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

We present the clinical, hematologic, and radiographic findings in two brothers with Sneddon's syndrome (stroke and livedo reticularis) and antiphospholipid antibodies. Patient 1 had anticardiolipin antibody and patient 2 had lupus anticoagulant, which we detected only upon repeated blood testing. One should test for both anticardiolipin antibody and lupus anticoagulant and repeat the screenings before determining a Sneddon's syndrome patient's antiphospholipid antibody status. Both Sneddon's syndrome and the primary antiphospholipid antibody syndrome are potentially familial causes of stroke. In familial cases, an inherited predisposition to antiphospholipid antibody production may be involved in disease pathogenesis.
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PMID:Familial Sneddon's syndrome: clinical, hematologic, and radiographic findings in two brothers. 814 5

Cerebral infarction in the young is likely to be non-atheromatous. While in previous studies no cause has been found in 40% to 50% of patients, an increasing role for haemorheological factors is becoming apparent. Among these, an association between antiphospholipid antibodies (aPLs) and ischaemic cerebrovascular disease is now well-recognised. This entity has not been previously reported in Malaysian patients. In a study of 80 patients with stroke below the age of 50 years who were seen at the University Hospital, Kuala Lumpur, between January 1982 and May 1992, 3 patients with ischaemic cerebral infarction were found to have aPLs. aPLs was detected using ELISA method for anticardiolipin antibodies (aCLs), and presence of lupus anticoagulant (LA) was established by kaolin clotting time, thromboplastin inhibition test and platelet neutralisation procedure. Only 1 patient had active systemic lupus erythematous. Cerebrovascular events were recurrent in one of the 2 non-lupus patients. aPL-related stroke should be considered in young patients who have cerebral ischaemia occurring without obvious cause. More cases are likely to emerge in Malaysia with active screening.
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PMID:Antiphospholipid antibodies and stroke in the young--a study of three cases. 818 47

Despite extensive evaluation, the cause of many childhood ischemic strokes remains unexplained. Two children are reported with stroke and lupus anticoagulant. Both had family members with features of the antiphospholipid antibody syndrome. Children with unexplained ischemic stroke should be evaluated for lupus anticoagulant and anticardiolipin antibodies.
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PMID:Childhood stroke and lupus anticoagulant. 819 73

Antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibodies) are regarded as important risk factors for ischemic stroke and transient ischemic attacks in young subjects. In fact the interaction of these antibodies with phospholipid may impair the coagulation system at several steps, promoting thrombosis. A variety of therapeutic strategies including corticosteroids, immunosuppressive drugs, antiplatelet agents and anticoagulants have been prescribed in stroke patients with aPLs, but the efficacy of these drugs has not been established yet.
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PMID:Antiphospholipid antibodies and cerebrovascular disease. 824 74

To determine whether young patients who suffered a stroke in the past, have a higher prevalence of ACA of LAC as compared to healthy controls, we evaluated 44 stroke patients and 46 controls in a case-control study for the presence of ACA and LAC. All the patients had had a stroke under the age of 50 yr and the stroke date was less than 5 yr ago (mean 2.5 yr). Stroke was defined as an ischaemic cerebral infarction and was confirmed by angiography, CT-scan or MRI. An age- and sex-matched group of healthy volunteers served as controls. The mean age of the patients was 41.4 yr (range 22-52 yr), and of the controls 36.8 yr (range 24-50 yr). Serum and plasma from both groups was examined for IgM- and IgG-ACA and LAC. One patient was positive for both IgG- and IgM-ACA, whereas 3 controls were found positive for IgG-ACA. For 2 patients and 5 controls an equivocal result was obtained for IgG-ACA or IgM-ACA. None of the patients or controls were positive for LAC. The differences between the patient and control group were statistically not significant. In conclusion, no difference was found in the prevalence of cardiolipin antibodies in sera from patients with a stroke within the last 5 yr and an age- and sex-matched control group. There was no correlation either between the presence of lupus anticoagulant and the occurrence of a stroke in the past.
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PMID:Cardiolipin antibodies and lupus anticoagulant in young patients with a cerebrovascular accident in the past. 831 30

