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)

Fernando and Chir 1st reported an association between chorea and oral contraceptives (OCs) in 1966. Differential diagnosis of chorea, in addition to Sydenham chorea, include Wilson disease; encephalitis; Huntington chorea; drug intoxication; benign familial chorea; pregnancy; systemic lupus erythematosus; Henoch-Schonlein purpura; polycythemia vera; hypocalcemia; hyperthyroidism; carbon monoxide poisoning; cerebral infarction, and; intracranial tumor. Chorea can also occur as an untoward side-effect of OC therapy, as shown by the case report of a 20-year old white woman. Chorea associated with OC therapy occur unilateraly but has also been bilateral in 37% of reported cases. 8 of 24 reported cases (33%) had a prior history of rheumatic fever - mean age of patient was 22 years (range, 16 to 40 years). The time between initiation of OC therapy and appearance of choreiform movements can vary from 6 days to 9 months, with a mean of 3 months. Time between discontinuation of OC therapy and cessation of symptoms vary from 3 days to 3 months, with a mean of 5 weeks. Speculations by various authors on the pathogenesis of chorea are described.
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PMID:Chorea associated with oral contraceptive therapy. 739 41

This is a report of cerebral infarction and cerebral hemorrhage derived from systemic lupus erythematosus. A 49-year-old male was admitted to our hospital due to dysarthria and supranuclear facial palsy. He had been suffering from SLE and medicated incompletely since 9 years prior to admission. A CT scan showed a small infarction in the left parietal area. An angiography revealed a tapering stenosis of the left carotid siphon and an occlusion of the left vertebral artery at the cisternal portion. On the 13 days after the admission, he complained of a high fever and right hemiparesis. The CT scan disclosed newly multiple small infarctions in the left parietal area. The angiography showed the progressing of the tapering stenosis at the left carotid siphon, and demonstrated the narrowing of the left superior temporal artery and ophthalmic artery in addition to the disappearance of a left posterior communicating artery. High dose of steroid was given to him, but cerebral hemorrhage and huge left cerebral infarction were complicated. On the 26 days after the admission, his general condition was worsened and died. It was considered that the cerebral infarction and hemorrhage might be derived from the vasculitis of SLE.
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PMID:[A case of systemic lupus erythematosus associated with cerebral infarction and cerebral hemorrhage]. 757 35

We reported a case of malignant rheumatoid arthritis (MRA) with cerebral infarction associated with a possible cause of lupus anticoagulant. The patient was a 68-year-old woman who had received treatment for rheumatoid arthritis (RA) from 15 to 16 years ago. She consulted to our hospital with a major complaint of right hemiplegia. Brain CT revealed a low density area in the left hemisphere. She was diagnosed as cerebral infarction and hospitalized. Since she was noted to have hypocomplementemia, interstitial pneumonia and pericarditis, she was diagnosed as MRA. Coagulation test disclosed positive lupus anticoagulant (LA). Generally, CNS disorders in MRA are uncommon. Cerebral infarction was complicated in the present case, suggesting the involvement of antiphospholipid antibodies as its pathogenesis.
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PMID:[A case of malignant rheumatoid arthritis with lupus anticoagulant and cerebral infarction]. 777 8

The authors report a thirty-seven-year-old woman with systemic lupus erythematosus (SLE), a coronary aneurysm, and myocardial infarction. SLE was diagnosed at twenty-three years of age and treated with prednisolone. Seven years later, she developed inferior myocardial infarction, and coronary angiography showed an aneurysm in the proximal right coronary artery without associated stenosis. At the age of thirty-seven years, she died from cerebral infarction and sepsis. Autopsy revealed an aneurysm (6 mm in diameter) in the proximal right coronary artery and an old inferior myocardial infarction. Histologic examination showed recanalization and fibrosis in the media of the aneurysm wall. This case suggests that coronary aneurysm may cause myocardial infarction in SLE and that aneurysm formation may be a sequela of arteritis.
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PMID:Myocardial infarction secondary to coronary aneurysm in systemic lupus erythematosus. An autopsy case. 778 96

One of the clinical hallmarks of antiphospholipid syndrome is the development of neurological complications, namely cerebral ischaemia, chorea, multi-infarct dementia, amaurosis fugax, migraine and transverse myelitis. An animal model should include the development of measurable neurological deficits and evidence of cerebral infarction. Although there are a number of mouse models for fetal loss, there has been no convincing model for the neurological complications of the antiphospholipid syndrome. One explanation for the high frequency of neurological events in antiphospholipid syndrome is a vulnerability of the cerebral vasculature to the hypercoagulable state associated with the syndrome. A greater appreciation of the differences in the regulation of coagulation between the systemic and cerebral vasculatures may be key to understanding the apparent predilection for central nervous system involvement in the antiphospholipid syndrome.
Lupus 1994 Aug
PMID:Models for central nervous system complications of antiphospholipid syndrome. 780 11

