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)

The prevalence of lupus anticoagulant (LAC) and its relation with reported clinical associations has been determined in 55 patients with systemic lupus erythematosus (SLE) from northern India who were studied prospectively. Kaolin clotting time was used to screen for LAC, which was detected in seven (13%) of the patients. Significant associations were found between LAC and thrombotic events, onset of disease at an early age, and disease of shorter duration. No statistically significant association could be found between LAC and recurrent abortions, pulmonary hypertension, thrombocytopenia, and neurological manifestations. It is concluded that LAC is a useful marker for a subset of patients with SLE at risk of thromboembolic events.
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PMID:Lupus anticoagulants in systemic lupus erythematosus: prevalence and clinical associations. 212 9

In recent years an association has been described between, on the one hand, an in vitro prolongation of phospholipid-dependent coagulation tests (the 'lupus anticoagulant') or the demonstration of antiphospholipid antibodies and, on the other, clinical events, particularly recurrent thrombosis (usually venous but sometimes arterial), thrombocytopenia, and also recurrent mid-term fetal loss. Other less well-documented associations with haemolytic anaemia, livedo reticularis, strokes and other neurological syndromes have been suggested. The antibodies are present temporarily in many infections, are usually of IgM isotype and thrombosis does not occur. However, they are persistently present and mainly of IgG isotype in a number of auto-immune disorders associated with thrombosis, in particular systemic lupus erythematosus, in which 50% of patients will show antibody of one isotype or another. The strongest association is with antinuclear factor-negative lupus and 'lupus-like' disorders in which a full diagnosis of classical lupus cannot be made. The clotting test abnormality and antiphospholipid antibodies may be found also in otherwise normal individuals suffering thrombosis or fetal loss--the so-called primary antiphospholipid syndrome. These data raise important questions for management, but many details are controversial despite a decade's work; this review examines the present position and outlines some of the difficulties, particularly from the point of view of nephrology and paediatrics.
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PMID:The 'antiphospholipid syndrome' and the 'lupus anticoagulant'. 212 60

The frequency of "Lupus anticoagulant" (LA), was studied in 51 patients with systemic lupus erythematosus (SLE), 15 patients with chronic immune thrombocytopenic purpura (ITP) and 3 other patients with prolonged partial thromboplastin time (PTT), two of which had suffered episodes of CVA, and the other had a diagnosis of Paroxysmal Nocturnal Hemoglobinuria. Lupus anticoagulant was determined in each patient by the plasma recalcification time and the Russell's viper venom clotting time. Eight patients with SLE, (15.6%) 6 with chronic ITP (40%) and the three patients with prolonged PTT were positive for LA. All patients with LA were female, whose ages ranged from 19 to 59 years, and all except two patients were under steroid therapy. Thrombocytopenia was the most frequent manifestation in the patients with LA, followed by recurrent fetal death and thrombosis. Only the patients with ITP had hemorrhagic complications and one of them also had CVA in one occasion. The immunosupressory therapy may have played a role in diminishing the frequency of LA in the patients studied.
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PMID:[Presence of lupus-type anticoagulant, in systemic lupus erythematosus and other clinical entities]. 212 14

Hematologic abnormalities are common in association with collagen diseases, specially Systemic Lupus Erythematosus and include anemia, neutropenia, thrombocytopenia with alterations in lymphocyte subpopulations. On the other hand, patients with unexplained fibrosis of the bone marrow (the syndrome of idiopathic myelofibrosis or primary myelofibrosis) have clinical and laboratory evidence of immunologic dysfunction. Clinical findings include the presence of arthritis, vasculitis and erythema nodosum. Laboratory abnormalities include the presence of circulating immune complexes, antinuclear antibodies, positive direct Coombs test, elevated latex fixation and a circulating lupus type anticoagulant. Total hemolytic complement markedly depressed has also been reported. These data suggest that immunologic mechanisms associated with activation of the complement system play an important role in the disease process of some patients with agnogenic myeloid metaplasia with myelofibrosis. A review of the literature revealed that myelofibrosis occurring in the setting of collagen diseases is rare. However, a role for immunologic factors in the pathogenesis of myelofibrosis is also supported by the patients with coincident well defined collagen disease and myelofibrosis. In this report, we present two patients with such an association. Case 1 was a 58-year-old male with a two year duration history of rheumatic arthritis. He had bone erosions on hands, splenomegaly and myelofibrosis. Rheumatoid factor (latex) was positive: 1:2560. He had positive LE cells and hypocomplementemia: 37 CH50/ml (NV 70-150). The patient did not meet criteria for SLE. Case 2 was a 36-year-old female admitted because of dyspnea and fever. Diagnosis of myeloid metaplasia with myelofibrosis and progressive systemic sclerosis had been made four years before hand.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coexistence of myelofibrosis and collagen diseases]. 213 Feb 12

