Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anticardiolipin antibodies (ACA) and lupus-like anticoagulant (LLAC) have been studied in a group of 142 non-hospitalized and a group of 72 hospitalized HIV infected patients. We observed a variable frequency of ACA positivity ranging from 7.7% to 30.3% according to the groups of patients and the isotype of immunoglobulin fraction containing ACA activity. None of the patients investigated presented a prolongation of the activated partial thromboplastin time (APTT) compatible with the presence of a LLAC. Some patients presented a weak anticoagulant activity only detected by the tissue thromboplastin inhibition (TTI) test. No positive correlation was found between this latter test and ACA. We conclude that, like in syphilitic patients, ACA present in HIV infected patients are most often not associated with LLAC.
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PMID:Anticardiolipin antibodies (ACA) are most often not associated with lupus-like anticoagulant (LLAC) in human immunodeficiency virus (HIV) infection. 190 97

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

Eight cases with lupus anticoagulants (LA) were diagnosed over the last five years (1984-88). Of these, three were established cases of systemic lupus erythematosus (SLE), where bad obstetric history (2 cases) and recurrent deep venous thrombosis (DVT--1 case) prompted execution of laboratory tests for LA. In the remaining 5 cases, there was no clinical evidence of SLE. However, one case developed laboratory findings suggestive of SLE at a later date. One of these 5 patients was referred for unexplained abnormality in partial thromboplastin time (K). Three had recurrent abortions (one with additional history of DVT) while one had DVT with raised PTT (K). The clinical findings and laboratory tests by which lupus anticoagulants can be diagnosed have been discussed.
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PMID:Lupus anticoagulant. A report of 8 cases. 190 56

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

The significance of anticardiolipin antibodies and the lupus anticoagulant was studied in 58 consecutive patients with systemic lupus erythematosus. On 85 occasions serum IgG and IgM anticardiolipin antibodies were measured by an enzyme linked immunosorbent assay (ELISA), and simultaneous plasma samples tested for lupus anticoagulant activity. The most significant association with clinical events (previous thrombosis or thrombocytopenia occurring in 11/58 patients) was with prolonged tissue thromboplastin inhibition time (TTIT) followed by prolonged kaolin cephalin clotting time (KCCT) then raised IgG anticardiolipin antibody concentrations and dilute Russell's viper venom time. Although IgG anticardiolipin antibodies or KCCT were the most sensitive tests in identifying this group, the TTIT was the most specific (98%). Nine patients were IgG anticardiolipin antibody positive and lupus anticoagulant negative, of whom one had thrombocytopenia but none had thrombosis. The presence of a lupus anticoagulant in anticardiolipin antibody positive patients increases specificity for certain adverse clinical events.
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PMID:Lupus anticoagulant: clinical significance in anticardiolipin positive patients with systemic lupus erythematosus. 190 18

A 37-year-old man with acute myeloblastic leukemia (FAB M2) in first remission underwent a bone marrow transplant (BMT) following conditioning with high-dose cytarabine and total body irradiation. The donor was an HLA-identical brother. Graft rejection occurred and a second BMT was performed from the same donor following conditioning with cyclophosphamide. Engraftment was achieved, but the patient developed severe jaundice and died of respiratory failure on day +46 after the second BMT. Liver biopsy revealed luminal narrowing of the central veins and a diagnosis of hepatic veno-occlusive disease (VOD) was made. The coagulation studies showed a prolonged kaolin clotting time which was not corrected by 1:1 mixture with normal plasma, and the platelet neutralization test was positive. Dilute tissue thromboplastin time and dilute Russell viper venom time were also prolonged. These results fulfilled the criteria for lupus anticoagulant, which may have contributed to VOD in this patient.
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PMID:Hepatic veno-occlusive disease in a patient with lupus anticoagulant after allogeneic bone marrow transplantation. 193 57

Antiphospholipid antibodies have been associated with an increased risk of thromboses, most of which occur in veins. We observed a very unusual association of cerebral and renal thromboses, in 2 patients with systemic lupus and anti-prothrombinase, in whom arterial occlusions were clearly documented. Immunosuppressive treatment was followed by a dramatic improvement in both. In the literature, no treatment clearly prevents the recurrence of these thromboses. This could be partly explained by our current ignorance of their pathogeny.
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PMID:Cerebral and renal arterial thromboses in systemic lupus erythematosus with antiphospholipid antibodies: a report of two cases. 196 52

