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A young man presenting with recurrent deep venous thrombosis was found to have a lupus type coagulation inhibitor. He showed neither clinical nor serological evidence of systemic lupus. The value of the Russell viper venom coagulation time in the detection of the inhibitor is demonstrated. Anticoagulant therapy has not caused any bleeding complication despite the presence of the inhibitor.
Familial cases of lupus anticoagulant were rarely described. We report the observation of two sisters with lupus anticoagulant, one with thrombocytopenic purpura and the other with systemic lupus erythematosus.
Plasma from a patient with early manifestations of disseminated lupus erythematosus, a prolonged partial thromboplastin time with kaolin, mildly prolonged prothrombin time, and a circulating inhibitor affecting the assay of several clotting factors was investigated. The most sensitive test for the inhibitor was found to be the Russell viper venom time without phospholipid. A decrease in phospholipid concentration as well as decreased sodium chloride levels both significantly enhanced the effect of the inhibitor in several coagulation tests. Of various phospholipid substitutes tested phosphatidyl ethanolamine was the most effective in partially correcting for the inhibitor. The inhibitor was not localized to the patient's platelets, which were also found to partially neutralize its effect. Since lupus erythematosus is sometimes accompanied by thrombocytopenia the coagulation disorder may be aggravated by such a deficiency of phospholipid. The inhibitor appears to act by preventing binding of phospholipid to the Xa/V/thromboplastin complex. It was characterized as a gamma globulin of mixed class.
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We studied the natural inhibitors (NI) of blood coagulation and fibrinolysis in 50 patients with lupus anticoagulant (LA), in order to identify possible alterations of these NI, that could favour thrombotic manifestations. We found no statistically significant difference in antithrombin III, protein C and alpha 2-antiplasmin between controls and patients with LA, irrespective of their clinical manifestations. We found an increase of plasminogen activator inhibitor (PAI, P < 0.001) and a decrease of free protein S (PSf, P < 0.001) and total protein S (PSt, 0.01 < P < 0.05) in the patients with LA when compared with the control group. We found no difference in the levels of NI between patients with thrombosis (n = 19) and without thrombosis (n = 31) nor between patients with (n = 25) or without thrombosis and/or foetal loss (n = 25). In contrast, we observed a decrease of PSf in women with foetal loss (n = 10) as compared with women without foetal loss (n = 22, 0.01 < P < 0.05) and a decrease of PSf when comparing 19 patients with systemic lupus erythematosus (SLE) with 31 patients without SLE (0.01 < P < 0.05). These findings show that the patients with LA had several abnormalities in the NI system, but there was no significant association between levels of PAI, PSf, PSt and a history of thrombosis.
Sciatic nerve palsy is an uncommon complication of cardiac surgery and is thought to be induced by a combination of reduced femoral artery blood flow, small vessel vascular disease or prolonged hypoxia. We here describe a new case which is the first described with transient elevation of antiphospholipid antibodies. Although transient elevation of lupus coagulation inhibitor is known to occur frequently in patients treated in an intensive care unit, there are very few data about the possible role of antiphospholipid antibodies in the generation of ischemic neuropathies. We can not prove that the ischemic neuropathy in our case has been favored by the presence of lupus coagulation inhibitor and antiphospholipid antibodies as the occurrence of the symptoms seemed to precede the transient elevation of lupus coagulation inhibitor. This case suggests that antiphospholipid antibodies and lupus coagulation inhibitor should be included in the work up of patients who present nerve damage after cardiac surgery but further studies are needed to ascertain this association.
Antiphospholipid antibodies(APA) have been reported to be a heterogeneous family of immunoglobulins. Some APA can be detected via phospholipid dependent coagulation assays when they present as an aspecific coagulation inhibitor, lupus anticoagulant(LA), other antibodies can be measured via immunological assays mostly via their capability to bind to immobilized cardiolipin (anticardiolipin antibody; aCL). Despite their name, APA associated with antiphospholipid syndrome(APS) do not bind phospholipids, but are directed at plasma proteins bound with anionic phospholipids. The antigenic targets of these antibodies include beta 2 glycoprotein I(beta 2 GP I), prothrombin, high- and low-molecular-weight kininogens, annexin V, protein C and protein S. In this article, the current knowledge on the methods of detection and their functional properties are reviewed, and the interaction of these antibodies and acquired activated protein C resistance are discussed.
