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)

We utilized a kaolin-activated partial thromboplastin time (APTT) using rabbit brain phospholipid, in which the capacity of a fourfold increased "high" phospholipid concentration (PC) to normalize the abnormal "standard" PC-APTT in patients with lupus anticoagulants is assessed. This system was also used to measure factors VIIIC, IX, and XI. The tissue thromboplastin inhibition test (TTI), a prothrombin time system in which the activity of a lupus anticoagulant is unmasked by the use of dilute thromboplastin, was simultaneously evaluated. Test sensitivity was defined by results on 31 consecutive patients with standard PC-APTT inhibitors and no bleeding tendency. Specificity was based on 94 patients with various other coagulopathies, including coagulation factor inhibitors, severe congenital factor deficiencies, hepatic insufficiency, and warfarin and heparin treatment. Twenty-one patients with lupus erythematosus and standard PC-APTT results within normal limits were also tested. Sensitivity of the APTT system was superior to that of the TTI (97% v 58%); high PC normalized clotting time ratios and factor levels. Positive results were common with both assays in the group of 20 heparinized patients. The APTT system had superior specificity in remaining cases; there were no positive tests among 74 patients. The lupus erythematosus group had a significant decrease in the clotting time ratio with high PC, indicating that low-level lupus anticoagulants are quite prevalent in this group. The kaolin clotting time using rabbit brain phospholipid in standard and high concentrations is a simple, sensitive, and specific technique for diagnosis of lupus anticoagulants.
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PMID:Lupus anticoagulants: improved diagnosis with a kaolin clotting time using rabbit brain phospholipid in standard and high concentrations. 373 Jun 11

Potent lupus inhibitors from various patients were mixed with platelet free normal plasma and were compared in activated partial thromboplastin time (APTT), dilute prothrombin time (dil. PT), kaolin clotting time (KCT), contact product clotting time (CPCT), and Russell viper venom clotting time (RVVCT) tests. In the last three tests platelets and platelet lipid substitutes were avoided to enhance the sensitivities of these tests for the lupus anticoagulant. Correlations between the KCT and the other tests were mostly good, indicating that different lupus inhibitors functioned by a similar mechanism. There was no significant trend between particular clinical symptoms and individual coagulation test combinations. The KCT was found to be the most sensitive test for the lupus inhibitor, followed by the CPCT, RVVCT, dil. PT and APTT tests. Activated platelets tended to correct the APTT lupus inhibitor defect in all except the strongest inhibitor cases.
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PMID:Similar mechanism of various lupus anticoagulants. 392 78

To define clinical and laboratory characteristics of the lupus anticoagulant (LA), we reviewed our experience (219 subjects). Subjects were divided into group A, those with the LA and the diagnosis of lupus erythematosus, group B, those with the LA but nonlupus diagnoses, and group C, those with drug-related lupus syndromes. The typical laboratory findings consisted of a prolonged and inhibited plasma clot time (an average of 1.9 times control time) which was proportionately more prolonged than the partial thromboplastin time or activated partial thromboplastin time (APTT) (average 1.3 times control). Ninety-eight percent had a prolonged plasma clot time and 94% had a prolonged partial thromboplastin time. The prothrombin and thrombin times were prolonged in 33 and 25% of subjects, respectively. Washed platelets shortened the APTT in the 22 subjects so tested. Monoclonal protein peaks were seen in 7% of patients. Seventeen episodes of bleeding were observed, but in all but one instance there was another hemostatic defect present. In the 18 patients who underwent major operations, there were no hemorrhagic complications. Fifty-eight episodes of thrombosis were observed with the same incidence in group A (25%) as in group B (26%). Bleeding is rare with the LA but thrombosis is common even without SLE and lupuslike syndromes. The plasma clot time in platelet-rich plasma is more prolonged, and in our experience, is more sensitive in detecting the lupus anticoagulant than is the partial thromboplastin time.
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PMID:Lupus anticoagulant: an analysis of the clinical and laboratory features of 219 cases. 392 59

Clinical and laboratory experience with circulating lupus anticoagulant in 3 patients undergoing coronary artery bypass procedures is reported. This circulatory anticoagulant inhibits activation of prothrombin by the prothrombin activator complex (factor Xa, factor V, and phospholipid). The presence of lupus anticoagulant was initially detected because of a prolonged activated partial thromboplastin time and a normal or mildly prolonged prothrombin time. The 3 patients underwent uncomplicated coronary artery bypass grafting and experienced no abnormal bleeding postoperatively. The lupus anticoagulant is a rare cause of bleeding after open-heart surgery. It appears to be a problem only when an additional coagulation defect is present.
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PMID:Coronary bypass surgery in patients with circulating lupus anticoagulant. 392 5

Approximately 2% of the patients screened in our laboratories with activated partial thromboplastin times are found to have a lupus anticoagulant. Recognition of lupus anticoagulants has assumed new importance because of a number of associated clinical conditions. Recurrent spontaneous abortions, arterial and venous thrombotic disease, and polyneuropathy have been described in patients with lupus anticoagulants. Although the clinical heterogeneity of these patients has been recognized increasingly, the laboratory identification of the lupus anticoagulant is still confusing and frustrating. In many cases, the diagnosis of this inhibitor is one of exclusion following a series of ambiguous mixing studies and variable factor assays. We studied ten patients with atypical laboratory results. Of particular significance are patients with a time-dependent enhancement of the lupus anticoagulant effect and patients with lupus anticoagulants that manifest a preferential inhibition of the prothrombin time rather than the activated partial thromboplastin time. We also confirmed the sensitivity of the platelet neutralization procedure in the identification of the lupus anticoagulant.
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PMID:The laboratory heterogeneity of lupus anticoagulants. 392 47

