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)

Eight attacks of transient global amnesia were observed in a female patient who suffered from livedo reticularis and a series of other neurological symptoms, which were transient in most stances. The neurological deficits include focal epileptic attacks, unilateral loss of vision, paresis of left arm and/or leg and dysarthria. The first amnestic attack was seen at the age of 19. The episodes lasted from a few to 3 days. The intervals between the amnestic episodes varied between a few days and 11 years. The livedo reticularis became more obvious during each neurological episode and was less pronounced during the time of remission. A benign type of essential hypertension and parproteinemia (gamma-M) was found. The investigations failed to show any evidence of essential thrombocythemia, polyarteriitis nodosa, lupus erythematodes and other immune complex diseases. The underlaying disease remained unclear.
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PMID:Recurrent transient global amnesia in a case with cerebrovascular lesions and livedo reticularis (Sneddon Syndrome). 9 41

We examined the prevalence of the antibodies to cardiolipin measured by solid-phase enzyme immunoassay during a prospective study of patients with subacute cutaneous lupus erythematosus (SCLE). Seven of 44 (16%) consecutive patients with SCLE had positive anticardiolipin antibodies; of these only three satisfied the American Rheumatism Association's revised criteria for the classification of systemic lupus erythematosus. Clinical findings probably associated with the positive anticardiolipin antibodies were found in four cases, including clotting abnormalities, thrombocytopenia, hemolytic anemia, livedo reticularis, chilblain lupus erythematosus lesions, migraine, leg venous thrombosis and pulmonary embolism after surgery, and spontaneous abortion. Our data suggest that it is reasonable to screen SCLE patients for these antibodies to confirm the presence of the antiphospholipid syndrome.
Lupus 1992 Aug
PMID:Prevalence of anticardiolipin antibodies in subacute cutaneous lupus erythematosus. 130 91

We compared the clinical and serological characteristics of 15 patients with onset of systemic lupus erythematosus after the age of 50 with those of 232 younger patients. The sex distribution was similar in both groups. All 15 patients were Caucasian. Autoimmune thyroiditis was found in 20% of the elderly patients. Initial manifestations, which presented more frequently in the older group, included thrombocytopenia (P < 0.05), sicca syndrome (P < 0.01) and cardiomyopathy (P < 0.005), whereas butterfly rash (P < 0.05) presented more frequently in the younger group. Analysis of cumulative clinical symptoms showed that butterfly rash (P < 0.05) and livedo reticularis (P < 0.05) were less frequent in the elderly. However, this group presented a significantly increased incidence of sicca syndrome (P < 0.005) and cardiomyopathy (P < 0.005). Antibodies to double-stranded DNA tended to occur less frequently in older patients (P < 0.05).
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PMID:Systemic lupus erythematosus in 50 year olds. 143 23

We report the case of a young man suffering from the rare combination of livedo reticularis and recurrent ischemic cerebrovascular disease (Sneddon's syndrome). He also had a circulating anticardiolipin antibody. in the absence of systemic lupus erythematosus, we suggest the likelihood of a primary antiphospholipid syndrome.
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PMID:Sneddon's syndrome associated with anticardiolipin antibody: a case report. 144 2

As many as 30 patients suffering from systemic lupus erythematosus (SLE) with the clinical signs of central nervous system derangement were examined. The mean age of the patients was 31.1 years. Using EIA, antibodies against cardiolipin (a-CL) were detected in 21 patients (70%). A-CL were revealed in all the patients with cerebral circulation impairment (CCI), choreic hyperkinesis, and convulsive syndrome. A-CL were discovered in 12 out of 18 SLE patients suffering from migraine-like headaches and in 4 out of 5 patients with mental disorders. Antibodies reacting with cardiolipin were mostly represented by the IgM isotype (80%) whereas a-CL-IgG were only identified in 13% of the patients, being associated in all the cases with a-CL-IgM. The high level of a-CL-IgG in blood serum was recorded in patients with the gravest patterns of nervous system derangement: CCI, occlusion of the retinal artery, psycho-organic and convulsive syndromes. All these patients demonstrated generalized reticular livedo. The high levels of a-CL-IgM were observed in SLE patients with choreic hyperkinesis and migraine-like headaches. Thus, the studies made it possible to trace the relationship between the development of certain neurological disorders (CCI, chorea, convulsive syndrome) in SLE patients and a-CL.
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PMID:[The clinico-immunological characteristics of central nervous system involvement in systemic lupus erythematosus: the relationship with antibodies to cardiolipin]. 145 60