A variety of immune phenomena have been associated with chlorpromazine. One such factor, the lupus-like anticoagulant, while nonspecific, has been reported in 26 to 75% of chronic chlorpromazine recipients, although the exact incidence is unknown and requires further investigation. Such patients may have an enhanced risk of bleeding profiles (hemophilia-like) or, conversely, thrombotic events. A case of such a lupus-like anticoagulant with a circulating inactivator of coagulation is discussed in light of the recent literature.
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This study describes the use of a modified dilute thromboplastin assay for demonstration of the lupus coagulation inhibitor in plasma. A one-stage clotting inhibition assay is used in which the ability of the test plasma to prolong the clotting time of normal plasma is measured. The method is easy to perform and suitable for routine use. Clinical and laboratory data from five patients with the inhibitor but without systemic lupus erythematosus are presented. Thromboembolic manifestations were observed in three patients and obstetric complications possibly due to placenta thrombosis in two. One patient showed a bleeding tendency, associated with prothrombin deficiency. A number of pathological coagulation analyses and other laboratory data may be due to affinity of the lupus inhibitor for negatively charged phospholipids in vitro.
The clinical features in 12 women with a circulating coagulation inhibitor (lupus 'anticoagulant') were studied and correlated with findings in 22 renal biopsies in these patients. Four of 12 women had serological evidence of systemic lupus. Only two of 23 pregnancies in these women were successful. Lesions in all biopsies were remarkably similar. Seven biopsies taken during or soon after pregnancy showed acute fibrinoid lesions. 'Acute' lesions consisted of fibrin thrombi in glomeruli arterioles and arteries and double contours in glomerular capillary walls. Biopsies carried out remote from pregnancy in these seven patients showed persisting double contours in glomeruli together with narrowing of arteries due to recanalizing thrombi and cellular intimal proliferation. All other biopsies showed similar lesions. The lesions were essentially the same as those of thrombotic microangiopathy and those described previously in post-partum renal failure. Renal function was severely impaired in four patients and showed moderate impairment in two patients at the time that acute thrombotic lesions were demonstrated in glomeruli. Renal function in two patients improved during plasma exchange therapy. Because all biopsies showed either acute, healing or healed, thrombotic lesions, it is proposed that these lesions are characteristic of the renal findings in patients with a lupus 'anticoagulant'. In all but two cases the acute lesions were seen during or soon after pregnancy.
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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Liposomes of pure phospholipids were used in a modified APTT test system and the role of phosphatidyl serine (PS) in determining the sensitivity of the test system to the presence of lupus anticoagulants was assessed. Six consecutive patients with lupus anticoagulants and seven haemophiliacs with anticoagulants directed at specific coagulation factors, were studied. Increasing the concentration of phospholipid in the test system markedly reduced the sensitivity to lupus anticoagulants but had marginal effect on the specific factor inhibitors. The same effect was achieved when the content of PS alone was increased in a vehicle liposome of constant composition. The results suggest that the lupus anticoagulants can best be detected by a screening method using an APTT test with a reagent of low PS content. The use of a reagent rich in PS will largely abolish the lupus anticoagulant's effect on the APTT. An approach using the two different types of reagent may facilitate differentiation of lupus inhibitors from other types of anticoagulant.
Mixtures of various patient lupus inhibitor-containing plasmas and normal plasma were tested concurrently with the dilute tissue thromboplastin inhibition (DTTI) test and the kaolin clotting time (KCT). The KCT was found to be more sensitive to the presence of the lupus inhibitor than the DTTI. The principle of reducing the platelet phospholipid content in the KCT test plasma to enhance sensitivity for the lupus inhibitor was extended by using plasmas filtered through 0.22-micron cellulose acetate filters.
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