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)

An 11-year-old boy developed florid choreic movements in his right extremities after having had an episode of febrile illness. He was evaluated at our hospital where MRI disclosed a honeycomb-like low signal intensity area rimmed by a thin Gd-enhanced layer in the left putamen. Arteriography revealed the lenticulostriate arteries being segmentally narrowed and a "ground glass" staining was observed in the left putamen in late venous phase. Sydenham's chorea, that had been the initial impression, was not substantiated because of negative pharyngeal culture for streptococci, negative ASLO/ASK titers and because of lack of clinical stigmata of rheumatic fever. However, prothrombin time was prolonged, and activated partial thromboplastin time (APTT), that had been also prolonged, was not normalized by adding healthy serum, indicating the presence of lupus anticoagulant. VDRL was false positive and anticardiolipin antibodies, both IgM and IgG classes, were also detected. However, systemic lupus erythematosus was unlikely in view of negative antinuclear antibody and LE phenomenon. He deteriorated rapidly due to development of severe bilateral chorea, thereby he was unable to walk or feed himself. He received a 3-day course of mega-dose intravenous methylprednisolone, that temporarily lessened the chorea, but soon it became worse. A second course of mega-dose methylprednisolone was given, followed by daily maintenance dose of prednisolone. His chorea gradually improved in severity and after 2 months only a trace of choreic movements was detected in his hands. He has been followed at our outpatient clinic where he no longer shows chorea and the APTT has improved to nearly normal time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of chorea as a sole presentation of primary anti-phospholipid antibody syndrome]. 181 92

Fifty patients with systemic lupus erythematosus were studied for the presence of lupus anticoagulant using three different assays--kaolin clotting time, platelet neutralization test, and tissue thromboplastin inhibition test. Lupus anticoagulant could be detected in seven cases (14%) with the use of one test in cases with a partial prothrombin time with kaolin more than five seconds greater than normal. The detection rate rose to 20% (10 cases) when using all three tests, so a panel of three assays could identify lupus patients apparently at risk for thrombotic complications.
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PMID:Assays for lupus anticoagulant: the sensitivity of different assays. 190 73

An iliac crest bone marrow aspiration in a 24-year-old man was followed by severe haemorrhage into the iliopsoas muscle. A lupus anticoagulant and severe hypoprothrombinaemia, as well as clinical and laboratory pointers to suggest the presence of a systemic lupus erythematosus-like syndrome, were demonstrated. Therapy with prednisone was commenced following recurrent severe epistaxis. His prothrombin time, activated partial thromboplastin time and prothrombin activity improved promptly and his bleeding ceased. The lupus anticoagulant is commonly encountered in the laboratory, but acquired hypoprothrombinaemia is extremely rare. The condition is reviewed and its treatment discussed.
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PMID:Acquired hypoprothrombinaemia and lupus anticoagulant: response to steroid therapy. 190 19

We report the case of a patient with SLE who had repeated ulceration of the small intestine requiring emergency surgery. Pathologic examination revealed microthrombosis and vasculitis at the site of the intestinal ulcers. High levels of antiphospholipid antibodies, thrombocytopenia, and prolonged prothrombin time coincided with the episodes of intestinal ulceration. Antiphospholipid antibodies may be involved in the development of thrombosis resulting in the repeated episodes of intestinal ulceration in this patient. This possibility should be considered in patients with SLE who have intestinal ulceration and appropriate antithrombotic medication should be administered.
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PMID:Repeated intestinal ulcerations in a patient with systemic lupus erythematosus and high serum antiphospholipid antibody levels. 201 44

We have identified an inhibitor of the protein C anticoagulant pathway in the plasma of a patient with systemic lupus erythematosus and a history of recurrent deep vein thrombosis, fetal wastage, and seizures. The patient's plasma contained anticardiolipin antibodies as well as a weak lupus anticoagulant. Examination of this patient's plasma revealed normal levels of protein C and protein S antigen, normal levels of functional protein C, as well as essentially normal levels of every blood coagulation factor. In a modified prothrombin time assay, the activated protein C-mediated prolongation of the clotting time observed in normal plasma was not observed in this patient's plasma. Gel permeation chromatography of the patient's plasma revealed that the inhibitory material was a high molecular weight protein that coeluted with the IgM peak. The inhibitor did not appear to circulate as a complex with protein C, since the inhibitor could easily be separated from protein C during fractionation procedures, and did not interfere with the activation of protein C in plasma as assessed by a functional amidolytic assay. Our findings suggest that the recurrent thrombotic episodes observed in this patient may have occurred as a result of the patient's antiphospholipid antibody neutralizing specific phospholipids essential for the full expression of the anticoagulant activity of activated protein C.
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PMID:Impairment of the protein C anticoagulant pathway in a patient with systemic lupus erythematosus, anticardiolipin antibodies and thrombosis. 210 91

