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 relatively high incidence of heart failure is noted among patients with systemic lupus erythematosus (SLE) without clearly defined clinical causes. To evaluate left ventricular performance in patients with SLE without evidence of cardiovascular disease, noninvasive measurement of the systolic time intervals was carried out. Simultaneous recording of the electrocardiogram, phonocardiogram and carotid arterial pulsation were obtained in 25 patients with systemic lupus erythematosus and compared with 22 normal subjects. The patients with SLE had a shorter left ventricular ejection time (P less than 0.05), a longer pre-ejection period (P less than 0.02) and an increased ratio of pre-ejection period/left ventricular ejection time (P less than 0.005). These abnormalities on ventricular function were independent of age, duration of the disease, hypertension, renal involvement, anemia, immunologic activity and corticosteroid treatment. Several etiologic possibilities are discussed and the clinical usefulness of this method to detect and follow-up the cardiac dysfunction in systemic lupus erythematosus is emphasized.
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PMID:Myocardial involvement in systemic lupus erythematosus. A noninvasive study of left ventricular function. 69 53

Anemia occurs in more than one half of patients with systemic lupus erythematosus and is usually attributed to "chronic disease." Approximately 10% of patients with a positive Coombs' test manifest clinically significant hemolysis. Leukopenia affects both granulocytic and lymphocytic lines and may be caused by autoantibodies. Nevertheless, enhancement of B lymphocyte function occurs in active disease, perhaps due to a loss of regulatory T cells. Most patients have increased production and increased peripheral destruction of thrombocytes, with a normal circulation platelet count. Thrombocytopenia is usually caused by increased destruction. Qualitative abnormalities of platelet aggregation also occur. Circulation anticoagulants are not rare; however, spontaneous bleeding is uncommon. The anticoagulants, immunoglobulins directed against clotting factors, assume importance for invasive procedures. Most clinically significant hematopoietic abnormalities can be suppressed by corticosteroids; however, splenectomy, or immunosuppressive agents, or both, may be indicated for patients who respond inadequately to corticosteroids.
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PMID:Hematologic aspects of systemic lupus erythematosus. Current concepts. 83 48

A 73-year-old woman was found to have clinically significant pancytopenia in association with procainamide hydrochloride ingestion. The syndrome, resembling systemic lupus erythematosus, which has been reported to develop in patients treated with this agent, is characterized by mild to moderate anemia and mild to moderate granulocytopenia. Severe granulocytopenia in patients taking procainamide and unrelated to a lupus syndrome has not previously been reported in association with significant thrombocytopenia. The clinical severity of this patient's presentation, suggesting an aleukemic leukemia, and its complete remission after cessation of procainamide administration occasional this report.
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PMID:Severe transient pancytopenia associated with procainamide ingestion. 103 16

A case of hyperglobulinemic purpura of Waldenstrom with involvement of trunk and arms of 10 years duration has been presented. The patient had mild anemia, hepatosplenomegaly, positive rheumatoid factor and no evidence of immonological abnormalities associated for with systemic lupus erythematosus. A brief review of clinical manifestation and pathogenesis is cited.
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PMID:Purpura hyperglobulinemica (Waldenstrom). 105 27

A 21-year-old woman was admitted to our hospital because of high fever, cough, and headache. Other clinical manifestations included hepatosplenomegaly, anemia, leukopenia, and mild liver dysfunction. As she had been diagnosed to have systemic lupus erythematosus (SLE) previously, we first suspected that this disease had become exacerbated. However, the titers of anti-EB virus (VCA-IgG) and some other viruses were high on admission, and hemophagocytosis by macrophages was observed on bone marrow examination. Therefore, she was diagnosed to have virus-associated hemophagocytic syndrome (VAHS). Prednisolone therapy was then initiated, but the patient responded poorly. We next tried gamma globulin, and the clinical findings and laboratory data were improved. Our patient showed a very favourable clinical course following gamma globulin therapy, suggesting that steroid and gamma globulin should be considered as a treatment even in the early stages of this syndrome in adults.
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PMID:[Steroid and gamma globulin therapy against virus-associated hemophagocytic syndrome]. 127 36

Since 1981 when anti-Ro (SS-A) and/or anti-La (SS-B) antibodies were described to be present in infants with neonatal lupus erythematosus (NLE) and their mothers, subsequent studies have demonstrated the almost universal association of NLE with either or both of these autoantibodies. To our best knowledge, three cases of NLE were reported to be negative in anti-Ro (SS-A) and anti-La (SS-B) antibodies. We report one infant born to a mother with systemic lupus erythematosus (SLE). He had neonatal pancytopenia (thrombocytopenia, anemia, and leukopenia) which got resolved after intravenous immunoglobulin (IVIG) administration. Both anti-Ro (SS-A) and anti-La (SS-B) antibodies were not detectable in his serum by immunodiffusion method while other such as RNP (nonspecific, including U1,U2,U3,...,U6), Sm and Scl-70 antibodies were all positive. This mother had all the above antibodies detectable in her serum. After excluding other possibilities, his pancytopenia was most likely to be attributed to neonatal lupus. We suggest that autoantibodies such as RNP and Sm antibodies may play an important role in the pathogenesis of thrombocytopenia of NLE.
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PMID:Neonatal lupus erythematosus with negative anti-Ro and anti-La antibodies: report of one case. 129 48

