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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of antiphospholipid syndrome (APPS) is presented. A 33-year-old female presented with a right hemispheric stroke secondary to thrombosis of the middle cerebral artery. Shortly thereafter, she developed thrombosis of the right brachial artery. Despite thrombolytic therapy, progressive occlusion of this artery occurred as demonstrated by a follow-up angiogram. The patient had a history of multiple recurrent spontaneous abortions. Lupus anticoagulant, anticardiolipin antibodies, and VDRL were positive on two different occasions. The angiographic findings of multiple and progressive arterial thrombosis in young women should alert the angiographer to the possibility of APPS.
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PMID:Angiographic findings in a patient with primary antiphospholipid syndrome: case report. 139 62

The association of ischemic cerebrovascular lesions with livedo reticularis is known as Sneddon syndrome. It affects young subjects, primarily women, and its neurological manifestations are TIAs, ischemic stroke, progressive dementia and epileptic seizures. Its etiopathogenesis has still to be clarified. Some authors have associated it with an antiphospholipid antibody syndrome. Recently it has been assumed that a defect in blood coagulation may be involved in its pathogenesis. Here we report a case in which both an increase in coagulation factor VII activity and a deficiency in free protein S were documented.
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PMID:Cerebral ischemia and livedo reticularis in a patient with impairment of coagulation factor VII and free protein S. 142 96

A plasma protein is required as a cofactor for the binding of antiphospholipid antibodies to phospholipids. This protein has been identified as beta 2-glycoprotein I, an apolipoprotein that binds to negatively charged phospholipids and is a natural inhibitor of the coagulation cascade. It is not certain whether antiphospholipid antibodies bind to beta 2-glycoprotein I alone, to beta 2-glycoprotein I-phospholipid complex, or to a phospholipid epitope modified by beta 2-glycoprotein I. We used isolated beta 2-glycoprotein I and purified IgG and IgM antiphospholipid antibodies from serum or plasma of patients with the antiphospholipid syndrome to study the relation between antiphospholipid antibodies and beta 2-glycoprotein I in enzyme-linked immunosorbent assays. IgG antiphospholipid antibodies did not bind to beta 2-glycoprotein I when it was used as an antigen on the assay plate. The binding of IgG and IgM antiphospholipid antibodies to phospholipid was enhanced when beta 2-glycoprotein I was added to the phospholipid antigens either before or together with the antiphospholipid antibodies. The degree of enhancement varied across patients. IgM antiphospholipid antibodies required less cofactor for binding to phospholipid antigens. These results confirm the requirement of beta 2-glycoprotein I as a cofactor for the binding of autoimmune antiphospholipid antibodies to phospholipids.
Stroke 1992 Feb
PMID:Antiphospholipid cofactor. 144 Jul 26

Antiphospholipid antibodies (APA) have been described not only in systemic lupus erythematosus but also in several inflammatory diseases of the connective tissue, some infections, neoplasms, in pregnancy and even in apparently healthy individuals. Arterial and venous thrombosis are some of the clinical manifestations most frequently associated with APA. Two patients with ankylosing spondylitis with antiphospholipid antibodies are presented. The first patient developed a infarct in the pons as a complication at 34 years of age, with high titres of anticardiolipin antibodies as the only factor predisposing a cerebral vascular accident. The second patient had deep vein thrombosis with the presence of circulating anticoagulant. These are the first cases of antiphospholipid syndrome associated to ankylosing spondylitis in the literature.
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PMID:[Antiphospholipid syndrome in patients with ankylosing spondylitis. Presentation of 2 cases]. 156 71

Sneddon syndrome is know as the association of idiopathic livedo reticularis and cerebrovascular lesions. The most characteristic trait of this syndromes is a non-inflammatory arteriopathy in medium caliber vessels. The pathogenic role of antiphospholipid antibodies in this disease is not clear. Clinical characteristics and etiopathogenic features of eight patients with Sneddon's syndrome are reviewed, specially regarding its relationship with primary antiphospholipid syndrome. A female predominance was found (3:1) as well as a relationship with hypertension (five patients suffered hypertension), but no relation was found with contraceptive use. Three patients showed evidence of antiphospholipid antibodies, present as anticardiolipin antibodies with significative titers in three cases and lupus anticoagulant in one. Digital artery biopsy performed in four patients showed in all of them the pathologic features characteristic of this disease. Seven patients were treated with platelet activity inhibitors and one with oral anticoagulants. Six of them have had a year and half follow-up without showing any new ischemic stroke. The main etiopathogenic factor on Sneddon's syndrome is the presence of a non-inflammatory arteriopathy in medium caliber vessels. Blood hypertension and antiphospholipid antibodies could play a role in the development of cerebrovascular lesions in some cases. No relationship has been found with oral contraceptives in this series of patients. Medium term prognosis with platelet activity inhibitors therapy seems benign.
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PMID:[Sneddon's syndrome: its clinical characteristics and etiopathogenic factors]. 846 57

