-PT. Anti-PS-PT antibody is closely related to LA. Antinuclear antibody was detected in 79% of the patients with aPS and/or aPI. We compared the carotid ultrasonographic findings in positive aPI or aPS patients with those in negative ones. Increased IMT, plaque score and carotid stenosis were more common in aPI and aPS-positive patients than in negative ones Three of 5 patients who showed positive beta2-GPI, aCL and LA, simulataneously, had sysyemic lupus erythematosus as an immulological background. Two of 3 patients with PI and/or PS and beta2-GPI and/or LA were patients with SLE. Antiphospholipid antibody was considered to be a risk factor of stroke, especially in SLE and/or young female patients. The incidence of lupus anticoagulant is more common than beta2-GPI aCL in ischemic stroke. In SLE patients with stroke, multi-antiphospholipid-protein antibodies was inclined to be present. LA is closely related to ant-PS-PT and aPI and aPS are associated with anti-nuclear antibody and precipitation of atherosclerosis.
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PMID:[Antiphospholipid syndrome and stroke]. 1644 44

A 39-years-old woman was admitted to our hospital with musculoskeletal complaints (myalgias and symmetric arthralgias in proximal interphalangeal, metacarpophalangeal joints of the hands and in knees), systemic symptoms like fever, fatigue, malaise and a six months previous history of a transient ischemic attack. The presence of antibodies to double-stranded deoxyribonucleic-acid (DNA) and antiphospholipid antibodies led to the diagnosis of systemic lupus erythematosus with secondary antiphospholipid syndrome. Cerebral infarction develops significantly more often in patients with lupus and antiphospholipid antibodies, but other clinical syndromes are associated with lupus anticoagulant: cognitive dysfunction, seizures, polyneuropathy, aseptic meningitis, myelopathy.
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PMID:[Systemic lupus erythematosus with neurologic onset and secondary antiphospholipid syndrome. A Case Study]. 1660 81

The importance of cerebral disease in patients with the Hughes syndrome is now becoming more widely recognized. The range of neuropsychiatric manifestations of APS is comprehensive, and includes focal symptoms attributable to lesions in a specific area of the brain as well as diffuse or global dysfunction. Patients with APS frequently present with strokes and TIA, but a wide spectrum of other neurologic features-also including non thrombotic neurologic syndromes-has been described in association with the presence of aPL. The recognition of APS has had a profound impact on the understanding and management of the treatment of CNS manifestations associated with connective tissue diseases, in particular, SLE. Many patients with focal neurologic manifestations and aPL, who a few years ago would have received high-dose corticosteroids or immunosuppression, are often successfully treated with anticoagulation. In our opinion, testing for aPL may have a major diagnostic and therapeutic impact not only in patients with autoimmune diseases and neuropsychiatric manifestations, but also in young individuals who develop cerebral ischemia, in those with atypical multiple sclerosis, transverse myelitis, and atypical seizures. We would also recommend testing for aPL for young individuals found with multiple hyperintensity lesions on brain MRI in the absence of other possible causes,especially when under the age of 40 years. It is our practice to anticoagulate patients with aPL suffering from cerebral ischemia with a target INR of 3.0 to prevent recurrences. Low-dose aspirin alone (with occasional exceptions)does not seem helpful to prevent recurrent thrombosis in these patients. Our recommendation, once the patient has had a proven thrombosis associated with aPL, is long-term (possibly life-long) warfarin therapy. Oral anti coagulation carries a risk of hemorrhage, but in our experience the risk of serious bleeding in patients with APS and previous thrombosis treated with oral anticoagulation to a target INR of 3.5 was similar to that in groups of patients treated with lower target ratios. Although a double-blind crossover trial comparing low molecular weight heparin with placebo in patients with aPL and chronic headaches did not show a significant difference in the beneficial effect of low molecular weight heparin versus placebo, in our experience selected patients with aPL and neuropsychiatric manifestations such as seizures, severe cognitive dys-function, and intractable headaches unresponsive to conventional treatment may respond to anticoagulant treatment. The neurologic ramifications of Hughes syndrome are extensive, and it behoves clinicians in all specialties to be aware of this syndrome because treatment with anticoagulation may profoundly change the outlook for these patients.
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PMID:Cerebral manifestations in the antiphospholipid (Hughes) syndrome. 1688 79

A 46-year-old white male diagnosed with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) was seen for audiological testing 15 minutes following a sudden onset hearing loss in the right ear. The test battery included pure-tone audiometry, word-recognition testing, speech-recognition threshold (SRT) testing, immittance testing, and distortion-product otoacoustic emissions (DPOAE) testing. Testing revealed a sensorineural hearing loss in the right ear. Shortly after testing, the patient indicated that his condition had improved. Testing was repeated, and the second round of tests revealed normal hearing in both ears. Four days later, a follow-up test again indicated normal hearing in both ears. Possible connections of this brief occurrence of idiopathic hearing loss with the patient's medical conditions are discussed. Specifically, symptoms were consistent with a transient ischemic attack (TIA) affecting his right cochlea in the stria vascularis region, resulting in a temporary, sensorineural hearing loss. No residual effects were observed clinically.
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PMID:Spontaneous recovery of sudden sensorineural hearing loss: possible association with autoimmune disorders. 1692 14

