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)

The prevalence of immunologic and coagulation disorders in 75 schizophrenic patients treated with chlorpromazine or other antipsychotic drugs was evaluated. Four groups were studied: Group A, chlorpromazine treatment for more than 2 1/2 years; Group B, chlorpromazine and other antipsychotic drug treatment for more than 2 1/2 years; Group C, chlorpromazine treatment for less than 2 1/2 years; Group D, no chlorpromazine, but other antipsychotic drug treatment. Significant elevation of serum IgM and prolongation of partial thromboplastin time were noted in patients who had long-term chlorpromazine treatment. The latter was caused by a circulating inhibitor resembling that seen with systemic lupus erythematosus. There was a significant correlation between the IgM level versus chlorpromazine dose or duration of treatment and the partial thromboplastin time versus chlorpromazine dose or duration of treatment. In Groups A and B, 63% had a positive antinuclear antibody test (greater than or equal to 1:80), 40% had antibodies to native DNA, and 58% had antibodies to nucleoprotein. These antibodies were negative in the other groups. The percentages of T lymphocytes were below normal in 13 of 41 patients treated with chlopromazine. Twenty of 42 patients in Groups A and B, and none of 28 in Groups C and D had splenomegaly. This study indicates that most patients on long-term chlorpromazine treatment develop one or more immunologic abnormalities.
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PMID:Immunologic and coagulation disorders in chlorpromazine-treated patients. 31 32

An acquired inhibitor of blood coagulation, similar to that described in patients with Systemic Lupus Erythematosus (SLE), was detected during routine coagulation screening in 10 patients who did not meet the criteria for a diagnosis of SLE. The lupus-like anticoagulant (LLAC) was diagnosed on the basis of prolonged activated partial thromboplastin time (APTT) and/or prothrombin time (PT) which failed to correct when patient plasma was added to normal plasma; an additional criterion was an abnormal tissue thromboplastin inhibition test. No patient had a specific inhibitor directed against factors VIII and IX. Demonstration of LLAC was highly dependent upon the type of reagents adopted in the APTT and PT: the abnormality was detected consistently by one reagent only. One-stage assays of factors VIII and IX were characteristic of the presence of an inhibitor, showing non-parellel dose-response curves or decreased activity at low dilutions which were partially corrected at higher dilutions. Although 7 patients were free of abnormal bleeding, unequivocal signs of haemorrhagic tendency after a surgery were present in the remaining 3 patients. The findings suggest that LLAC is a non-exceptional cause of prolonged coagulation screening tests, and that it may sometimes be associated with impaired haemostasis.
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PMID:The varied sensitivity of partial thromboplastin and prothrombin time reagents in the demonstration of the lupus-like anticoagulant. 47 62

We studied a patient being treated with procainamide in whom we observed a high antinuclear antibody titer and prolonged activated partial thromboplastin (PTT), prothrombin (PT), and Stypven times (ST). Serum antibody concentrations against single-stranded DNA were elevated while those aginst native DNA were not elevated, suggesting the procainamide-induced lupus syndrome. Dilution of the patient's plasma with normal plasma failed to correct the PTT and PT, indicating the presence of an inhibitor(s) to blood coagulation. The anticoagulant activity was associated with the IgG fraction of the patient's serum. Addition of purified or partially purified human factors IX, X, VIII, VII, XIa, prekallikrein, high molecular weight kininogen, or phospholipids to the patient's plasma failed to correct the PTT, PT, or ST; however, purified human factor XII and prothrombin corrected the PTT and ST, respectively. These results indicate that production of antibodies directed against antigenic determinants on coagulation proteins can be a manifestation of procainamide-induced lupus erythematosus.
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PMID:Circulating inhibitors of blood coagulation associated with procainamide-induced lupus erythematosus. 71 99

A lupus-type anticoagulant which causes strong inhibition of the partial thromboplastin time with kaolin (PTTK), the stypven time, and the thrombin generation tests has been investigated. All tests for platelet function were normal, as were all specific coagulation factor assays with the exception of a slightly reduced factor XI in this patient. A diethylaminoethyl-cellulose-immunoglobulin (DEAE-cellulose-IgG) fractionation of the patient's plasma produced two peaks containing inhibitory activity in the PTTK test. The first of these peaks had a cloudy appearance, suggesting the presence of immunoglobulin aggregates. Studies with IgG aggregates prepared from normal IgG and from the patient's IgG demonstrated that such aggregates were not the cause of inhibition. It was possible to neutralize the inhibitory activity of the purified IgG but not platelet-poor plasma (PPP) with a rabbit anti-IgG. The inhibition of the patient's PPP in the thrombin generation, the contact product, and the stypven time tests were corrected by the inclusion in the test system of platelets activated either by aggregation due to adenosine diphosphate (ADP) or formalin fixation and washing. These studies lend support to earlier findings that platelets interact at several sites in the coagulation cascade.
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PMID:Demonstration of a platelet bypass mechanism in the clotting system using an acquired anticoagulant. 73 36

An inhibitor of blood coagulation was detected in the plasma of four schizophrenic patients receiving long-term chlorpromazine therapy. The partial thromboplastin time (PTT) was prolonged in all four patients and the prothrombin time (tpt) was prolonged in one. The inhibitor which resembled in many respects that seen in patients with systemic lupus erythematosus (SLE), was shown to be associated with the tigM-rich fractions of the serum. None of the patients manifested a clinical bleeding tendency and in two, discontinuation of the chlorpromazine was followed by a decrease in the activity of the anticoagulant. While three of the patients had a positive antinuclear antibody test (ANA) and the fourth a false positive serology for syphilis, no further evidence for SLE was found.
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PMID:A chlorpromazine-induced inhibitor of blood coagulation. 88 26