Antiphospholipidsyndrome is a well-defined entity characterized by spontaneous abortion, thrombocytopenia and recurrent arterial and venous thromboses. The diagnosis is biochemically verified by the presence of antibodies binding to negatively charged phospholipids. A patient with recurrent thromboembolic complications over the years eventually developed a rapidly progressing dyspnoe. Two-dimensional echocardiography showed a large right atrial mass which at operation proved to be a thrombus. Coombs test was positive as were lupus anticoagulans and antibodies against cardiolipin, in addition to thrombocytopenia and prolonged bleeding time. The author reviews the literature and discusses problems regarding diagnostical criteria for antiphospholipidsyndrome, pathogenesis of the "procoagulopathy" and thrombembolic complications associated with the syndrome. Special consideration is given to non-invasive diagnostic methods for distinguishing between atrial myxom and floating thrombus.
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PMID:[Antiphospholipid syndrome with massive right atrial thrombus. Differential diagnosis of myxoma]. 213 29

This review presents a unifying hypothesis that provides a connection between several types of hypersensitivity reactions associated with several types of drugs and explains some of the therapeutic effects (antiinflammatory activity and antithyroid effects) of these same drugs. This hypothesis centers on the oxidation of these drugs to chemically reactive metabolites by peroxidases. The drugs of interest have functional groups that are easily oxidized. The major peroxidase involved in this hypothesis is MPO because of its critical location in leukocytes which play a key role in the function of the immune system. However, thyroid peroxidase can probably also oxidize many of the same drugs to reactive metabolites, and this may be responsible for the thyroid autoimmunity observed in connection with some hypersensitivity reactions. Peroxidases have also been described in the skin and in platelets, and their presence may be responsible for the high incidence of skin reactions in the hypersensitivity response and the occurrence of immune-mediated thrombocytopenia, respectively. Involvement of other peroxidases, such as prostaglandin peroxidase, may also be important for antiinflammatory effects of drugs. In addition, leukocytes contain prostaglandin synthetase, and the activation of leukocytes leads to the release of arachidonic acid and the production of prostaglandins. This process may also lead to the metabolism of drugs to reactive metabolites. In studies of the metabolism of procainamide and dapsone, aspirin and indomethacin did not inhibit the formation of the hydroxylamine by neutrophils and mononuclear leukocytes. This is evidence against the involvement of prostaglandin synthetase in these oxidation; however, preliminary studies with other drugs suggest that prostaglandin synthetase may contribute to the metabolism of some drugs by leukocytes. Furthermore, the metabolism of phenylbutazone, phenytoin, and tenoxicam, as well as our preliminary work with other drugs such as carbamazepine, suggests that the range of drugs that are metabolized to reactive metabolites by peroxidases may be broader than initially suspected. There are several other drugs that do not fit into the functional group classes covered in this review but have similar properties. A good example is alpha-methyldopa, which is associated with drug-induced lupus, immune-mediated hemolytic anemia, and other hypersensitivity reactions. Such drugs may also be metabolized to reactive metabolites by peroxidases. Another aspect of the hypothesis is that an infection, or other inflammatory condition, may be an important risk factor for a hypersensitivity reaction because such a stimulus leads to activation of leukocytes which can lead to formation of reactive metabolites from certain drugs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Drug metabolism by leukocytes and its role in drug-induced lupus and other idiosyncratic drug reactions. 217 25

Antiphospholipid antibodies including the false-positive serologic test for syphilis, the lupus circulating anticoagulant, and the anticardiolipin antibody can be associated with recurrent thrombotic events, recurrent fetal loss, and thrombocytopenia. A range of other possible clinical associations also exists, including neurologic events, skin lesions, and cardiac lesions. The pathology of these lesions and the pathophysiology are discussed. Treatment is controversial but when indicated is directed toward prevention of recurrent episodes using anticoagulants including antiplatelet agents, warfarin, and heparin as well as occasionally prednisone with or without immunosuppressive agents.
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PMID:Vasculopathy associated with the antiphospholipid antibody syndrome. 218 63

