Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with a documented diagnosis of polyarteritis nodosa and laboratory evidence of a circulating lupus anticoagulant is described. Additional clinical features suggestive of the antiphospholipid antibody syndrome were found. The patient underwent amputation of the first two digits of the foot due to ischemic necrosis. Steroid and immunosuppressive treatment resulted in clinical improvement and disappearance of the circulating anticoagulant, without necessitating additional treatment with oral anticoagulants. The presence of the lupus anticoagulant might have worsened the vascular damage done by polyarteritis nodosa in this patient.
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PMID:Association of lupus anticoagulant with polyarteritis nodosa: report of a case. 170 11

The antiphospholipid syndrome was diagnosed in 19 of 1078 patients treated between 1987 and 1991. All patients with antiphospholipid syndrome had either anticardiolipin antibody (16/19) or lupus anticoagulant (10/19); three patients had thrombocytopenia, eight patients had a prolonged partial thromboplastin time, and 10 patients had an elevated erythrocyte sedimentation rate. The most common site of involvement was the cerebral circulation (nine patients), manifested by transient ischemic attacks or stroke. Eight patients had upper extremity disease, characterized by symptoms of Raynaud's phenomenon, with angiographic lesions involving the brachial, radial, ulnar, and/or digital arteries. Lower extremity disease occurred in seven patients, with clinical presentations similar to those of atherosclerosis and varying angiographic patterns. In comparison with the population having atherosclerosis, patients with arterial manifestations of antiphospholipid syndrome were more likely to be women (13 of 19 versus 411 of 1078, p less than 0.02), were significantly younger (46.2 years versus 63.6 years, p less than 0.0001), did not smoke (1 of 19 patients versus 700 of 1078, p less than 0.0001), had a higher percentage of upper extremity involvement (8 of 18 versus 13 of 1078, p less than 0.0001), and had a higher incidence of early graft failure (9 of 12 grafts versus 13 of 371 grafts, p less than 0.0001). The syndrome is associated with the repetitive failure of vascular reconstructions and occlusion of native vessels. Antiphospholipid syndrome should therefore be suspected in young, female, nonsmokers with vascular disease, especially those with involvement of the upper extremity, cerebrovascular disease with normal findings on extracranial carotid angiography, and premature graft failure.
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PMID:Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis. 172 74

Lupus anticoagulant (LA) and anticardiolipin antibodies (ACA) have been associated with thrombotic events and recurrent fetal loss. In order to assess the role of LA with the thrombotic tendency in various disease states we evaluated 38 patients with confirmed LA [tissue thromboplastin index (TTI) greater than 1.3; circulating anticoagulant index (CAI) greater than 15], subgrouped as follows: a) LA associated with systemic lupus erythematosus (SLE) (n = 13); b) primary antiphospholipid syndrome (PAPS) (n = 16); and c) LA associated with other disorders (n = 9). Male/female ratio differed between the groups: 0/13, 6/10 and 4/5, respectively. Venous and arterial thrombotic events were more common in the PAPS group (87%) compared with the SLE group (61%) and the other disorders group (22%). Serum ACA antiphospholipid IgG levels by ELISA were increased in the SLE and PAPS patients, but did not differ between the groups (167 +/- 24 vs. 190 +/- 28 mu respectively). Antiphospholipid IgM levels were higher in the SLE group compared with the PAPS group (127 +/- 15 vs. 67 +/- 16 mu). Mean TTI and CAI levels did not differ between the SLE, PAPS and other disorders groups (1.8 +/- 0.19, 2.8 +/- 0.9, 2.0 +/- 0.3 for TTI; 25 +/- 4, 33 +/- 4, 32 +/- 5 for CAI). Likewise TTI, CAI and ACA levels did not differ in patients with or without thrombosis. We conclude that the prevalence of thrombotic manifestations varies among patients with similar serum intensities of LA and levels of ACA, suggesting that other factors may be involved in the pathogenesis of thrombosis in these patients.
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PMID:Association of lupus anticoagulant and anticardiolipin antibodies with thrombosis in patients with systemic lupus erythematosus, primary antiphospholipid syndrome and other disorders. 173 97

A 15-year-old girl with right-sided cerebral infarct in association with lupus anticoagulant is described. The literature on the primary antiphospholipid syndrome and its neurological complications is reviewed.
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PMID:Cerebral infarct associated with lupus anticoagulant in an adolescent girl: a case report with review of the literature. 175 10

