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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

New details have been added to the description of the antiphospholipid antibody syndrome. These include quantitation of risk of stroke; delineation of an associated acute occlusive vasculopathy syndrome, including its pathology; increased awareness of the association of adrenal insufficiency with antiphospholipid antibody; new demonstration of placental pathology in cases of fetal death; and new details on the persistence or transience of antibody in patients with systemic lupus erythematosus. There are several animal models for the antiphospholipid antibody syndrome. Assay standardization and reproducibility issues, more for the lupus anticoagulant than for the enzyme-linked immunosorbent assay for antiphospholipid antibody, remain as important barriers to progress. Antibody characteristics of activity, isotype, and subclass must be considered in assay interpretation; antigen characteristics of fatty acid chain and lipid phase are also important variables. Other circulating proteins may have clinical importance. Several laboratories have commented that antiphospholipid antibody interferes with protein C. A cofactor, apolipoprotein H, enhances binding of some antiphospholipid IgG antibodies. Other phospholipid-binding proteins are known. Isolation, purification, and perhaps cloning of many of these factors should lead to a better understanding of the pathogenesis of the syndrome.
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PMID:Antiphospholipid antibody and antiphospholipid antibody syndrome. 183 43

Recently, the association between anti-phospholipid antibodies (false positive VDRL, lupus anticoagulant or anti-cardiolipin antibody) and diverse clinical manifestations has been termed antiphospholipid syndrome. We report 6 female patients with "primary" antiphospholipid syndrome, not related to connective tissue disorders. Their age ranged from 23 to 66 years and they were followed from 1 to 27 years (mean 9.2). Venous occlusion developed in 4, arterial occlusion in 4 (TIA, convulsive episode and cutaneous thrombotic microangiopathy). Three of 5 had fetal loss and 3/6 developed thrombocytopenia. Leg ulcer, migraine and mitral valvulopathy and peripheral facial paralysis were isolated manifestations in different patients. High titers for type IgG anticardiolipin antibodies were present in all patients. Low titers for IgM antibodies were present in 2. The pathogenesis of this syndrome is discussed.
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PMID:[Primary antiphospholipid syndrome: clinical experience of 6 patients]. 184 92

A prospective echocardiographic study was carried out on 55 patients with the recently described 'primary' antiphospholipid syndrome derived from three university medical centres. The prevalence of valvular lesions in patients with this syndrome was 38% compared with 4% in a control group of 55 healthy volunteers (P < 0.001). Mean age of patients with valve abnormalities was 42 +/- 12 years and of those without, 30 +/- 10 years (P < 0.05). One patient had a morphologic echocardiographic pattern suggestive of non-infective verrucous mitral endocarditis. Twenty patients had a two-dimensional or Doppler echocardiographic pattern of significant valvular dysfunction--either regurgitation or stenosis--without evidence of vegetations. Mitral and aortic regurgitation were the most common lesions in these patients. During follow-up of patients with valvular disease, haemodynamically significant clinical valve disease developed in four and surgery was required in one. Eleven patients had cerebrovascular occlusions. Thus, valvular heart disease, particularly affecting the mitral and aortic valves, is common in patients with the 'primary' antiphospholipid syndrome, especially in those over 40 years old.
Lupus 1991 Nov
PMID:High prevalence of significant heart valve lesions in patients with the 'primary' antiphospholipid syndrome. 184 63

Leg ulcers are associated with antiphospholipid antibodies in patients with systemic lupus erythematosus. They may also occur in patients with primary antiphospholipid syndrome(PAPS). Histopathologic findings at the edges of the ulcers may give insight into their pathogenesis. In a patient with PAPS and a leg ulcer, a biopsy of the ulcer's edge revealed a peculiar small vessel nodular proliferation in the upper and lower dermis. There was mild mixed inflammatory infiltrate in the surrounding connective tissue, a few vessels with fibrin thrombi, and some with fibrin deposition within their walls. A review of the literature revealed similar findings in other skin ulcers associated with lupus anticoagulants. This suggests peculiar pathogenetic mechanisms that may be akin to those responsible for antiphospholipid arterial vasculopathy.
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PMID:Leg ulcers in the primary antiphospholipid syndrome. Report of a case with a peculiar proliferative small vessel vasculopathy. 190 10


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