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

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

Having reviewed the literature on the association of aPL antibodies with clinical manifestations, it is clear that this group of autoantibodies are of considerable importance. The presence of aPL antibodies in some but not all individuals confers a risk of a clinical syndrome characterized by recurrent arterial or venous thrombosis, thrombocytopenia, hemolytic anemia, or positive Coombs' test, and in females, recurrent idiopathic fetal loss. In SLE, the risk is approximately 40%, compared with a risk of 15% in the absence of aPL antibodies. However, only one half of persons possessing these antibodies have SLE, and overall the risk is around 30%. In some circumstances, such as in chlorpromazine or infection-associated aPL antibodies, there appears to be no increased risk. At the other end of the spectrum are seen patients whose only clinical manifestations comprise features of this clinical syndrome, and this entity has been designated the primary antiphospholipid syndrome (PAPS). aPL antibodies are also important because they are not uncommon. They have been found frequently in women with idiopathic recurrent fetal loss (30%), in non-autoimmune patients with ischemic heart disease (20%), or venous thrombosis (up to 30%), or stroke (4-47%), and in chronic immune thrombocytopenia (30%). These autoantibodies can be detected using sensitive solid-phase immunoassays employing the CL antigen, or in appropriate coagulation tests to detect LA activity. These assays are simple to perform but require care in selection of the best test and in interpretation of results. Current tests do not distinguish between those persons at risk of the clinical events and those not at risk. Detection of specific isotypes (especially IgG) and antibody level may aid in such a designation. Treatment of aPL antibody-associated syndromes remains a controversial subject. Since thromboses are associated with significant morbidity and potential mortality, there is a good argument for long-term preventive antithrombotic therapy, at least for as long as the antibodies are detectable, in those patients in whom clinical complications have previously occurred. It is not generally recommended that this treatment be offered to individuals in whom aPL antibodies are detected but who have not suffered previous thromboses, since the risk of such events does not appear to be equal within a group of aPL antibody-positive persons. This particularly applies to pregnant women, since live births and uncomplicated pregnancies are observed regularly in the presence of aPL antibodies without specific treatment. A previous history of at least one unexplained, late fetal loss is considered a prerequisite before intervention in subsequent pregnancies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunology and clinical importance of antiphospholipid antibodies. 185 85

Anticardiolipin antibodies (aCL), one of a group of antiphospholipid antibodies which include the lupus anticoagulant (LA), may occur in association with systemic lupus erythematosus (SLE) and are less commonly detected in other diseases. We retrospectively reviewed the clinical and immunological features of 39 consecutive patients with abnormal aCL identified by one laboratory, to examine the spectrum of neurological disease in those patients without SLE. Fourteen patients in this category are described, 6 of whom did not have evidence of LA. All but 1 presented with neurological symptoms. Stroke and migraine dominated the clinical presentation, but many patients had features to suggest the presence of a hypercoagulable state. This study lends support to the concept of a primary antiphospholipid syndrome.
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PMID:Neurological disease associated with anticardiolipin antibodies in patients without systemic lupus erythematosus: clinical and immunological features. 196 May 45

In a 2-year prospective study of 146 patients with cerebral ischemia, we compared vascular risk factors for stroke with clinical and laboratory findings, particularly antiphospholipid antibodies. Ten patients (6.8%) were positive for at least one antiphospholipid antibody; one patient had systemic lupus erythematosus, one had rheumatoid arthritis, and the remaining eight fulfilled criteria for the diagnosis of primary antiphospholipid syndrome. These patients were predominantly male, not necessarily young, and 50% of them did not have any other vascular risk factors; there were no significant clinical or paraclinical differences between these patients and those without antiphospholipid antibodies. Outcome in the 10 patients was good, and platelet antiaggregating drugs proved to be useful in preventing further cerebrovascular ischemic events in our patients.
Stroke 1991 Jun
PMID:Antiphospholipid antibodies in cerebral ischemia. 205 74


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