The objective of this study was to analyse whether primary antiphospholipid syndrome (PAPS) may precede and modify the characteristics of systemic lupus erythematosus (SLE). Out of the total 362 SLE patients in our service, 223 patients had antiphospholipid antibodies (aPL), of whom 110 met the criteria of antiphospholipid syndrome. In 26 cases (7.2%) PAPS appeared 5.5 years before the onset of lupus (PAPS+SLE Group). Their clinical findings were compared to lupus patients without (SLE only Group, n = 26) and with secondary APS (SLE+SAPS Group, n = 26). The prevalence of deep venous thrombosis, stroke/TIA, recurrent fetal loss, coronary heart disease and myocardial infarction was significantly higher in PAPS+SLE Group as compared to SLE only Group. The difference in prevalence of fetal loss (P = 0.014) between PAPS+SLE and SLE+SAPS Groups was also recorded. On comparison to PAPS+SLE Group, patients without APS (SLE only Group) were younger at onset of lupus, with more frequent flares and a higher prevalence of WHO type III/IV nephritis (P = 0.007), requiring higher doses of cyclophosphamide and corticosteroids. Lupus started in the form of PAPS in 7.2% of our SLE patients, who presented with more thrombotic and less inflammatory complications than in SLE patients without a prior or with a following secondary APS. Considering the long latency between the two diseases, PAPS may be a forerunner of lupus, but it may also coexist with SLE as an independent autoimmune disorder.
Lupus 2007
PMID:Primary antiphospholipid syndrome as the forerunner of systemic lupus erythematosus. 1757 33

Thrombophilia-hypofibrinolysis may play an important role in rare premature (< or = age 45 years) arterial occlusive events in atherothrombotic cardiovascular (ATCVD) disease, particularly in normolipidemic patients. Whether thrombophilia-hypofibrinolysis contributed to ATCVD < or = age 45 years was assessed in 78 men and 40 women with 230 ATCVD events (myocardial infarction (MI) [n = 60], coronary artery bypass graft [CABG, n = 33], angioplasty [n = 52], chronic angina [n = 41], ischemic stroke [n = 11], transient ischemic attack [TIA, n = 24], claudication [n = 9]). Cases were compared with healthy normal adult controls (44 men and 76 women). In men, the Factor V Leiden mutation was present in 6/63 (10%) cases versus 0/44 (0%) controls (P = 0.042), Factor VIII was high (>150%) in 16/60 (27%) cases versus 1/42 (2%) controls (P = 0.001), Factor XI was high (>150%) in 9/57 (16%) cases versus 0/42 (0%) controls (P = 0.009), and plasminogen activator inhibitor activity (PAI-Fx) was high (>21.1 U/mL) in 15/63 (24%) cases versus 3/43 (7%) controls (P = 0.023). In women, protein C was low (<73%) in 4/26 (15%) cases versus 0/74 (0%) controls (P = 0.004), and free protein S was low (<66%) in 5/27 (19%) cases versus 2/74 (3%) controls (P = 0.014). In women, Factor XI was high (>150%) in 3/27 (11%) cases versus 1/74 (1%) controls (P = 0.057), and the lupus anticoagulant was present in 9/32 (28%) cases versus 2/51 (4%) controls (P = 0.002). In patients with ATCVD < or = age 45 years, thrombophilias (Factor V Leiden, Factor VIII, Factor XI, protein C and S deficiency, lupus anticoagulant) and hypofibrinolysis (PAI-Fx, Lp[a]) may promote arterial thrombosis, which is synergistic with atherosclerotic endothelial injury.
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PMID:Thrombophilia-hypofibrinolysis and atherothrombotic cardiovascular disease < or = age 45 years. 1765 28

The ocular manifestations are described in autoimmune disease, being most common associated with systemic lupus erythematosus, scleroderma, rheumatoid arthritis, insulin-dependent diabetes mellitus, and dermatomyositis. Nonetheless, the antiphospholipid syndrome is a relatively newly recognized autoimmune disorder. Ocular conditions in which to consider antiphospholipid syndrome include amaurosis fugax, transient ischemic attack, retinal haemorrhages and cotton wool spots, central retinal vein and artery occlusion, anterior ischemic optic neuropathy, ophthalmic and cilioretinal artery occlusions. Ocular features due to antiphospholipid antibodies - induced thrombosis should be treated with anticoagulant drugs. In opposition, for the treatment of ocular features due to immunological mechanisms such as vasculitis, immunosuppressants seem to be more suitable. The aim of this article is to underline the mainly ocular features of Hughes' syndrome and for the most part attention should be paid to the patients with central retinal vascular occlusion with no cause but most likely caused by lupus anticoagulant.
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PMID:Ocular manifestations of antiphospholipid (Hughes)' syndrome--minor features? 1806 49


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