The clinical and serological features of 38 aCL-positive patients were compared to those of 45 aCL-negative patients. A significantly higher incidence of thrombophlebitis and livedo reticularis was found in aCL-positive patients. There were 13 aCL positive patients with thrombophlebitis and/or arterial thromboses and these 13 patients were designated as having the antiphospholipid syndrome (APS) while the remaining 70 patients were diagnosed as having Systemic Lupus Erythematosus (SLE). APS patients also had a high incidence of arterial occlusions, recurrent abortions and strokes compared to SLE patients. Patients with high levels of IgG-aCL were more likely to have APS, while patients with low levels of IgG-aCL or IgM-aCL only were more likely to have SLE without the clinical features of APS. Since aCL antibodies have recently been shown to interact with a phospholipid-binding plasma protein beta 2-glycoprotein-I (beta 2-GPI), we measured the beta 2-GPI levels in these patients and found that beta 2-GPI levels are significantly higher in APS compared to SLE patients negative for aCL antibodies. Since beta 2-GPI is known to exert multiple effects on coagulation processes the interaction of aCL antibodies with this glycoprotein may play a pathogenic role in APS.
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PMID:Patients with anticardiolipin antibodies with and without antiphospholipid syndrome: their clinical features and beta 2-glycoprotein-I plasma levels. 151 96

Autoimmune aPL are associated with a well-defined clinical syndrome of vascular thromboses, recurrent fetal loss, thrombocytopenia, livedo reticularis, and valvular and neurologic abnormalities. A clinical diagnosis of SLE need not be present, and aPL syndrome in the absence of other well-defined autoimmune disease is termed PAPS. A positive test for aPL is defined by enzyme-linked immunoassay (aCL) or by functional coagulation assay (LAC). Anticardiolipin antibody and LAC are similar but probably not identical antibodies. The false-positive test for syphilis is less closely associated with clinical complications than are aCL and LAC. The mechanism of action of aPL is not yet known, although many theories have been advanced. Recent identification of beta 2-glycoprotein I, a serum glycoprotein, as an aPL cofactor suggests that inhibition of this protein's anticoagulant activity may be important. Autoimmune aPL differ from infection-induced aPL in important antibody characteristics, including IgG subclass, light chain preference, antibody avidity, and cofactor requirement. Both recognize negatively charged phospholipids, but various physical characteristics of the phospholipids alter the recognition patterns. Treatment of the aPL syndrome is not well defined. Anticoagulation with heparin, coumadin, or aspirin are currently widely used. Although corticosteroid, immunosuppressive therapy, and plasmapheresis may be used for severe, fulminant thrombosis, the efficacy of this treatment has yet to be proved.
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PMID:Antiphospholipid antibody syndrome. 156 40

We report the case of a 74-year-old patient with HLA-B27 negative spondylarthropathy presenting with acute disseminated vascular occlusions. The presence of livedo reticularis prompted a search for antiphospholipid antibodies which were found to be markedly elevated. Histopathological examination revealed noninflammatory vascular obstruction. The clinical evolution was rapidly fatal in spite of corticosteroid treatment. Livedo reticularis can be an important diagnostic clue to various types of underlying disease. Increased levels of antiphospholipid antibodies have been associated with thrombosis and thromboembolism, especially in the context of autoimmune diseases such as systemic lupus erythematosus. This paper reports antiphospholipid antibody-associated noninflammatory vascular occlusions in a patient with HLA-B27 negative spondylarthropathy. The pathogenetic mechanism of antiphospholipid antibody-mediated vascular occlusions is not completely understood and optimal therapy remains to be defined.
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PMID:[Livedo reticularis and multiple vascular occlusions in a patient with HLA-B27-negative spondyloarthrosis and antiphospholipid antibodies]. 162 51

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

Twenty-three patients with the 'primary' antiphospholipid syndrome were studied over 2-6 years. Twenty-two (96%) had antiphospholipid antibodies detected by ELISA (87% had antibodies to thromboplastin and 70% to cardiolipin), and 18 out of the 21 tested patients (86%) had lupus anticoagulant activity by coagulative assays. Mean age of the cohort was 29.9 years and the sex ratio (female:male) 4.75:1. Eleven patients presented 18 venous and/or arterial thrombosis and 13 had 25 foetal losses (84% occurred during the second and third trimester). Other clinical features were migraine, livedo reticularis, and epilepsy. Three patients had relatives with systemic lupus erythematosus. Thrombocytopaenia was seen in 33%, antinuclear antibodies in low or moderate titre in 30%, and haemolytic anaemia in 13%. During the follow-up, two patients presented recurrent thrombosis despite anticoagulant therapy, one of them dying because of recurrent pulmonary thromboembolism. Four patients achieved successful term pregnancies after treatment with aspirin and a further patient after treatment with aspirin and low dose prednisolone. No patient developed systemic lupus erythematosus or any other definable connective tissue disease. The 'primary' antiphospholipid syndrome may exist as a distinct clinical entity and all younger patients presenting with thrombotic events, foetal losses and/or thrombocytopaenia, without any evidence of a well defined disease, should be tested for antiphospholipid antibodies in order to rule out this syndrome.
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PMID:The 'primary' antiphospholipid syndrome: antiphospholipid antibody pattern and clinical features of a series of 23 patients. 166 49


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