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)

A patient with IgM-secreting B-cell lymphoma developed demyelinating peripheral neuropathy, nodular regenerative hyperplasia of the liver, coagulopathy, and terminal miliary lymphomatous spreading. Serologic auto-antibody activities directed against myelin associated glycoprotein, prothrombinase complex (i.e. lupus anticoagulant) and smooth muscle cells were detected. It is suggested that there is a link between the IgM gammopathy, the immunological abnormalities and the various clinico-pathological conditions.
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PMID:Peripheral neuropathy, coagulopathy and nodular regenerative hyperplasia of the liver in a patient with multiple serologic auto-antibody activities and IgM B-cell lymphoma. 255 47

Thirty SLE patients underwent clinical neurological examination, electrophysiological studies, cerebral computer tomographic (CT) scans, and blood sampling. Nineteen patients (63%) had clinical neuropsychiatric and 10 patients (33%) had clinical neuromuscular manifestations. Migrainous headache affecting 11 patients (37%) was the most prevalent clinical manifestation. Electrophysiological testing revealed abnormal electroencephalography in 10 patients (33%). Abnormal electromyography and nerve conduction velocity were found in 13 (43%) and 7 (24%) patients respectively. Abnormal visual evoked response was detected in 2 patients. Cerebral CT scans displayed cerebral atrophy in 20 patients (71%), while 6 patients (21%) had cerebral infractions. Disease activity assessed by two different tests revealed a higher prevalence of cerebral infarctions, classical migraine, muscular weakness, and pathological electromyography and nerve conduction velocity in the higher disease activity groups. Cerebral infarctions were only found among anti-Ro negative patients, but apart from this, no significant association could be found between coagulopathy, circulating immune complexes, cryoglobulins, routine immunological tests, medication, and any clinical, electrophysiological or cerebral CT pathology.
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PMID:Clinical neurological, electrophysiological, and cerebral CT scan findings in systemic lupus erythematosus. 259 48

Coagulopathy leading to arterial and venous thrombosis is sometimes seen in patients with systemic lupus erythematosus (SLE). It is caused by antiphospholipid antibodies reacting with negatively charged phospholipid constituents of membranes and coagulation factors. The patients may also suffer from recurrent fetal loss and neurological manifestations, and may have intermittent thrombocytopenia and low serum concentration of complement factor C4. Patients without evidence of SLE or other immunological disorders may also exhibit this antiphospholipid antibody-associated thrombotic tendency. The patients are often young women, and it is important to be aware of this kind of coagulopathy, because it may take a most severe course in some of the persons affected.
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PMID:[The antiphospholipid syndrome]. 259 85

We studied 15 patients with angiographically documented intraluminal clot in the vertebrobasilar (VB) circulation and ischemic stroke. Progressive brainstem signs were the most common presentation; the neurologic deficit was maximum at stroke onset in 4. Seven experienced their first symptoms during sedentary activities. Thirteen of the initial 15 CTs revealed infarcts in the VB territory, 7 with multiple foci. Intraluminal clot was present in the vertebral artery in 7 patients (2 bilateral), basilar artery in 7, posterior cerebral artery in 5, and superior cerebellar artery in 1. Multiple clots were seen in 5 patients. Stroke risk factors were present in the majority of cases. Although cardiac source embolism was the most common single etiology (4 patients), most patients had other causes including migraine, coagulopathy associated with malignancy and nephrotic syndrome in systemic lupus erythematosus, vertebral artery dissection with local embolism, delayed irradiation arteriopathy, and a fusiform, ectatic basilar artery. Six (40%) died within 5 months of follow-up. Intraluminal clot in the posterior circulation is a marker for multiple stroke mechanisms, not all of which are embolic. Intraluminal clot should prompt investigations into occult risk factors when no cause appears obvious.
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PMID:Intraluminal clot in the vertebrobasilar circulation: clinical and radiologic features. 292 76

