Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A young man who had suffered several episodes of deep-vein thrombosis of the legs since the age of 20 had a myocardial infarction at the age of 33, at which time both a prolonged partial thromboplastin time (PTT), compatible with a lupus anticoagulant (LA), and decreased fibrinolytic capacity (FC) were found. His sister presented with deep-vein thrombosis of a leg and subsequent pulmonary embolism when she was 18 years old. She had a miscarriage three years later and developed a hemolytic-uremic syndrome at the age of 35. The PT and FC were normal. Laboratory investigations of the parents revealed positive antinuclear antibodies in the mother's serum but no anomaly in the father. This study suggests a familial tendency to develop autoimmune disorders associated with LA and thromboembolic complications related to decreased FC.
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PMID:Different clinical presentations of a lupus anticoagulant in the same family. 190 97

Two cases of primary antiphospholipid syndrome are described. A girl presented with myocardial infarction at the age of 6. afterward developed chorea, livedo reticularis, thrombocytopenia and circulating lupus anticoagulant (LAC). A boy, age 7, had an episode of intracranial hypertension and a deep venous thrombosis of a lower left limb, both recurrent in the following years. A high titer of IgG anticardiolipin antibodies (aCI) was detected. These observations suggest that both LAC and aCI tests should be performed in children with thromboembolic phenomena when the criteria for a definite autoimmune disease are lacking.
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PMID:Primary antiphospholipid syndrome: a report of two pediatric cases. 192 Mar 12

Forty-one patients (31 women, 10 men) aged 15-56 (mean age, 38) with Sneddon's syndrome characterised by cerebrovascular disease and widespread livedo reticularis in the absence of typical lupus features were studied. 16 patients (39%) had clinical and/or electrocardiographic signs of ischemic heart disease, with 2 of them having survived myocardial infarction. Cardiac murmurs (usually mitral systolic) were heard in 15 patients (37%). Echocardiography revealed mitral valve thickening in 13 of 32 tested patients (41%). Anticardiolipin antibodies were found in 22 patients (54%) and lupus anticoagulant in 25 of 38 tested patients (66%). In 6 patients (15%) neither anticardiolipin antibodies nor lupus anticoagulant were observed. Anticardiolipin antibodies were more often present in patients with ischemic heart disease (12 of 16), than in those without (10 of 25) (p less than 0.05). Mitral valve thickening was revealed more often in patients with antiphospholipid antibodies (12 of 26 patients) than in those without (1 of 6); however, a statistically significant difference was not observed.
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PMID:Sneddon's syndrome: cardiac pathology and antiphospholipid antibodies. 193 83

A 64-year-old man with both Factor XI deficiency and a lupus anticoagulant who suffered two myocardial infarctions within a 3-month period is described. Although thromboembolic disorders, including myocardial infarction, have been associated with the antiphospholipid syndrome, myocardial infarction in patients with Factor XI deficiency is rare. The potential role of Factor XIa in fibrinolysis is discussed.
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PMID:Myocardial infarction in a patient with factor XI deficiency and a lupus anticoagulant. 193 5

We report the generation and serologic, cellular, histologic, and genetic characteristics of a BXSB/MpJScr substrain, termed BXSB/MpJScr-ll/ll, that has lost early-life male lupus disease. Classic genetic analysis suggested that delayed disease expression results from the action of a single autosomal recessive gene. This putative gene, referred to as ll (long-lived), causes a significant delay in expression of autoimmune serology (total serum IgG and anti-nuclear antibodies levels), monocytosis, and of immune complex-mediated histopathologic changes such as glomerulonephritis, arteritis, and myocardial infarction. Presumably as a consequence of the delayed immunopathology male BXSB/MpJScr-ll/ll mice live three to four times longer than regular BXSB/MpJScr. This strain might be useful for analysis of single genes responsible for severe autoimmune disease expression.
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PMID:An autosomal recessive gene that delays expression of lupus in BXSB mice. 199 74

