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 woman with a history of polyarthralgias appeared to develop systemic lupus erythematosus and lymphoma simultaneously. The diagnosis of the concurrent lymphoma was made on biopsy of a left axillary lymph node. Generalized lymphadenopathy, splenomegaly and pruritus had given rise to suspicion of an underlying lymphoma. The lymphoma responded well to chemotherapy. Her condition was further complicated by an arterial occlusion involving the right 2nd toe which was eventually amputated, transient ischemic attacks (amaurosis fugax), livedo reticularis and thrombocytopenia which were accompanied by elevations of IgM anticardiolipin antibodies and a biological false test for syphilis. The lupus anticoagulant test was not performed as she was given anticoagulation therapy.
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PMID:Systemic lupus erythematosus and lymphoma: association with antiphospholipid syndrome. 202 23

This report illustrates the importance of serologic techniques for defining the etiology of neonatal thrombocytopenia. In Case 1 the maternal count was low normal to normal during the first postpartum week. Several weeks later the appearance of persistent maternal thrombocytopenia led to the demonstration of anti-GP IIb-IIIa in stored and freshly obtained maternal sera, suggesting that the mother had an autoimmune type of thrombocytopenia. The mother of Case 2 had systemic lupus erythematosus. However, serologic testing revealed that the infant's thrombocytopenia was not related to the mother's lupus but was secondary to alloimmunization with the PlA1 antigen. An algorithm for defining etiologic mechanisms in infants with antibody-mediated forms of thrombocytopenia is presented.
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PMID:Importance of platelet serologic testing for defining the cause of neonatal thrombocytopenia. 202 82

In order to detect diagnostic clues to identify patients with chronic immune thrombocytopenia which is likely to develop systemic lupus erythematosus (SLE), a retrospective study was conducted. Of 39 patients with chronic immune thrombocytopenia, 4 fulfilled the diagnostic criteria being between 4.5 and 14 years after the initial diagnosis of "idiopathic" thrombocytopenic purpura. The remaining 35 patients were found to be idiopathic thrombocytopenic purpura (ITP) after at least a 5-year follow-up. It was noted that in patients with SLE who had thrombocytopenia at presentation, only 4 or 5 findings of diagnostic criteria were observed. Of particular interest, all patients who developed SLE were positive for anti-SS-A antibody, in contrast none of the patients with ITP had this antibody. Furthermore, despite the few clinical manifestations, we noted lupus peritonitis in 1 patient and pulmonary hypertension in another patient. In conclusion, the anti-SS-A antibody is an excellent clue for the early detection of SLE occurring as "idiopathic" thrombocytopenic purpura.
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PMID:Thrombocytopenia subsequently develops systemic lupus erythematosus--can anti-SS-A antibody predict the next event? 208 72

We studied the sera of 36 patients with lupus anticoagulant and IgG antibodies against both phosphatidylserine and cardiolipin. Most sera also had IgG antibodies against other phospholipids: 97% against phosphatidylinositol, 91% against phosphatidylglycerol, and 82% against phosphatidylethanolamine. IgG2 was the predominant subclass against cardiolipin and phosphatidylserine; 35 of 36 patients (98%) had IgG2 against both phospholipids. Most patients also had the IgG1 subclass; 32 of 36 (89%) against cardiolipin and 25 of 36 (69%) against phosphatidylserine. IgG3 and IgG4 subclasses were present at very low concentrations and in only a minority of the sera. The antibody response against phosphatidylserine was characterized by significantly less IgG1 than was the response against cardiolipin (P less than 0.01), although the IgG2 responses against each phospholipid were not different. IgG subclasses were unrelated to any other aspect of the patients' history, including a history of thrombocytopenia or thrombosis, a positive antinuclear antibody test, or a diagnosis of systemic lupus erythematosus.
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PMID:IgG1 and IgG2 are the predominant subclasses of antiphospholipid antibody in women with the lupus anticoagulant. 210 89

A 37 year-old female was admitted to our hospital because of hypermenorrhea, prolonged bleeding time, thrombocytopenia and the diagnosis of idiopathic thrombocytopenic purpura (ITP) was made. Though activated partial thromboplastin time (APTT) was markedly prolonged, her coagulation factors were within normal ranges. Activities of the circulating lupus anticoagulant (LAC) was suggested. Kaolin clotting time of the platelet poor plasma was used as a sensitive screening test using the mixture of normal and patient's plasma for the detect of LAC. As a result, LAC positive pattern was observed. The treatment with high-dose gammaglobulin brought out a transient increase of the platelet count, but the prolongation of APTT was not corrected. Both the platelet count and the prolongation of APTT were significantly improved after the treatment with betamethasone.
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PMID:[Idiopathic thrombocytopenic purpura complicated with circulating lupus anticoagulant]. 210 46