Eighty-three patients with circulating anticoagulants were studied at The New York Hospital. The lupus-type anticoagulant, an inhibitor of the prothrombin activator complex, was demonstrated in 58 patients. The inhibitor was identified using the blood and tissue thromboplastin inhibition tests. Inhibition by the lupus anticoagulant was augmented in 67% of these patients by a cofactor present in normal plasma. The lupus inhibitor was detected primarily because of an unsuspected abnormal coagulation test. One-half of the patients with the lupus-type anticoagulant did not have systemic lupus erythematosus.
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PMID:A clinical study of the lupus anticoagulant. 96 90

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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PMID:Studies on phospholipids in the action of a lupus coagulation inhibitor. 122 21

Prevalence of lupus anticoagulant (LA) in patients with systemic lupus erythematosus (SLE) and clinical manifestations vary widely between different clinical series. We investigated the relation between LA, autoimmune hemolytic anemia (AIHA), thrombocytopenia and platelet dysfunction in 80 unselected patients with SLE. AIHA was found in 6 patients (7.5%) and thrombocytopenia in 10 patients (12.5%), which was not related to platelet aggregation abnormalities. Compared to controls, patients with SLE showed significantly prolonged aPTT and kaolin clotting time (KCT), but platelet aggregation induced by both collagen and thrombin was not impaired. LA activity as defined by Rosner et al. (index for LA/ICA) was found in 15 patients (18.9%). Only 7 of these patients showed a positive platelet neutralization test (Triplett) and 9a positive tissue thromboplastin inhibition test (Schleider). In our SLE patients 23.7% have suffered from at least one thrombotic complication. In patients with LA activity thromboembolic complications were increased (p < 0.05). Thrombocytopenia was found in 6% of LA-negative but in 20% of LA-positive patients.
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PMID:[Prevalence of lupus anticoagulant, autoimmune hemolysis, thrombocytopenia and disorders of platelet function in unselected patients with SLE]. 128 63

Antiphospholipid antibodies (APA) are a family of immunoglobulins that react with anionic phospholipids, or anionic phospholipids-protein complexes. Recent evidence would support the latter definition. Lupus anticoagulants (LA) inhibit in vitro phospholipid dependent coagulation tests [e.g., activated partial thromboplastin time (APTT), prothrombin time (PT), and dilute Russell viper venom time (dRVVT)]. This inhibition appears to be specific for reagent phospholipids. The addition of freeze-thawed platelets or activated platelets will result in correction of the LA-induced abnormality. Anticardiolipin antibodies (ACA) are related to LA but appear to be distinct. ACA are detected by solid phase assays (ELISA, RIA) and require a plasma cofactor: beta 2 Glycoprotein-I (beta 2 GPI). ACA and LA activities can be separated in individual patient plasmas by affinity chromatography. In some instances they are of differing isotypes. Preliminary evaluation of beta 2 GPI in coagulation assays suggests it may function as a cofactor for LA activity. Recent work also suggests human prothrombin may represent a necessary cofactor for in vitro LA activity. Paradoxically, patients with LA/ACA may sustain thromboembolic events involving both venous and arterial sites. The prothrombotic properties of LA/ACA have not been satisfactorily characterized. A number of proposals have been reported, including inhibition of prostacyclin (PGI2) generation by endothelial cells, decreased activity of the protein C system, impaired fibrinolysis, and inhibition of beta 2GPI. Among these various hypotheses, down regulation of the protein C system appears most plausible. Also, LA/ACA may interfere with the phospholipase A2-phospholipid substrate complex involved in the generation of arachidonic acid from membrane phospholipids.
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PMID:Antiphospholipid antibodies: proposed mechanisms of action. 128 81

Lupus anticoagulant (LA) and anticardiolipin antibodies (ACA) have been reported to be associated with fetal loss. OBJECTIVE. Our aim was to estimate the incidence of LA and to examine the correlation between LA and ACA in pregnant women. To investigate the clinical significance of LA and ACA in an obstetric population. STUDY DESIGN. A prospective, cross sectional study of 2856 consecutive women admitted to a department of obstetrics and gynecology for delivery or due to pregnancy complications during an 11 month period. METHODS. Activated partial thromboplastin time (APTT) was determined in all patients. LA and ACA were determined if APTT > or = 35 sec. For reference ACA was determined in a group of randomly selected patients with APTT < 35 sec. The results were analyzed in relation to the obstetrical records. RESULTS. Overall incidence of APTT > or = 35 sec.: 7.0%, significantly more frequent in patients with early spontaneous abortion (18.6%) and intrauterine growth retardation (17.5%). Incidence of LA 0.07%. The patients had undetectable ACA and no clinical condition related to LA. Incidence of ACA class IgM (IgM-ACA) in patients with APTT > or = 35: 20.4%, significantly higher than in the reference group (9.6%). Uncomplicated pregnancy in 84% of patients with IgM-ACA. No cases of ACA class IgG (IgG-ACA) in patients with APTT > or = 35 but two cases in the reference group (one normal pregnancy, one spontaneous abortion). CONCLUSION. LA is a rare manifestation with uncertain significance in otherwise healthy pregnant women. IgM-ACA in low titer occurs relatively frequently during normal pregnancy.
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PMID:Lupus anticoagulant and anticardiolipin antibodies in an obstetric population. 133 19


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