The purpose of this study was to measure plasma platelet-activating factor (PAF) concentration, PAF-acetylhydrolase activities, anti-phospholipid antibody (aPLs) titers, and platelet function in patients with subarachnoid haemorrhage (SAH) and to assess the association of these variables with the development of cerebral vasospasm. Thirty-two patients with SAH due to ruptured cerebral aneurysm were studied. Plasma PAF concentration, PAF-acetylhydrolase activity, platelet count and aggregability, and plasma factor 4 (PF4) concentrations were measured regularly until approximately 2 weeks after SAH. aPLs, including lupus anticoagulant and anti-cardiolipin IgG and IgM were measured within 3 days after SAH. Plasma PAF concentration in patients with SAH showed the highest value on the occasion during 5 to 9 days after SAH. The concentrations were higher in patients with infarction due to vasospasm than in patients without cerebral infarction on any occasions after SAH. Plasma PAF-acetylhydrolase activities did not change in patients, regardless of the presence of cerebral infarction after SAH. Increased platelet consumption and aggregability and higher concentrations of PF 4 were detected in patients with cerebral infarction and not in patients without cerebral infarction. The patients with cerebral infarction due to cerebral vasospasm had aPLs more frequently than the control volunteers. Our findings indicate that increased plasma PAF and aPLs may contribute to the pathogenesis of cerebral vasospasm after SAH.
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PMID:Platelet-activating factor and antiphospholipid antibodies in subarachnoid haemorrhage. 784 32

Elevated levels of anticardiolipin antibodies (ACA) have recently been found to be associated with occlusive diseases such as myocardial or cerebral infarction or venous thrombosis. In a prospective study anticardiolipin antibodies (both IgG and IgM) were measured by ELISA in 140 patients with acute vascular occlusions of the eye. Patients with clinical evidence for lupus erythematodes, HIV infection or elevated concentrations of antinuclear antibodies (IIFT with HEp-2 as antigen, LD Diagnostika, Heiden, FRG) were excluded. Elevated concentrations of IgG-ACA and IgM-ACA were found in 9% of the cases, with no correlation with the type of ocular vascular occlusion (retinal artery occlusion, retinal vein occlusion, anterior ischemic optic neuropathy). These results indicate that the anticardiolipin syndrome with elevated concentration of anticardiolipin antibodies may also have a causal role in some patients with occlusive eye diseases, whereas in most patients the concentrations were within normal ranges.
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PMID:[Anticardiolipin antibodies in vascular occlusions of the eye]. 784 29

The pathogenesis of migrainous stroke is controversial. The possibility that a number of migraine-related strokes is associated with the presence of antiphospholipid antibodies, a condition predisposing to coagulopathy, has been suggested. We investigated the prevalence of lupus anticoagulant and anticardiolipin antibodies in patients with migrainous stroke. In 6 out of 16 patients with migrainous cerebral infarction, the presence of antiphospholipids antibodies was detected. In such patients, the presence of other risk factors for stroke was significantly lower (chi 2 = 5.6; p = 0.01) with respect to patients with negative results for antiphospholipid antibodies. These results suggest that antiphospholipid antibodies associated with migraine may be an important marker for ischemic stroke.
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PMID:Migrainous stroke and the antiphospholipid antibodies. 785 51

Two depressive patients with systemic lupus erythematosus (SLE) and cerebral infarction, while being treated with corticosteroid, are described. In both cases, lithium was remarkably effective and no severe side-effects occurred. These findings suggest that lithium can be a useful antidepressant agent in the treatment of depressive SLE patients.
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PMID:Antidepressant effect of lithium in patients with systemic lupus erythematosus and cerebral infarction, treated with corticosteroid. 779 82

A 26-year old woman, who was diagnosed as having systemic lupus erythematosus at the age of 23 year old, presented diarrhea and headache. She showed severe hypoproteinemia (serum total protein 3.7 g/dl, serum albumin 1.4 g/dl) and hyperlipidemia. She revealed to have protein-losing enteropathy with the result of alpha-1-antitrypsin clearance test using stool. Increase of prednisolone improved the loss of albumin into the bowel and abnormal laboratory findings. She also showed watershed infarction in the area of middle cerebral artery and posterior cerebral artery. Protein-losing enteropathy is a rare complication of SLE, only 18 cases are available on literature. No case is found to have cerebral infarction in patients with protein-losing enteropathy associated with SLE. It is known that blood levels of anticoagulation factors decrease in protein-losing enteropathy due to the leakage of plasma protein into intestinal lumen. Serum antithrombin III was decreased in this case. Hyperlipidemia found in this case seems to be caused by same mechanism in nephrotic syndrome. Lupus anticoagulant was also positive in this patient. These factors seems to be related to the occurrence of cerebral infarction. This case suggests the possibility of cerebral infarction in patients with protein-losing enteropathy in SLE.
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PMID:[Protein-losing enteropathy and cerebral infarction associated with systemic lupus erythematosus]. 814 30


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