Antibodies against negatively charged phospholipids, such as those to cardiolipin, can often be detected in the serum of patients with autoimmune related conditions, chronic infections and in patients treated with phenothiazines. In the present study, peripheral blood lymphocytes from nine healthy controls and eight patients with phenothiazine-induced IgM anticardiolipin antibodies (ACA) and the lupus anticoagulant were placed in vitro. Culture supernatants were assayed for ACA by measurement of optical densities using an ELISA. A significant difference (p less than 0.05) was demonstrated between the mean concentration of culture supernatant ACA from the patients as compared to healthy controls. The concentration of ACA in culture supernatants strongly correlated (r = 0.85) with that from the serum. There was a weak correlation between serum and culture supernatant ACA concentration and the lupus anticoagulant activity as measured by prolongation of the partial thromboplastin time. This technique uses readily accessible peripheral blood lymphocytes and should permit dissection of cytokine and cellular immune pathways regulating APA production.
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PMID:Production of anticardiolipin antibodies by cultured human lymphocytes. 196 31

Ninety-seven psychiatric patients who have been treated with the antipsychotic drug chlorpromazine or another phenothiazine have been investigated for the presence of antiphospholipid antibodies. A variety of coagulation studies and specific antiphospholipid immunoassays were performed to define the spectrum of antigen specificity of these antibodies. Coagulation studies showed an increasing sensitivity for the lupus anticoagulant with reagents of differing phospholipid content. Prolonged activated partial thromboplastin times (APTTs) were found in five patients with the use of an insensitive APTT reagent and in 14 patients with a lower phospholipid content reagent. In every case, attempted correction of the clotting time with normal plasma was unsuccessful. Twenty-one patients had abnormal kaolin clotting time profiles. In seven of these patients, test results with both APTT reagents had been normal. Antibody reactivity was tested against three negatively charged phospholipids, phosphatidyl-serine, cardiolipin, and phosphatidylinositol. Only five patients demonstrated reactivity against phosphatidylinositol, whereas high antibody titers were observed in 28 patients against one or both of phosphatidylserine and cardiolipin. Twenty-three of these patients were found to have elevated anticardiolipin-specific IgM antibodies. Overall, 41 of the patients had at least one laboratory abnormality suggestive of antiphospholipid antibody activity. Seven of the 26 patients, taking phenothiazines other than chlorpromazine, had positive test results for antiphospholipid antibodies. No clinical thromboembolic events were recorded in any patient. These findings demonstrate the heterogeneity of antiphospholipid antibody specificity induced in patients treated with various phenothiazine drugs and indicate that none of these patterns of reactivity marks a predisposition for thromboembolism in this population.
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PMID:Heterogeneity of laboratory test results for antiphospholipid antibodies in patients treated with chlorpromazine and other phenothiazines. 197 39

The primary anti-phospholipid syndrome is characterized by recurrent venous and arterial thromboembolic phenomena, recurrent fetal loss, thrombocytopenia, and serological evidence of anti-cardiolipin (aCL) antibodies or/and the presence of lupus anticoagulant (prolonged activated partial thromboplastin time). The exact role of aCL antibodies in pathogenesis is not clear and the mechanism by which the antibodies may induce the various manifestations is unknown. In the current study we evaluated the effect of passive transfer of aCL antibodies (to the tail vein of naive mice) on fecundity, fetal loss (fetal resorption), and the weight of embryos and placentae. Two types of aCL antibodies were employed: (i) mouse monoclonal aCL antibodies derived from a BALB/c mouse in which experimental systemic lupus erythematosus was induced by a pathogenic idiotype (idiotype 16/6) of anti-DNA antibodies and (ii) polyclonal IgG and IgM aCL antibodies derived from serum of a patient with primary anti-phospholipid syndrome. After infusion of either antibody (10 micrograms per mouse) we could demonstrate lower fecundity rate, increased resorption index of embryos (equivalent to recurrent fetal loss), lower number of embryos per pregnancy, and lower mean weights of embryos and placentae in comparison to mice infused with appropriate control immunoglobulins. We conclude that the aCL antibodies may have direct effects on fecundity and on the outcome of pregnancy.
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PMID:Induction of anti-phospholipid syndrome in naive mice with mouse lupus monoclonal and human polyclonal anti-cardiolipin antibodies. 201 26


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