Antiphospholipid antibodies have been reported to occur in ischemic stroke patients, but there have been no previous reports linking these antibodies to spinal cord infarction. A case of spinal cord infarction associated with primary antiphospholipid syndrome in a 6-year-old boy is reported. Magnetic resonance imaging clearly demonstrated marked swelling of the thoracolumbar spinal cord with gadolinium-diethylenetriamine pentaacetic acid enhancement at an acute stage, followed later by cord atrophy. Serological study disclosed positive lupus anticoagulant and immunoglobulin G anticardiolipin antibody. It is suggested that the role of antiphospholipid antibodies as an etiological factor for spinal cord ischemia should be recognized among causes that might have been categorized as either spontaneous spinal cord infarction or myelitis.
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PMID:Spinal cord infarction associated with primary antiphospholipid syndrome in a young child. Case report. 836 Jul 45

To determine the utility of magnetic resonance imaging (MRI) of the brain in diagnosing active neuropsychiatric disease in systemic lupus erythematosus (NP-SLE), a prospective study of 51 hospitalized systemic lupus erythematosus (SLE) patients during 64 separate episodes of suspected NP-SLE was initiated. In addition to standard hematology, chemistry, and serological tests, the workup included MRI in all patients. A computed tomographic scan of the brain was obtained in patients enrolled in the first year of the study. Of the 64 neuropsychiatric episodes, 42 were attributable to NP-SLE and 22 were attributed to causes other than SLE. Neuropsychiatric complaints unrelated to lupus included depression (n = 6), seizures (n = 5), headache (n = 3), altered mental status (n = 2), aseptic meningitis (n = 2), cardiovascular accident (n = 2), transient ischemic attack (n = 1), and vertigo (n = 1). The MRI was abnormal in 34 of 64 (53%) episodes. MRI abnormalities were more common in patients with focal neurological deficits (19/26) than in those without focal findings (15/38; P = .008) and in patients with nephritis (19/24) than in those without renal disease (15/40; P = .002). MRI abnormalities were as frequent in NP-SLE (25/42) as in cases with non-NP-SLE-related causes (9/22). Periventricular increased signal (PIS) was a frequent MRI finding (10/64). Enlargement of the prepontine cistern, an MRI finding not previously described in NP-SLE, was seen (14/64). Both findings were associated with the presence of hypertension and lupus nephritis. PIS similar to that seen in our patients has been described in otherwise healthy elderly individuals with risk factors for stroke, suggesting that vascular abnormalities may be important in the etiology of these lesions. In conclusion, abnormalities in brain MRI occur frequently in NP-SLE, especially in patients with focal neurological deficits. However, the presence of similar MRI abnormalities in SLE patients with neuropsychiatric symptoms and findings with non-SLE-related causes limits the specificity of the MRI for diagnosing NP-SLE.
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PMID:Magnetic resonance imaging of the brain in neuropsychiatric systemic lupus erythematosus. 851 97

Records of 108 patients with lupus erythematosus beginning in childhood (1953-1990) were reviewed; 25 had recorded neurologic findings. This is the largest group of childhood lupus erythematosus patients with neurologic disease that has been reported. The average age of children at the time of diagnosis of lupus was 154 months. There were 22 girls and 3 boys in the group. All patients met at least four of the 1982 American Rheumatism Association criteria for the classification of systemic lupus erythematosus. Average age at onset of neurologic difficulties was 168 months. In 4 patients, the neurologic symptoms preceded the diagnosis: 1 month (spastic diplegia), 1 month (bilateral weakness and spasticity), 24 months (chorea), and 26 months (chorea), respectively. Four patients had neurologic symptoms coincident with the diagnosis of lupus erythematosus. In those patients whose symptoms followed the diagnosis of lupus erythematosus, the average elapsed time until symptoms appeared was 33 months; the single lowest and highest outliers were discounted. Most frequent findings were headache (16/25) and behavioral aberrations (10/25). All behavioral manifestations were depression except in 1 patient. Other prevalent findings included hemichorea or chorea (7/25), cerebrovascular accident with hemiplegia or diplegia (7/25), seizures (5/25), visual loss (3/25), and cranial neuropathy (2/25). Vertigo and myelopathy occurred in 1 patient each. All patients were treated primarily with corticosteroids and azathioprine; in the presence of active disease, the drug dosages were increased with significant improvement in neurologic symptoms. Resolution usually occurred from days to months; most improved in a few days to a few weeks; 3-4 months was the longest period until symptoms subsided.
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PMID:Neurologic characteristics of childhood lupus erythematosus. 855 56