Prolongation of partial thromboplastin time was noted in patients with acquired immunodeficiency syndrome (AIDS) who were admitted to the hospital for diagnosis of opportunistic infection. As biopsy procedures were often indicated, detailed investigation of the abnormal coagulation study was performed in four patients. Results confirmed the presence of a lupus anticoagulant. Partial thromboplastin times of 34 consecutive subsequent patients hospitalized with the diagnosis of AIDS-associated opportunistic infection were recorded; prolongation was noted in 24 of these. None of these 38 patients exhibited clinical evidence of bleeding. One patient had a confirmed thrombotic episode. Prolonged partial thromboplastin time is a common finding in hospitalized patients with AIDS and opportunistic infection. If no clinical history of unusual bleeding is noted, the lupus anticoagulant should be suspected. Many patients with AIDS require invasive procedures for disease management; the lupus anticoagulant, an in vitro phenomenon, should not prevent these studies.
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PMID:Lupus anticoagulant in the acquired immunodeficiency syndrome. 308 92

We describe the coagulopathy of a 65-year-old woman with a thrombotic disorder associated with dysfibrinogenemia and lupus anticoagulant (LA). The patient's prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), and batroxobin time were prolonged and could not be corrected by mixing with equal volumes of normal plasma. Fibrinogen quantitation showed approximately twice as much immunoreactive as thrombin-clottable protein. The batroxobin and thrombin clotting times of the patient's isolated fibrinogen were prolonged and could not be corrected by mixture with normal fibrinogen. Turbidimetrically assessed fibrin monomer aggregation in response to thrombin, ancrod, or batroxobin and fibrin monomer reaggregation experiments disclosed clearly delayed onset and a lower maximum opacity. In other turbidimetric and clotting-time experiments, the patient's fibrinogen displayed a dose-dependent inhibition of the reaggregation of normal fibrin. Fibrinopeptide A and B release rates and sialic acid content were normal. Assessed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of reduced samples, the subunit structure of the patient's fibrinogen and its fully cross-linked fibrin was normal. The presence of LA was established by two techniques, the blood thromboplastin inhibition test and the platelet neutralization procedure (PNP). A positive PNP could not be produced by mixing afibrinogenemic plasma with the patient's purified fibrinogen. The patient's inactivated serum and her isolated IgG prolonged the PT and PTT of normal plasma but showed no inhibitory effect on the clotting of purified normal fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dysfibrinogenemia and lupus anticoagulant in a patient with recurrent thrombosis. 311 49

In spite of recent advances in knowledge concerning the detailed biochemistry of blood coagulation, the diagnosis of haemostatic disturbances remains an important problem of clinical judgement in many instances. Laboratory support relies initially on a series of screening tests designed to investigate the general nature of blood clotting. Recent interest in these aspects is centred on standardization and quality assurance of methods and results. Procedures have been recommended in an attempt to unify data. Several aspects of conventional laboratory investigations have been modified and the reliability of diagnostic information has been improved. Some relatively recent findings have extended the application to coagulation studies. For example, the discovery of protein C, a potent physiological inhibitor of blood coagulation, has clarified the nature of the clotting disorder in some patients with hereditary thrombosis disease. In addition, close analysis of plasma from patients with systemic lupus erythematosus has stimulated interest in the association between the haemostatic, neurological and immunological abnormalities recorded in these patients. More recently, sophisticated techniques for the diagnosis of many coagulation factor defects have been developed. Carrier detection of the sex-linked disorders is undertaken widely with reasonable success and reliable prenatal diagnosis procedures have been established in specialized centres. Unequivocal information regarding the diagnosis of carrier status in some families is obtained by the use of gene analysis and linked polymorphisms. Precise details of the genes for several clotting factors have been recorded. Future development in this field is likely to improve the clinical course of many coagulation disorders.
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PMID:Laboratory support in the diagnosis of coagulation disorders. 389 45

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

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

The case of a young man with the plasma cell type of Castleman's disease is described. Beyond the well known systemic manifestations the coagulation tests showed a decrease in the activity of factors V, VIII and X due to the presence of lupus-like circulating anticoagulants. After surgical excision of the mediastinal mass both hematochemical pathological data and the coagulation defect disappeared. It is suggested that the lupus-like anticoagulant was secreted by the tumor.
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PMID:Castleman's disease with coagulation defect. A case report. 646 80


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