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)

Thirty-three cases of systemic lupus erythematosus in women are studied in retrospect. Eight patients (24 percent) presented a total of ten neuropsychiatric episodes that could be attributed to the underlying disease. The neuropsychiatric manifestation that was most often observed was cerebrovascular stroke (40 percent) followed by psychic disturbances and convulsions. A facial paralysis coinciding with an hypertensive crisis was noticed in one case. Another patient presented a peripheral sensitive neuropathy. Five episodes occurred prior to diagnosis or during the first year of the disease. In two patients the neuropsychiatric manifestations constituted the initial symptom of systemic lupus erythematosus. ECG proved to be one of the most valuable diagnostic tools among the complementary studies. It was altered in cases of organic pathology and normal when disturbances were of psychic origin. The C3 fraction of the serum complement revealed a definite difference between patients with and without neuropsychiatric manifestations. Concentrations were lower in persons which psychic disturbances than in patients without them. The pathogenesis of neuropsychiatric manifestations of systemic lupus erythematosus is discussed. They cannot be attributed exclusively to coagulation disturbances nor to treatment with corticosteroids. The immediate prognosis of neuropsychiatric episodes was good: there was partial or total recuperation in eight of the ten episodes. However, the long-term course of systemic lupus erythematosus shows that these manifestations represent an unfavourable prognostic factor in this disease.
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PMID:[Neuropsychic manifestations in systemic lupus erythematosus (author's transl)]. 43 Nov 77

An 11-month-old girl had systemic lupus erythematosus with a widespread skin rash. She manifested five of the criteria necessary for the diagnosis: oral ulcerations, alopecia, positive lupus erythematosus preparations, convulsions, and thrombocytopenia with leukopenia. Direct immunofluorescence showed deposits of IgG and C3 at the dermoepidermal junction of both abnormal and clinically uninvolved skin, and in subepithelial deposits along the glomerular basement membrane.
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PMID:Systemic lupus erythematosus in a 1-year-old child. 113 Mar 30

A 1987 questionnaire sponsored by the Health and Welfare Ministry concerning the clinical subsets and severity of systemic lupus erythematosus (SLE) was distributed to 93 medial facilities. A clinical analysis of the outcome and treatments was accomplished on one thousand six hundred and fourteen SLE patients fulfilling ARA criteria. The outcome was evaluated into 6 categories, namely; complete remission, incomplete remission, no change, gradual worsening, rapid worsening and unknown. Treatments included (1) anti-inflammatory drugs, (2) initial dose of prednisolone (PSL) below 29 mg/day, (3) initial dose of PSL from 30 to 59 mg/day, (4) initial dose of PSL above 60 mg/day, (5) pulse therapy, (6) immunosuppressants, (7) plasmapheresis, and (8) hemodialysis. Statistical significances were determined with ridit analysis. The severity of the disease for 1,614 SLE patients was evaluated by the judgement of each medical facility independently, separating it into 3 grades. As a result, 16.8% was evaluated as severe, 54.6% was evaluated as moderate, and 28.6% was evaluated as mild. Clinical subsets were divided into 3 categories according to the outcome; (1) those with high complete remission rates (serositis, convulsion, oral ulcers, unconsciousness, hemolytic anemia and so on), (2) those with high incomplete remission rates (lupus nephritis, digital gangrene, hypertension, peripheral neuropathy, erythema, Raynaud's phenomenon and so on), and (3) those with high rates of no change or worsening (aseptic bone necrosis, pulmonary hypertension, pneumonitis, chronic renal failure and so on). SLE patients with persistent proteinuria below 3.4 g/day, pulmonary hypertension, or pneumonitis treated with large doses of PSL such as an initial dose of PSL above 60 mg/day and/or pulse therapy had a significantly higher remission rate than those treated with small dosages of PSL. Hereafter, the establishment of modes of treatments for increasing the remission rates of intractable clinical subsets in highly desired.
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PMID:[Studies on clinical subsets and severity of systemic lupus erythematosus based on a 1987 questionnaire conducted in Japan--clinical analysis of the outcome and treatments in clinical subsets]. 160 13

The authors report a case of lupus showed in labour by the presence of generalised convulsions and coma after the crisis. This was followed by labile transitory hypertension, by massive proteinuria which cleared in 15 days, by major hyperthermia (higher than 39.5 degrees) and transitory agranulocytosis. The infant had a purely biological neonatal lupus. Pregnancy in a lupus patient has two risks: the mother's relapses of lupus, it is usual that renal failure is the worst of the prognostic features, but in this patient cerebral complications were much more serious. In the fetus there is a risk of spontaneous abortion linked to the anticardiolipin antibody level, and the risk of disease in the heart due to the anti-SSA (or anti-Ro) factor giving rise to congenital auriculo-ventricular blocks. The therapeutic possibilities are classically treated with immunosuppressants, mainly corticoids, which is added to low doses of aspirin. Plasmaphoresis and immunoglobulin treatments are being tried out.
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PMID:[Disseminated lupus erythematosus discovered during delivery: a difficult diagnosis]. 162 23

