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

Lupus anticoagulants have been recognized as significant causes of morbidity in patients for many years. They were originally regarded by physicians and researchers as a nuisance. However, the name is a misnomer that has resisted change over the years. The riddle of the anticoagulant effect in vitro and the apparent procoagulant effect in vivo remains unsolved. Since a lupus anticoagulant can exist in virtually every patient population, it is no longer a topic of interest limited only to the hematologists, but has achieved multidisciplinary attention. The presence of a lupus anticoagulant should be evaluated in any patient who presents with new onset transient ischemic attack or cerebral vascular accident, unexplained deep venous thrombosis, or recurrent fetal wastage.
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PMID:Lupus anticoagulant. 214 Mar 51

More than a dozen primary hematologic disorders have been associated with ischemic stroke. Inherited deficiencies of antithrombin III, protein C, and protein S have been linked with stroke in case reports; optimal screening requires functional as well as antigenic assays. Antiphospholipid antibodies and lupus anticoagulants are the most frequently identified acquired states associated with ischemic stroke. Polycythemia vera, sickle cell anemia, sickle-C disease, and essential thrombocythemia are the major disorders of formed blood elements causing stroke. Special, step-wise screening for occult prothrombotic entities in stroke patients is recommended for young persons with stroke of uncertain cause, for those with prior venous thrombosis, for those with a family history of unusual thrombosis, and for those with no other explanation for recurrent stroke. Acquired, perhaps transient, abnormalities of platelets, coagulation inhibition, and fibrinolysis may contribute importantly to brain ischemia in synergy with other mechanisms, but at present these remain ill-defined. The contribution of prothrombotic diatheses to stroke is probably underrecognized and warrants further investigation.
Stroke 1990 Aug
PMID:Hematologic disorders and ischemic stroke. A selective review. 186 63

A case of systemic lupus erythematosus (SLE) with subarachnoid hemorrhage due to a ruptured intracranial aneurysm is reported. A 31-year-old woman who had been treated with steroid for SLE was admitted to our department with severe headache, and nausea. CT scan showed subarachnoid hemorrhage and the left carotid angiogram revealed a small aneurysm at the supraclinoid portion of the left internal carotid artery. She had no neurological deficit. Hematological examination on admission showed disseminated intravascular coagulation (DIC), therefore, we decided to perform an intentionally delayed operation. In the meantime we treated the patient for DIC with FOY and methylprednisolone. The operation was performed after two weeks, when DIC had been eliminated completely. Postoperative hematological examination showed severe thrombocytopenia. We considered that SLE had come to the fore again, so we used Danazol in company with FOY and steroid. It seemed that Danazol was very effective for her. She was discharged about two months after admission with no problem. Cerebral apoplexy, such as cerebral infarction and cerebral hemorrhage, has often been seen in SLE, but subarachnoid hemorrhage due to a ruptured aneurysm is very rare. We could find only five reports of this phenomenon. Their prognoses were all, unfortunately, poor. It should be born in mind for therapy that a patient in SLE has a tendency to bleed. It seems that repeated hematological examinations and quick and proper management are important. We think that the aneurysmal formation in SLE is due to lupus vasculitis or the fragility of blood vessels due to a long use of Steroid.
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PMID:[A case of systemic lupus erythematosus with subarachnoid hemorrhage due to ruptured aneurysm]. 220 86

We investigated the clinical and pathologic characteristics of stroke in 234 patients with systemic lupus erythematosus. Thirteen patients (5.6%) developed cerebrovascular disease. Cerebral infarction was noted in eight, cerebral hemorrhage in two, and subarachnoid hemorrhage in three. In seven (54%) of these 13 patients, stroke occurred less than or equal to 5 years after systemic lupus erythematosus was diagnosed. Among the predisposing risk factors for stroke, hypertension was the most important. Lupus anticoagulant was detected in three (38%) and anticardiolipin antibody in three (43% of seven investigated) of the patients with infarction. Evaluation of the clinical manifestations and autoantibodies indicated that renal involvement and high titers of anti-deoxyribonucleic acid antibody were more frequent in the stroke group than in the non-stroke group. Autopsy studies on six of the patients with stroke revealed small infarcts and hemorrhages in all, but in no case was true angiitis observed. Libman-Sacks endocarditis was found in two of the three patients with infarction. In conclusion, the important contributory factor to the development of stroke in patients with systemic lupus erythematosus is considered to be hypertension mediated by immunologic abnormalities. Antiphospholipid antibodies and Libman-Sacks endocarditis are closely associated with occlusive cerebrovascular disease.
Stroke 1990 Nov
PMID:Stroke in systemic lupus erythematosus. 223 45