The patient is a 23 y.o. man with acute nephritis and bleeding at presentation. Laboratory data consistent with the diagnosis of systemic lupus erythematosus. A lupus anticoagulant was found: tissue thromboplastin inhibition test (TTIT) ratio 3.4; diluted Russell viper venom (DRVV) ratio 2.6. Hypoprothrombinemia (FII:C less than 1%; FIIR:Ag 5%) was present; prothrombin survival time (FII concentrate infusion 60 U/kg): t1/2 approximately to 9 hours. A prothrombin antibody was identified: it is not neutralizing but forms an immunecomplex with prothrombin. The antibody was characterized as IgG2, IgA, k, lambda. The prothrombin survival time indicates that the hypoprothrombinemia is due to the clearance of the prothrombin-antiprothrombin complex in vivo.
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PMID:Prothrombin-antibody coexistent with lupus anticoagulant (LA): clinical study and immunochemical characterization. 210 92

The lupus anticoagulant is an antiphospholipid antibody found in association with systemic lupus erythematosus and in a variety of other diseases, as well as in healthy individuals. In the laboratory, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis, mainly of the larger veins and arteries. The case of a young woman who developed superficial migratory thrombophlebitis in association with a high titer lupus anticoagulant is presented. Her diagnosis was initially missed because the partial thromboplastin time was not elevated. This appears to have resulted from the use of a specific thromboplastin relatively insensitive to the presence of the antibody. Retesting with a more sensitive reagent showed a markedly prolonged partial thromboplastin time.
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PMID:Superficial migratory thrombophlebitis and the lupus anticoagulant. 211 May 53

Lupus anticoagulant was determined in lupus erythematosus as an antibody inhibiting prothrombin activation in phospholipid coagulation tests without specific suppression of any coagulation factors. The available information concerning properties and mechanisms of action of lupus anticoagulant are rather controversial as there exist a group of similar coagulation inhibitors that represent antiphospholipid antibodies. In spite of a considerable increase of a coagulation test time prothrombin time, partial thromboplastin time, the presence of the lupus anticoagulant is rarely followed by haemorrhagic diathesis. On the contrary, recurring thromboembolic complications, pathology of gestation are observed in patients with this or other antibodies against phospholipids. The appearance of the antiphospholipid antibodies is described in infections, haematological processes, systemic vasculitis, tumours, may be provoked by a long use of some medicinal preparations. Circulation of the lupus coagulant and other antibodies against phospholipids is of a chronic type while in infections diseases it is of an acute transitory character.
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PMID:[The antiphospholipid antibody syndrome: its pathogenesis and clinico-morphological manifestations]. 211 34

A 42-year-old Mexican migrant laborer with a previous history of neurofibromatosis presented with a stuffy nose and chronic ulceration of his soft palate. Multiple subcutaneous nodules were found on his skin, and laboratory investigation revealed an elevated activated partial thromboplastin time (APTT). Further laboratory evaluation showed a lupus-like circulating anticoagulant deemed IgM by quantitative immunoglobulin studies. Although coagulation defects in lepromatous leprosy are rare, the preoperative preparation of a patient with leprosy may require a screening prothrombin time (PT), APTT and platelet count. Abnormalities in these values may indicate the need for specific factor assays and a search for circulating anticoagulant.
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PMID:An unusual case of Hansen's disease (lepromatous leprosy) with circulating anticoagulant and macroglobulinemia. 211 10

A 56-year-old woman with autoimmune hyperthyroidism (Basedow) whose blood coagulation had at first been normal developed prolonged partial thromboplastin time (PTT) of 48 s and a fall in prothrombin time (Quick value) to 52%. At the same time, total activity of factor VIII was reduced to 18% and factor IX to 16%. These values not having changed after the addition of normal plasma, it is assumed that an acquired inhibitor of plasmatic coagulation was responsible. Such inhibitors were first described in lupus erythematodes and therefore called lupus anticoagulant, but later also demonstrated in other autoimmune diseases.
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PMID:["Lupus anticoagulant" in immune hyperthyroidism]. 190 Apr 65


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