We report a case of a 47-year-old man with anti-phospholipid antibody syndrome associated with subdural hematoma. The patient had several episodes of arthritis during his thirties. He developed venous thrombosis in his right lower leg at the age of 35, when laboratory studies demonstrated prolongation of activated partial thromboplastin time (APTT) and a biological false-positive result occurred on a syphilis test. When bulbar palsy and Horner's syndrome in the right eye suddenly appeared at the age of 42, he was diagnosed as having brain stem infarction. At the age of 47, he developed constructional apraxia, dyscalculia, skilled movement disturbances and generalized convulsions. Subdural hematoma and multiple lacunes in the cerebral white matter were demonstrated with brain MRI. Furthermore, the patient was positive for Rumpel-Leede phenomenon. Laboratory studies revealed mild thrombocytopenia, prolonged bleeding time and APTT, positive antinuclear antibody and positive test results for both lupus anticoagulant and an anti-cardiolipin antibody, namely anti-phospholipid antibodies. Based on these findings, we consider that the tendency of this patient to bleed may have been due to antiphospholipid antibodies, attacking the platelet membranes and that the bridging veins in the subdural space may be the site at which the bleeding tendency easily appears. Anti-phospholipid antibody syndrome accompanied by hemorrhagic complications had rarely been reported. We suggest that special attention should be given to hemorrhagic complications in patients with anti-phospholipid antibody syndrome associated with fragility of the vessels and/or platelet dysfunction.
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PMID:[A case of anti-phospholipid antibody syndrome associated with subdural hematoma]. 180 71

A 30-year-old woman, who in the past was diagnosed as having systemic lupus erythematosus (SLE) and had been treated accordingly, consulted us with neuropsychiatric symptoms, including mutism and catatonia. ANA and anti-dsDNA in serum were negative, and she did not fulfill the ARA criteria for a diagnosis of SLE. However, in view of her history and the fact that she developed convulsions and a transient, unexplained period of leukopenia during admission, her current illness could be interpreted as a cerebral manifestation of SLE. After increasing the dosage of prednisone, she recovered almost completely from this episode. The literature concerning possible procedures to diagnose neuropsychiatric manifestations of SLE is reviewed; it turns out that especially the primary form of cerebral SLE often causes diagnostic problems.
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PMID:[Cerebral disseminated lupus erythematosus; brain-racking for patient and physician]. 225 54

A 38-year-old woman suffering from systemic lupus erythematosus was treated with cyclophosphamide and prednisone. Two months later she developed mononeuritis multiplex. After one year, she showed a personality change with aggressiveness and paranoid delusions. Grand mal epileptic fits began to occur. An unenhanced CT-scan showed extensive and bilateral frontal hypodense lesions originally ascribed to vasculitis-caused infarcts. On autopsy, a primary intracerebral lymphoma with extensive necroses was demonstrated. The relationship between SLE, immunosuppressive treatment and primary intracerebral lymphoma is discussed.
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PMID:Primary intracerebral lymphoma in systemic lupus erythematosus treated with immunosuppressives. 267 4

Hypersensitivity drug reactions are a major source of serious adverse drug reactions, yet very little is known about their mechanism. Several drugs are oxidized by activated neutrophils and mononuclear cells to reactive metabolites. Jack Uetrecht explains that the pattern of hypersensitivity reactions associated with these drugs - drug-induced lupus, agranulocytosis, and generalized hypersensitivity reactions - fits a mechanism in which leukocyte-generated reactive metabolites initiate the hypersensitivity reaction. Because activation of the leukocyte is necessary for reactive metabolite formation, one risk factor for a drug hypersensitivity reaction may be an infection or other inflammatory condition.
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PMID:Mechanism of hypersensitivity reactions: proposed involvement of reactive metabolites generated by activated leukocytes. 269 59

Five hundred consecutive patients with systemic lupus erythematosus (SLE) were entered into a prospective study of anticardiolipin antibodies (ACLA) in their 3 major immunoglobulin isotypes and followed thereafter with repeated testing for a mean period of nearly 8 months. Manifestations of SLE that were strongly associated with ACLA included venous thrombosis (particularly when recurrent), thrombocytopenia, hemolytic anemia, recurrent fetal loss, and leg ulcers. Other manifestations found to be associated with ACLA were arterial occlusions, transverse myelitis, and pulmonary hypertension. Conversely, we found no relationship between ACLA and migraine, convulsions, transient ischemic attacks, psychoses, or avascular necrosis of bone. No relationship was found between the presence of ACLA and that of anti-DNA antibodies studied in the same serum sample. Association with ACLA grew stronger and titers became higher in patients with several of the associated manifestations. Statistical analyses revealed the existence of a syndrome, the antiphospholipid syndrome, comprising 2 or more manifestations in conjunction with ACLA titers 5 standard deviations above the mean of normal control subjects, particularly if ACLA had been positive on at least 2 occasions. We propose that such criteria could be applied to the definition of the antiphospholipid syndrome. The presence and the titers of these antibodies related to disease activity and titer decreased by treatment, particularly when they were of the IgM isotype. Patients in whom a thrombotic episode occurred during the course of the study were observed to have a coincident decrease in ACLA titers, a finding that might indicate consumption of the antibody during the event. Treatment and the resulting inactivation of disease appear to have independent effects on ACLA titers. Physicians should therefore be cautious in prescribing high doses of corticosteroids or immunosuppressants to patients with SLE solely because they have high titers of ACLA.
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PMID:Antiphospholipid antibodies and the antiphospholipid syndrome in systemic lupus erythematosus. A prospective analysis of 500 consecutive patients. 281 61

From the age of 17 a young man had recurrent venous thrombosis, with pulmonary embolism on two occasions. Laboratory investigations showed increased DNA binding, thrombocytopenia, positive antinuclear antibodies, and immunoglobulin A deficiency. A plasminogen activator deficiency was suspected because the euglobulin lysis time was considerably prolonged. Variant lupus was diagnosed. He had a severe myocardial infarct at the age of 20 and subsequent investigations showed the presence in serum of the lupus anticoagulant and antibodies to cardiolipin. The presence of these antiphospholipid antibodies explains the features of his illness and establishes that this case fits into a subset of systemic lupus erythematosus characterised by thrombotic events.
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PMID:Myocardial infarction in a young man with systemic lupus erythematosus, deep vein thrombosis, and antibodies to phospholipid. 308 42


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