We studied the patterns of cerebral blood flow (CBF), over time, in patients with systemic lupus erythematosus and varying neurologic manifestations including headache, stroke, psychosis, and encephalopathy. For 20 paired xenon-133 CBF measurements, CBF was normal during CNS remissions, regardless of the symptoms. CBF was significantly depressed during CNS exacerbations. The magnitude of change in CBF varied with the neurologic syndrome. CBF was least affected in patients with nonspecific symptoms such as headache or malaise, whereas patients with encephalopathy or psychosis exhibited the greatest reductions in CBF. In 1 patient with affective psychosis, without clinical or CT evidence of cerebral ischemia, serial SPECT studies showed resolution of multifocal cerebral perfusion defects which paralleled clinical recovery.
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PMID:Cerebral blood flow variations in CNS lupus. 229 89

Over 2 years, 104 patients underwent clinical evaluation and laboratory screening for the presence of abnormal anticardiolipin antibodies to determine the profile of laboratory and clinical findings in patients with stroke and other neurologic disorders. Seven with incomplete or ambiguous data were excluded; of the remaining 97 patients, 31 were greater than or equal to 65 years old. Nine patients suffered systemic lupus erythematosus, 45 suffered brain ischemia, and 43 suffered other nonischemic neurologic disorders. Cardiac arrhythmia, myocardial infarction, and cardiac valvulopathy were grounds for exclusion. The presence of anticardiolipin antibodies was not influenced by age. In the 88 patients without lupus, anticardiolipin antibodies were significantly more common in the group suffering brain ischemia than in the group with nonischemic neurologic disorders (29% versus 5%, p less than 0.01, chi 2 test). These controlled data demonstrate an association between the presence of circulating anticardiolipin antibodies with stroke, but not with other neurologic conditions.
Stroke 1990 Feb
PMID:Prospective study of anticardiolipin antibodies in stroke. 230 7

Anticardiolipin antibody (aCL) has been associated with thromboembolic phenomena, including stroke, in certain patients with systemic lupus erythematosus (SLE); however, the relation between this antibody and the central nervous system manifestations of SLE is unknown. Serum samples and cerebrospinal fluid from five patients with SLE and acute central nervous system manifestations were assayed for the presence of aCL. Anticardiolipin antibody was identified in sera from four of the five patients but in none of the cerebrospinal fluid samples. Nuclear magnetic resonance imaging showed 'infarct-like' lesions in these four patients. This preliminary study suggests that a correlation between serum aCL and cerebral infarcts in central nervous system lupus may potentially exist. From this limited study it seems unlikely that aCL has a direct pathogenic role in the diffuse encephalopathy of acute central nervous system lupus.
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PMID:Neuropsychiatric lupus erythematosus, cerebral infarctions, and anticardiolipin antibodies. 231 12

We describe three cases of extracranial vertebral artery dissection that are unusual in both their modes of presentation and their associations with other pathologic conditions. The first patient had Marfan's syndrome and migraine; his dissection was asymptomatic and was diagnosed by chance at the time of repeat angiography following a previous internal carotid artery dissection. The second patient had systemic lupus erythematosus and presented with a subarachnoid hemorrhage attributed to an intracranial vertebral artery dissection by the demonstration of an extracranial dissection. The third patient had a minor basilar artery stroke in which dissection had occurred beside a congenital hemivertebra deformity.
Stroke 1990 Apr
PMID:Three cases of spontaneous extracranial vertebral artery dissection. 232 44

We describe four elderly stroke patients--two men and two women--who had significantly elevated levels of anticardiolipin antibody in the absence of systemic lupus erythematosus or other connective-tissue disease.
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PMID:Anticardiolipin antibody associated ischaemic strokes in elderly patients without systemic lupus erythematosus. 233 6

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.
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PMID:Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases. 238 25


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