A prospective study of IgG and IgM isotypes of anticardiolipin antibodies (aCL) in a series of 100 patients with systemic lupus erythematosus was carried out. To determine the normal range of both isotype titres a group of 100 normal control serum samples was studied and a log-normal distribution of IgG and IgM isotypes was found. The IgG anticardiolipin antibody serum was regarded as positive if a binding index greater than 2.85 (SD 3.77) was detected and a binding index greater than 4.07 (3.90) was defined as positive for IgM anticardiolipin antibody. Twenty four patients were positive for IgG aCL, 20 for IgM aCL, and 36 for IgG or IgM aCL, or both. IgG aCL were found to have a significant association with thrombosis and thrombocytopenia, and IgM aCL with haemolytic anaemia and neutropenia. Specificity and predictive value for these clinical manifestations increased at moderate and high anticardiolipin antibody titres. In addition, a significant association was found between aCL and the presence of lupus anticoagulant. Identification of these differences in the anticardiolipin antibody isotype associations may improve the clinical usefulness of these tests, and this study confirms the good specificity and predictive value of the anticardiolipin antibody titre for these clinical manifestations.
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PMID:Isotype distribution of anticardiolipin antibodies in systemic lupus erythematosus: prospective analysis of a series of 100 patients. 210 99

71 patients with systemic lupus erythematosus (SLE) were studied for the occurrence of platelet antibodies by immunoblotting. Binding of IgG antibodies to platelet protein antigens was observed in 39 of the 71 patients. The most frequently detected and exceptionally strongly reacting antibodies were directed against platelet protein antigens with an approximate molecular weight of 65 kDa under nonreducing conditions. These antibodies were autoreactive and, when followed, they usually persisted. Interestingly, in this group of well-defined SLE patients, platelet antibodies against the most common targets (65 kDa) were significantly associated with the lupus anticoagulant, a history of thrombocytopenia and thrombosis, particularly with arterial occlusions. The lupus anticoagulant, on the other hand, correlated significantly only with venous thrombosis. In addition to the lupus anticoagulant, platelet antibodies against this unknown platelet protein may thus be a marker of a higher risk of thrombosis in SLE patients.
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PMID:Platelet autoantibodies detected by immunoblotting in systemic lupus erythematosus: association with the lupus anticoagulant, and with history of thrombosis and thrombocytopenia. 211 79

Both lupus anticoagulant and anticardiolipin antibody are groups of antiphospholipid antibodies associated with high frequency of thrombosis, fetal loss and thrombocytopenia. The hall marks of their identification is the prolongation of phospholipid-dependant coagulation tests. Much is written in literature about the successful management of lupus anticoagulant during pregnancy, via corticosteroid and acetyl salicylic acid (Aspirin) therapy; however, up to now only little has been mentioned about maternal and fetal complications associating lupus anticoagulant and its management. Here we present three cases with significant complications among patients with lupus anticoagulant managed in Sint Augustinus Hospital over the last 3 years. These complications were secondary to antiphospholipid syndrome or to therapy. Maternal complications included gastritis, atrophy of quadriceps muscle, resistant premature contractions and pre-eclampsia. One of our patients developed small lymphocytic lymphoma 1 year after her last labour. Fetal complications included: prematurity, suprarenal insufficiency (temporary) and delayed neuromuscular development found at the 2 year follow-up. As far as we know, some of these complications have never been mentioned in literature.
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PMID:Maternal and fetal complications associating lupus anticoagulant and its management; three case reports. 211 27

Twenty-one patients with anti-phospholipid antibodies (APLA), who were selected from 104 patients with antinuclear antibody or anti-DNA antibody, were studied to define clinical characteristics of APLA. Of the 21 patients, the incidences of IgG anti-cardiolipin antibody (ACA), IgM ACA, lupus anticoagulant (LAC) and BFP-STS were 20, 7, 11 and 12, respectively, and they were highly related with each other. The number of items of the 1982 ARA revised criteria for the classification of SLE was significantly low (mean value = 3.3), and also the level of serum C 4 was significantly high (mean value = 88% of normal) compared with those in patients without APLA. The incidence of thrombocytopenia and hemolysis was significantly high when compared with those in patients without APLA, and they were closely related to the presence of LAC. The incidence of thrombosis was markedly high (48%), 10 of 21 patients, especially those of cerebral infarction and deep vein thrombosis. Cerebral infarction was significantly associated with LAC. The obstetric complication was 4 of 13 patients (31%) in the incidence, which was significantly high compared with that in patients without APLA. Of them, natural abortion was closely associated with LAC. Based on these observations, it seems that autoimmunological disease activity in patients with APLA may be slight to mild, and strongly suggested that APLA may play an important role particularly in the pathogenesis of acquired thrombotic tendency.
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PMID:[Clinical characteristics of anti-phospholipid antibodies]. 211 74

Patients with systemic lupus erythematosus often develop thrombosis, recurrent abortion, thrombocytopenia and neurological disease, in association with serum antibodies against phospholipids, termed the secondary antiphospholipid syndrome. In our search for an animal model for the human antiphospholipid syndrome, we examined the MRL-1pr/pr mouse, which develops a lupus-like illness. These mice were found to have significantly elevated levels of serum antiphospholipid antibodies (aPL) and thrombocytopenia compared to normal mice. By immunodiffusion, these antibodies are similar to human aPL. We observed histologic evidence of central nervous system thromboses as well as perivascular infiltrates of the choroid plexus. The high titers of serum aPL, thrombocytopenia, and thrombosis establish this strain as an animal model for the secondary antiphospholipid syndrome.
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PMID:Autoimmune MRL-1 pr/1pr mice are an animal model for the secondary antiphospholipid syndrome. 212 Apr 36


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