A case of systemic lupus erythematosus (SLE) with subarachnoid hemorrhage due to a ruptured intracranial aneurysm is reported. A 31-year-old woman who had been treated with steroid for SLE was admitted to our department with severe headache, and nausea. CT scan showed subarachnoid hemorrhage and the left carotid angiogram revealed a small aneurysm at the supraclinoid portion of the left internal carotid artery. She had no neurological deficit. Hematological examination on admission showed disseminated intravascular coagulation (DIC), therefore, we decided to perform an intentionally delayed operation. In the meantime we treated the patient for DIC with FOY and methylprednisolone. The operation was performed after two weeks, when DIC had been eliminated completely. Postoperative hematological examination showed severe thrombocytopenia. We considered that SLE had come to the fore again, so we used Danazol in company with FOY and steroid. It seemed that Danazol was very effective for her. She was discharged about two months after admission with no problem. Cerebral apoplexy, such as cerebral infarction and cerebral hemorrhage, has often been seen in SLE, but subarachnoid hemorrhage due to a ruptured aneurysm is very rare. We could find only five reports of this phenomenon. Their prognoses were all, unfortunately, poor. It should be born in mind for therapy that a patient in SLE has a tendency to bleed. It seems that repeated hematological examinations and quick and proper management are important. We think that the aneurysmal formation in SLE is due to lupus vasculitis or the fragility of blood vessels due to a long use of Steroid.
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PMID:[A case of systemic lupus erythematosus with subarachnoid hemorrhage due to ruptured aneurysm]. 220 86

Autoimmune disorders such as SLE and ITP occur more commonly in young women and are the most common complications in pregnancy. There is considerable controversy concerning the risk to the mother and fetus, and the optimal prepartum management for minimizing that risk. 1. SLE is an autoimmune disorder in which IgG antibodies such as anti dsDNA-IgG, anticardiolipin IgG, and anti SS-A/Ro IgG are produced. Lupus nephropathy accompanied by diminished serum complement (CH50) and a rise in antibodies against dsDNA is a frequent clinical problem during pregnancy, which represents the adverse effect of hypertension or superimposed toxemia and causes fetal death or intrauterine fetal growth retardation. Habitual abortion or fetal death is common in a case with high anticardiolipin IgG titre. Anti SS-A antibodies are often found in the infants of antibody-positive mothers, and the deposition of antibodies in the perinodal region cause congenital heart block. IgG or immune complexes crossing the placenta directly injures the cardiac conduction system. In these cases which have high titre crossing the placenta directly injuries the cardiac conduction system. In these cases which have high titre of autoimmune antibodies, corticosteroid therapy should be started. 2. Management of ITP in pregnancy involves the consideration of three issues: 1) treatment of maternal thrombocytopenia, 2) prediction of fetal thrombocytopenia, 3) obstetrical management. ITP increases the risk for postpartum bleeding of sufficient severity to require blood transfusion. In most of these cases, maternal platelet counts are found to be less than 30,000/mm3. Women who have symptomatic severe steroid-unresponsive ITP may benefit from intravenous IgG(IvIgG) given as elective treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pregnancy complicated with autoimmune diseases]. 223 Apr 13

Antiphospholipid antibody is associated with a clinical syndrome of vascular thrombosis, thrombocytopenia, recurrent fetal loss, and livedo reticularis, whether or not a clinical diagnosis of systemic lupus erythematosus (SLE) coexists. A positive antiphospholipid antibody test is defined by enzyme-linked immunosorbent assay (ELISA) (antiphospholipid antibody itself) or by coagulation assay (lupus anticoagulant). These are similar but not identical antibodies. The test for syphilis is less closely related to the preceding two and is less regularly associated with clinical complications. The mechanism of action of either antiphospholipid antibody or lupus anticoagulant is as yet unknown. SLE-induced but not infection-induced antiphospholipid antibody has immunoglobulin G2 (IgG2) and IgG4 predominance. It recognizes all negatively charged phospholipids, but various physical characteristics of the phospholipids alter the recognition patterns. Treatment for the antiphospholipid antibody syndrome has not been clearly defined. Anticoagulation with aspirin, heparin, or warfarin is currently favored. A role for corticosteroid remains to be demonstrated.
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PMID:Antiphospholipid antibody syndrome: immunologic and clinical aspects. 225 9


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