A 60-year-old female was admitted to our hospital because of respiratory failure. She was diagnosed as having systemic lupus erythematosus (SLE) in 1971 and had been treated with low-dose oral corticosteroids for 13 years. She developed cough, fever and anemia several days after oral corticosteroids were tapered. Initially, she had no complications such as congestive heart failure, renal failure or bleeding tendency. Respiratory failure progressed without any response to antibiotic therapy. Chest roentgenogram showed bilateral diffuse infiltrates and air bronchograms. There was no improvement even with steroid pulse therapy, and she died of multiple organ failure. Autopsy revealed massive intra-alveolar hemorrhage and interstitial pneumonitis. Deposition of immunoglobulins in the lung was not seen. To our knowledge, this is the 11th reported case of SLE associated with pulmonary hemorrhage in Japan.
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PMID:[An autopsy case of massive pulmonary hemorrhage in systemic lupus erythematosus]. 143 30

A 46 year old woman presented with fever and normochromic anaemia followed rapidly by severe myocardial failure, unresponsive to maximum inotropic support and broad spectrum antibiotics. There were no classical clinical stigmata of systemic lupus erythematosus (SLE) but a possible immunological cause was looked for, and on the basis of her immuno-serology a diagnosis of SLE-like disease was made. She responded rapidly to high dose steroids. The importance of considering the possibility of SLE or 'lupus overlap' in an acutely ill 'undiagnosed' patient is emphasized. The relevance of instigating appropriate immuno-serological tests in the course of such an illness is discussed.
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PMID:Sub-clinical systemic lupus erythematosus presenting with acute myocarditis. 143 35

Farr's assay using double-stranded (ds) DNA from E. coli is a most sensitive and specific method for the detection of anti ds-DNA antibodies in patients with systemic lupus erythematosus (SLE). Because of the lack of sufficient DNA antigens, however, final antibody titers were hardly determined when the sera contained antibodies titered more than 100U/ml (or more than 60 per cent by DNA binding activities). In such sera DNA binding activities were measured by using ds-DNA tracer adjusted final concentration of NaCl to 125 mM. Higher binding activities measured by high-salt tracer are obtained significantly in SLE patients groups with nephrotic syndrome, proteinuria, cast, renal failure, diffuse proliferative nephritis, low serum complement levels, anemia and/or low IgG/IgA levels compared with the patients who lacked these clinical findings. In contrast the patients with digital rash or cramp showed significantly lower high-salt binding activities. The patients with pleuropericarditis tended to have lower bindings. The non-lupus patients including MCTD also had lower levels. These clinical characteristics could not be evaluated by standard Farr's assay. High-salt bindings suggest the presence of high avidity antibodies and also partly may mean the high levels of low avidity antibodies. The application of high-salt binding activities, thus, is a useful tool for the evaluation of clinical characteristics of SLE patients who had high levels of anti ds-DNA antibodies by standard Farr's assay.
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PMID:[Reassessment of measurement of anti double-stranded DNA antibodies by Farr's assay using double-stranded DNA from E. coli and application of DNA binding Activities in high salt solution]. 144 79

A male aged 58 was admitted to our hospital because of proteinuria, hematuria and bilateral pretibial edema. Laboratory tests showed normocytic, normochromic anemia and moderately impaired renal function. Antinuclear antibodies were negative. Neither M-protein nor Bence-Jones protein were detected. Light microscopic study on the biopsied renal specimen indicated a moderate mesangial proliferation accompanying with the deposition of PAS-positive and Congo red-negative materials in the subendothelial area. C3 accumulated segmentally along the capillary walls, which was clarified by immunofluorescence microscopy. Staining for IgG, IgA, IgM and light chains were negative. Electron microscopy demonstrated the deposition of microtubules in the mesangial, subepithelial and subendothelial areas. The diameter of these microtubules ranged from 40 to 80 nm. Such type of the microtubules have been reported to exist in the glomeruli in the patients with systemic diseases such as amyloidosis, systemic lupus erythematosus, cryoglobulinemia and light chain disease. In our patient, however, any clinical or serological findings suggestive of these systemic diseases were not obtained. On the other hand previous report pointed out that microtubules deposited in the glomeruli in the patients with immunotactoid glomerulopathy or other glomerulopathies. Our patient had the clinical features consistent with these glomerulopathies. However, no depositions of immunoglobulins were observed. This case is an atypical glomerulopathy accompanying with the glomerular microtubular deposits.
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PMID:[Glomerulopathy associated with glomerular microtubular deposits: a report of a case]. 148 13


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