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pubmed-article:1874623pubmed:dateCreated1991-9-26lld:pubmed
pubmed-article:1874623pubmed:abstractTextA 44-year-old female with Sneddon's syndrome, i.e. generalized racemose livedo and recurrent cerebrovascular disease, is presented. Significant levels of IgG anticardiolipin antibodies were found in her serum.lld:pubmed
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pubmed-article:1874623pubmed:monthMaylld:pubmed
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pubmed-article:1874623pubmed:authorpubmed-author:ZalaLLlld:pubmed
pubmed-article:1874623pubmed:authorpubmed-author:BraathenL RLRlld:pubmed
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pubmed-article:1874623pubmed:volume42lld:pubmed
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pubmed-article:1874623pubmed:pagination328-30lld:pubmed
pubmed-article:1874623pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:1874623pubmed:otherAbstractPIP: The entity of generalized livedo racemose and cerebrovascular bleeding disorders was introduced in 1965 by I. B. Sneddon describing 5 cases. it is not clear what role oral contraceptives and smoking play in the etiology of this syndrome. The case of a 44-year old multipara is described who had taken pills up to 1980 and smoked 5-10 cigarettes a day. In 1980 just before age 35 she suffered an apoplectic insult with hemisyndrome on the left side that she recovered from. An acute hypoglossal, and trigeminal paresis appeared on the left side. Computer tomogram showed a hypodense field in the area of both hemispheres of the brain. An audible mesosystolic click led to the diagnosis of suspecting cerebral embolism with mitral valve prolapse. Therapy was started with thrombocyte aggregation inhibitors. Although the prolapse could not be showed by echocardiography, the frontal mitral valve was slightly thickened. Another hospitalization in 1985 owing to a recurring attack of vertigo revealed higher blood pressure. She received betablocker treatment. In 1987 sudden weakness in the left arm and speech disorders ensued, and skin color alterations were manifest characteristic of generalized racemose livedo. Skin necrosis appeared on both toes. Sneddon syndrome was diagnosed, and full anticoagulation therapy was started with cumarin. The sensomotoric and speech symptoms receded only slightly. In 1988 a light cerebral insult occurred with the deterioration of the speech disorder. Laboratory finding showed immunoglobulin G (IgG) anticardiolipin antibodies (ACA) with 255 U/ml (normal range 0-10 U/ml), and normal IgM anticardiolipin antibodies with 8 U.ml (range of 0-10 U.ml). ACA has been detected in patients with lupus erythematosus and racemose livedo indicating the possible association of Sneddon syndrome with systemic lupus erythematosus.lld:pubmed
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pubmed-article:1874623pubmed:year1991lld:pubmed
pubmed-article:1874623pubmed:articleTitle[Sneddon syndrome].lld:pubmed
pubmed-article:1874623pubmed:affiliationDermatologische Universitätsklinik, Inselspital Bern.lld:pubmed
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pubmed-article:1874623pubmed:publicationTypeEnglish Abstractlld:pubmed
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