The lifetime prevalence of panic disorder in the United States is 1.5%; nearly 3 times that many Americans experience recurrent panic attacks. Both conditions are associated with diminished well-being, increased alcohol and drug abuse, suicide attempts, and financial dependency, at rates often exceeding those for other psychiatric disorders, including major depression. In spite of these considerable social consequences, panic disorder and panic attacks often go unrecognized. Because their symptoms can present as other medical disorders, including myocardial infarction, temporal lobe epilepsy, Cushing's disease, anemia, hypoglycemia, and lupus, these patients are instead often seen in emergency departments and cardiac and other medical clinics. General practitioners, and especially physicians working in emergency departments, should be alert to the possibility of panic disorder, especially if the patient has a first-degree family member suffering from panic disorder.
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PMID:The hidden patient: unrecognized panic disorder. 222 93

Between 1974 and 1988, 7 myocardial infarctions occurred in 6 (4 men, 2 women) out of 400 systemic lupus erythematosus patients. Their ages at the onset of lupus ranged from 13 to 44 years (m = 26). Four had renal involvement. Control of lupus in all 6 patients required high-dose steroids (at least 1 mg/kg/d of prednisone). Myocardial infarction occurred 4 to 19 years after the onset of lupus (m = 13). One patient died of cardiogenic shock. When the infarction occurred, only one patient was undergoing a lupus flare, while the disease was quiescent or slightly active in the 5 others. One patient had no risk factors for atheroma but had been taking steroids for 10 years. Among the other 4, one had hypertension, another had hyperlipidemia and 3 were smokers; they had been on steroids for 2, 4, 11 and 13 years. Coronary angiogram showed occlusion in all 4, but atheroma in only 2 patients. Lupus anticoagulant was present in 3 of these 4 patients. The mechanisms responsible for coronary occlusion in lupus patients are probably complex and interwoven. In addition to "classical" factors (i.e., vasculitis or steroid-induced atheroma), other factors, such as antiphospholipid antibodies and/or smoking, may play an important thrombogenic role.
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PMID:[Myocardial infarction in systemic lupus erythematosus. 7 cases in 6 patients]. 228 5

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.
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PMID:Prospective study of anticardiolipin antibodies in stroke. 230 7

Myocardial infarction has rarely been reported in patients with systemic lupus erythematosus but may develop late in the disease usually as a result of severe and accelerated atherosclerosis or coronary arteritis. A 32-year-old man with untreated and unrecognized systemic lupus erythematosus, in the absence of conventional coronary risk factors (except family predisposition) and definite extracardiac manifestations of systemic lupus erythematosus had a silent myocardial infarction early in the course of the disease. A coronary arteriogram revealed multiple stenosis of the left anterior descending artery and critical stenosis of the right coronary artery. It is our belief that lupus vasculitis is a likely contributing factor in the development of obstructive coronary disease in this patient.
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PMID:[Silent myocardial infarct as a main manifestation of systemic lupus erythematosus]. 232 60

Most patients with lupus anticoagulant (LA) activity have coincident antibodies to a group of negatively charged phospholipids, and its is suggested that LA and anticardiolipin tests detect antibodies with overlapping specificities. Some discordance between the two assays has been described, however. One patient presenting with severe thrombotic disease (recurrent deep vein thrombosis, pulmonary embolism, inferior venocaval obstruction, myocardial infarction, and digital gangrene) showed strong LA activity in February 1987. An enzyme linked immunosorbent assay (ELISA) showed no binding to the negatively charged phospholipids cardiolipin, phosphatidylserine, and phosphatidic acid, but binding to zwitterionic phosphatidylethanolamine (PE) was demonstrated. Inhibition studies and affinity purification confirmed this finding. Interestingly, the serum did not bind to the kaolin cephalin clotting time reagent when used as antigen in an ELISA. The pathogenic significance of anti-PE antibodies and their relation to LA remains to be clarified. Further studies of the occurrence of anti-PE antibodies in patients with LA activity who have negative anticardiolipin tests are suggested.
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PMID:Antibody to phosphatidylethanolamine in a patient with lupus anticoagulant and thrombosis. 249 57


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