We describe a 35-year-old man with a history of previous deep vein thrombosis who presented with hypertension. Renal investigations revealed failure to excrete contrast medium by the right kidney on intravenous pyelography. Digital subtraction angiography showed an 80% stenosis of the left renal artery. He was antinuclear antibody negative, as well as negative for antibodies to double stranded deoxyribonucleic acid and extractable nuclear antigens. The lupus anticoagulant test and antibodies to cardiolipin were positive. He conforms to a diagnosis of "primary" antiphospholipid syndrome.
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PMID:Hypertension, renal artery stenosis and the "primary" antiphospholipid syndrome. 175 47

The association of livedo reticularis and cerebrovascular lesions is known as Sneddon's syndrome. It affects young adults and is more common in females. Repeated strokes lead these patients to residual deficits. Recently, Sneddon's syndrome has been described in a subset of patients with systemic lupus erythematous and primary antiphospholipid syndrome. We report two cases, one of them with antiphospholipid antibodies. Antiphospholipid antibodies do not seem to explain the events of Sneddon's Syndrome. Perhaps, different pathogenic mechanisms play role in the clinical expression of this syndrome.
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PMID:[Sneddon syndrome: diagnostic value of antiphospholipid antibodies]. 846 57

In order to ascertain the role of the antiphospholipid antibody in the pathogenesis of thrombotic disorders, a study of 21 lupus anticoagulant-positive patients was done by a number of serologic and functional platelet tests. In immunofluorescent studies, we found that 80% showed a mitochondrial pattern on HEp cells and all patients gave an ubiquitously intense staining of donor platelets. By a microscopic spontaneous aggregation test, all lupus anticoagulant-positive patients showed accelerated platelet aggregation which was calcium-independent. The results show that the plasma of lupus anticoagulant-positive patients contains a platelet-binding antibody and causes spontaneous agglutination of platelets. These properties may play a role in the thrombogenesis common to the antiphospholipid syndrome.
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PMID:Platelet antibody binding and spontaneous aggregation in 21 lupus anticoagulant patients. 176 96

Antiphospholipid antibodies can be detected by three methods; agglutination reactions with a cardiolipid antigen (VDRL, Kline, Kolmer) as observed in false positive syphilitic serologies; secondly coagulation reactions using thromboplastin (activated cephalin time, diluted thromboplastin time, Stipven time...). These cases are called lupus-like or, better, antiprothrombinase circulating antibody; finally, solid phase immunological tests (ELISA, RIA) with purified phospholipids, usually cardiolipin. The antiphospholipid antibodies detected by this method are not the same and the percentage of concordance between the two tests does not exceed 50 per cent. These antibodies are present in 30 to 60 per cent of patients with disseminated lupus erythematosus and also, less frequently, in other connective tissue disorders. They are always found in the so-called primary antiphospholipid syndrome, featuring recurrent venous or arterial thrombosis, repeated abortion, thrombocytopenia, and often a livedo reticularis and leg ulceration. Arterial thrombosis may occur in any part of the body (eye, central nervous syste, visceral or peripheral arteries). Mortality is related to neurological or coronary complications. The pathogenicity of antiphospholipid antibodies has not been formally demonstrated, but they could interact with membrane phospholipids of the vascular endothelium and/or platelets. Immuno-suppressor therapy is not very effective and long-term anticoagulant and/or platelet antiaggregant therapy is usually required.
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PMID:[Anticardiolipin antibody in peripheral arterial diseases]. 176 82

We describe a 26-year-old patient with systemic lupus erythematosus and pulmonary and portal hypertension associated with the presence of anticardiolipin antibodies. Postmortem histological examination revealed the presence of recent thromboses of pulmonary and portal vessels. Our findings further support the concept of pulmonary hypertension being part of the antiphospholipid syndrome and suggest that portal hypertension due to intrahepatic portal vein thrombosis might be another manifestation of this syndrome.
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PMID:Portal and pulmonary vessel thrombosis associated with systemic lupus erythematosus and anticardiolipin antibodies. 179 32

The antiphospholipid antibody syndrome (APLAS) is a unique clinical syndrome with features of recurrent thrombosis, recurrent fetal loss, and thrombocytopenia. It is associated with a false positive test for syphilis, a prolonged partial thromboplastin time (PTT), a positive test for lupus anticoagulant (LA), and anticardiolipin antibodies (ACLA). A case report illustrating some of the clinical and laboratory abnormalities and therapeutic dilemmas is presented. The literature is then reviewed.
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PMID:Antiphospholipid antibody syndrome: a case report and review of the literature. 180 Nov 88


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