Histopathological changes in leptomeningeal and cerebral blood vessels in a case of subacute cutaneous lupus erythematosus (SCLE) with the involvement of the central nervous system are presented. A 46-year-old woman died because of cerebral stroke after a 19-year duration of the disease. The general autopsy showed changes in the kidneys, myocardium, spleen and pancreas, typical of systemic lupus erythematosus. The brain autopsy revealed large necrosis in the supply territory of the middle and posterior cerebral arteries in the left hemisphere. In addition, small focal necroses, partially hemorrhagic, were found in both cerebellar hemispheres. Small cortical necrosis was also visible in the right insular area. A diffuse damage of the blood vascular system in the form of fibrinoid necrosis of small sized cerebral blood vessels with inflammatory infiltrates of the vessel wall (necrotizing leukocytoclastic vasculitis) predominated in the microscopic examination of the brain. Vascular changes of vasculopathy type in the form of hyalinization of the vascular wall and fibrinoid necrosis with concomitant numerous, small necroses were observed. In the lumen of left internal carotid artery infiltrated by inflammatory cells, an organized thrombus was found. Giant cells were observed within vascular infiltration.
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PMID:Rare vascular changes in the brain in a case of subacute cutaneous lupus erythematosus. 867 32

IgG antibodies to cardiolipin and beta 2-glycoprotein I were looked for using an enzyme-linked immunosorbent assay (ELISA) in 19 patients with giant cell arteritis (meeting 1990 American College of Rheumatology criteria), including 16 with concomitant polymyalgia rheumatica (meeting Bird's criteria) and in three patients with isolated polymyalgia rheumatica. IgG anti-cardiolipin antibodies were demonstrated in eight patients (36%) and IgG anti-beta 2-glycoprotein I antibodies in two patients (9%) including one without anti-cardiolipin antibodies. Titers of anti-cardiolipin antibodies ranged from 27 to 190 units of IgG antiphospholipid antibodies (UGPL) (mean 71 UGPL). Of the eight patients with anti-cardiolipin antibodies, two had giant cell arteritis without polymyalgia rheumatica and six had polymyalgia rheumatica with clinical (n = 2) or histologic (n = 4) evidence of giant cell arteritis. None of the three patients with polymyalgia rheumatica but no giant cell arteritis had anti-cardiolipin or anti-beta 2 glycoprotein I antibodies. The VDRL was negative in the 14 patients who had this test. Tests for lupus anticoagulant were performed routinely, always with negative results. Among giant cell arteritis patients, those who tested positive for anticardiolipin antibody had significantly higher values for the erythrocyte sedimentation rate (p < 0.006) and for serum C-reactive protein (p < 0.03) and fibrinogen values (p = 0.05), and a trend toward higher platelet counts, as compared to those who tested negative for anticardiolipin antibody. The mean daily prednisone dose at the time of sampling was significantly lower in giant cell arteritis patients with anti-cardiolipin antibodies (p < 0.05); this difference may account for the apparent correlation between anti-cardiolipin antibodies and laboratory markers for inflammation. These data, as well as findings from serial measurements, suggest that anti-cardiolipin antibodies are present early in the course of giant cell arteritis and disappear within a few weeks of initiation of corticosteroid therapy in a dose of more than 25 mg prednisone per day. In this study, only one patient without anticardiolipin antibodies developed a cerebrovascular accident. Positive tests for anti-cardiolipin antibody or anti-beta 2 glycoprotein I antibody in a patient with polymyalgia rheumatica suggest a diagnosis of concomitant giant cell arteritis, which is usually symptomatic.
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PMID:Antibodies to cardiolipin and beta 2 glycoprotein I in patients with polymyalgia rheumatica and giant cell arteritis. 873 42


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