25 patients with lupus anticoagulant (LA) and a history of thrombosis are described and the cases reported in the literature with this association are reviewed. From the combined data it is concluded that the prevalence of thrombosis in patients with LA is about 30%, the thrombosis sites are the leg veins in about 66%, the cerebral arteries in 25% and the peripheral arteries in 10% of the patients. High anticardiolipin levels are associated with a higher risk, while age of less than 10 years, low prothrombin activity and a platelet count of less than 50,000/microliter is associated with a lower risk of thrombosis. Heparin and oral anticoagulants are effective in the treatment and prevention of thrombosis without untoward risk of bleeding.
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PMID:Lupus anticoagulants and thrombosis. A study of 25 cases and review of the literature. 393 Mar 50

A patient developed bleeding due to an acute acquired specific prothrombin deficiency. Unlike previously described patients, this patient had no evidence of an associated lupus anticoagulant. Prothrombin activity and antigen were decreased concordantly and the patient's plasma did not neutralize the activity of added prothrombin or interfere with its measurement by electroimmunoassay. Nevertheless, immunoelectrophoresis and experiments using 125I-prothrombin revealed a prothrombin-binding antibody. The residual prothrombin in the patient's plasma was in the form of a prothrombin-antibody complex. Administration of adrenal corticosteroids was associated with a rise in prothrombin activity and cessation of bleeding, but circulating prothrombin was still bound to the antibody. This suggests that non-neutralizing antibodies to prothrombin cause plasma prothrombin deficiency because of a rapid clearance of prothrombin-antibody complexes, which is slowed by adrenal corticosteroids. The antibody had a relatively low affinity for prothrombin (Kd 5 to 8 X 10(-7)) and was transient. It is possible, therefore, that the antibody arose not to prothrombin itself, but to an antigen sharing an epitope with prothrombin.
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PMID:Acquired hypoprothrombinemia due to non-neutralizing antibodies to prothrombin: mechanism and management. 399 83

Monocyte infiltration and activation of the coagulation system have been implicated in the pathophysiology of glomerulonephritis. In this study, spontaneous procoagulant activity (PCA) was measured in circulating mononuclear cells to determine whether elevated PCA correlated with the presence of proliferative glomerulonephritis in patients with systemic lupus erythematosus (SLE). No increase in PCA was found in 20 patients with end-stage renal failure, 8 patients with glomerulonephritis without SLE, and 10 patients undergoing abdominal surgical or orthopedic procedures as compared with 20 normal controls. In eight patients with SLE but with no apparent active renal disease, PCA was not elevated above normal basal levels. Seven additional patients with SLE who had only mesangial proliferation on biopsy also had no increase in PCA. In contrast, eight patients with focal or diffuse proliferative lupus nephritis, and one patient with membranous nephritis who ultimately developed a proliferative lesion, had a marked increase in PCA with greater than 100 times the base-line levels. The activity was shown to originate in the monocyte fraction of the mononuclear cells and was shown to be capable of cleaving prothrombin directly. The prothrombinase activity was not Factor Xa, because it was not neutralized by anti-Factor X serum and was not inhibited by an established panel of Factor Xa inhibitors. Monocyte plasminogen activator determinations did not correlate with renal disease activity. We conclude that monocyte procoagulant activity, a direct prothrombinase, seems to correlate with endocapillary proliferation in lupus nephritis and could be a mediator of tissue injury.
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PMID:Monocyte procoagulant activity in glomerulonephritis associated with systemic lupus erythematosus. 403 82

Circulating anticoagulant activity that had at least two distinct mechanisms--one directed against factor XII and one directed against blood thromboplastin (prothrombin activator complex)--developed in a patient with clinical and laboratory evidence of procainamide hydrochloride-induced systemic lupus erythematosus. The anticoagulant activity behaved as a gamma-globulin in chromatographic and electrophoretic analyses, with the majority of activity behaving as an IgM immunoglobulin. Despite markedly abnormal coagulation study results, no clinical bleeding occurred. Anticoagulant activity paralleled clinical and laboratory evidence of the inflammatory disease and improved on discontinuance of procainamide therapy.
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PMID:Studies on a circulating anticoagulant in procainamide-induced lupus erythematosus. 617 Dec 18

Antibodies that bind prothrombin without neutralizing its coagulant activity were demonstrated in the plasma of two patients with the acquired hypoprothrombinemia-lupus anticoagulant syndrome. The first patient's plasma contained less than 1% prothrombin activity and no detectable prothrombin antigen. The second patient's plasma contained about 6% of both prothrombin activity and antigen. Neither patient's plasma neutralized the prothrombin coagulant activity of normal plasma or of purified prothrombin added in vitro. Nevertheless, double immunodiffusion studies and binding experiments utilizing 125I-prothrombin demonstrated the presence of prothrombin antibodies in each patient's plasma. A Scatchard analysis of the binding data obtained with different concentrations of 125I-prothrombin and the first patient's plasma indicated the presence of a high affinity antibody, apparent Kd approximately 10(-10)M, and a lower affinity antibody, apparent Kd approximately 10(-9)M. Studies utilizing purified cleavage products of prothrombin suggested that the antibodies were directed against an epitope or epitopes located on the carboxyl-terminal, latent thrombin segment of the prothrombin molecule. We postulate that the acquired hypoprothrombinemia in these two patients and in other reported patients with the acquired hypoprothrombinemia-lupus anticoagulant syndrome stems from rapid clearance from the circulation of prothrombin antigen-antibody complexes.
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PMID:A mechanism for the hypoprothrombinemia of the acquired hypoprothrombinemia-lupus anticoagulant syndrome. 640 77


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