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)

Because of the possibility that immunological mechanisms might be involved in the pathogenesis of leukopenia accompanying systemic lupus erythematosus (SLE), the effect of lymphocytes on colony-forming units in culture (CFU-C) was compared. The colony formation of the bone marrow CFU-C of SLE patients was less than that of the healthy subjects. Lymphocytes of SLE patients and serum of some of the SLE patients remarkably inhibited colony formation by human bone marrow CFU-C. The results shown above suggest the possibility that immunocompetent cells of the patients are involved in the pathogenesis of leukopenia in SLE.
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PMID:Effect of peripheral blood lymphocytes from systemic lupus erythematosus patients on human bone marrow granulocyte precursor cells (colony-forming units in culture). 716 17

A patient with chronic discoid lupus erythematosus was admitted with fever, arthralia, pleuropericarditis, and a history of leukopenia. He was initially believed to have systemic lupus erythematosus (SLE), but extensive evaluation showed negative immunologic studies and the presence of acid-fast organisms on pericardial biopsy specimens with cultures positive for Mycobacterium tuberculosis. Discoid lupus erythematosus patients with extracutaneous manifestations should be carefully studied for concurrent illness, especially when serologic evidence fo SLE is negative.
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PMID:Discoid lupus erythematosus and tuberculosis simulating systemic lupus erythematosus. 739 2

Systemic lupus erythematosus (SLE) remains a disease of unknown origin, characterized by major alterations of both the cellular and the humoral arms of immunity. Hematological changes, including anaemia, leucopenia and thrombocytopenia, occur in more than one half of patients with this disease. Anaemia is the most common hematological abnormality seen in SLE. Its possible causes are anaemia of chronic disease (ACD), auto-immune haemolytic anaemia and hypoplastic anaemia. Leucopenia affects both granulocytic and lymphocytic lines and may be caused by autoantibodies. The influence of drugs, hypersplenism and marrow suppression are also possible. Thrombocytopenia occurs frequently and is almost invariably autoimmune. Patients with SLE are at increased risk of thrombosis. Haematological abnormalities in patients with this disease require careful long-term monitoring and prompt therapeutic intervention.
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PMID:[Hematologic problems in systemic lupus erythematosus]. 765 19

The primary antiphospholipid syndrome and the antiphospholipid syndrome in systemic lupus erythematosus (SLE) patients (defined as secondary antiphospholipid syndrome) are characterized by the presence of anticardiolipin antibodies, thrombosis, thrombocytopenia, and recurrent fetal loss. To determine the role of anticardiolipin antibodies in the pathogenesis of antiphospholipid syndrome, monoclonal anticardiolipin antibodies were derived from mice in which experimental lupus was induced by a murine monoclonal anti-16/6 Id antibody. Two murine monoclonal anticardiolipin antibodies (2C4C2, 2C4D1) were generated and characterized. The 2C4C2, but not the 2C4D1, monoclonal antibody demonstrated remarkable lupus anticoagulant activity. Furthermore, these murine anticardiolipin monoclonal antibodies appear to recognize antigenic epitopes similar to those recognized by anticardiolipin antibodies found in sera of SLE patients. The monoclonal anticardiolipin antibody 2C4C2 was injected into naive female mice. Following immunization, the mice developed high titers of autoantibodies reacting with cardiolipin, DNA, nuclear extract, 16/6 and anti-16/6 Id, and anticardiolipin antibodies. As early as 8 weeks after immunization these mice exhibited significant leukopenia, thrombocytopenia, and proteinuria with immune complex glomerulonephritis. Moreover, mating of 2C4C2-injected mice with allogenic males resulted in low pregnancy rates and a low number of fetuses with a high percentage of fetal loss. These studies provide a new experimental model for secondary antiphospholipid syndrome demonstrating the role of anticardiolipin antibodies in the pathogenesis of this syndrome.
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PMID:Monoclonal anticardiolipin antibodies derived from mice with experimental lupus erythematosus: characterization and the induction of a secondary antiphospholipid syndrome. 768 61

Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal anti-DNA Ab, bearing a major Id 16/6Id. Immunized mice initially produce Abs to 16/6Id, DNA and nuclear Ags, and subsequently develop various clinical manifestations including leukopenia and renal immune complex disease. MHC class I Ags play a critical role in the induction and progression of experimental SLE. The present study reports that ocular changes also occur in mice with experimental SLE. The ocular disease is characterized by bilateral subacute and chronic inflammation of the eyelids (blepharitis) with immune complex IgG deposition and hypertrophic meibomian glands. The severity of ocular changes was strain dependent: most severe in 129 mice, less intense in BALB/c animals and only minimal in C3H.SW mice. No blepharitis developed in mice deficient in MHC class I expression. Further, the disease was strongly inhibited in BALB/c mice treated with methimazole, an agent that has been shown to repress transcription of MHC class I. In these cases, there was no IgG deposition and a decreased infiltration of inflammatory cells in the eyelids. These observations thus suggest that, similar to the observation with experimental SLE, MHC class I is critical in the onset of this experimental autoimmune blepharitis. The new experimental eye disease described here provides an animal model for chronic blepharitis in humans, a common condition for which such a model has been sought.
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PMID:Periocular inflammation in mice with experimental systemic lupus erythematosus. A new experimental blepharitis and its modulation. 772 31

Since acute disseminated intravascular coagulation (DIC) often contributes to a fatal outcome in patients with systemic lupus erythematosus (SLE), prediction of its development is important to prevent the occurrence of such an event. To analyze the risk factor(s) contributing to the development of acute DIC in SLE, we carried out a retrospective study of a series of 129 SLE patients, eight of whom developed DIC during the course of this disease, to assess which of the easily assessable parameters, present at the time of first medical examination, were of predictive significance. The important individual variables, determined by univariate analysis, were male sex, leukopenia, and infection. These factors were placed in a multivariate logistic regression model, and only one factor, infection at first medical examination, was found to have predictive significance for the development of acute DIC in SLE patients. The prevention and control of infection in SLE patients might have implications for preventing the development of acute DIC.
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PMID:Risk factors for the development of acute disseminated intravascular coagulation in patients with systemic lupus erythematosus. 778 59

A 58 year old woman developed systemic symptoms, interstitial lung disease, splenomegaly, leukopenia and anti-histone and anti-nuclear antibodies (ANA), while treated with hydralazine for hypertension. Five months after presentation she was admitted with high fever, skin rash and atypical lymphocytosis due to acute cytomegalovirus (CMV) infection. Worsening leukopenia and increased ANA were found, and high titres of anti-DNA antibodies, anti-cardiolipin antibodies and rheumatoid factors appeared. Hydralazine was stopped and the patient gradually became asymptomatic. All autoantibodies spontaneously disappeared (over 16 weeks), and the white cell count and spleen size became normal. The patient was found to be a slow acetylator and to have both HLA-DR4 and selective IgA deficiency. Thus, a multifactorial genetic susceptibility to develop drug-induced lupus was brought out in stages first by hydralazine and then by CMV, yet all manifestations and autoantibodies resolved spontaneously, demonstrating the complex interplay of varied environmental factors with a genetic predisposition in the pathogenesis of autoimmunity.
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PMID:Effect of acute cytomegalovirus infection on drug-induced SLE. 783 Nov 73

Two women with the rare association of systemic lupus erythematosus (SLE) and myasthenia gravis (MG) are reported. The first patient developed SLE (arthritis, severe thymectomy for MG. The second patient developed SLE (oral ulcers, arthritis, serositis, leukopenia, high titres of anti-DNA and anti-nuclear antibodies) 4 years prior to the clinical and serological onset of MG. Lymphocyte subsets and in vitro proliferative responses of peripheral blood mononuclear cells to mitogens were normal in both patients. A review of the literature revealed 26 additional patients with definite SLE coexisting with MG. Besides the theoretical interest of this association, the differential diagnosis of fatigue in patients with SLE should always include the possibility of MG.
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PMID:The association of systemic lupus erythematosus and myasthenia gravis. 783 Nov 74

Induction of an experimental disease resembling murine systemic lupus erythematosus (SLE), has been achieved in mice by immunization with a human monoclonal anti-DNA antibody, bearing a common idiotype, designated 16/6 Id. In the present study we report the preparation of F(ab')2 proteolytic fragments of the human 16/6 Id mAb and the ability of the latter to induce experimental-SLE in mice. Following immunization with the F(ab')2 fragment, mice developed antibodies bearing the 16/6 Id, anti-16/6 Id and a variety of autoantibodies, similar to mice immunized with the whole 16/6 Id molecule. Serological manifestations of the disease such as leukopenia, proteinuria and renal damage, were developed following the immunization with the 16/6 Id F(ab')2 proteolytic fragments. These results demonstrate the pathogenic role of the F(ab')2 fragment that bears the 16/6 Id.
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PMID:Induction of experimental systemic lupus erythematosus in mice by immunization with the F(ab')2 fragment of the human anti-DNA monoclonal antibody carrying the 16/6 idiotype. 795 7

Out of 330 adult Systemic Lupus Erythematosus (SLE) cases who attended the Rheumatic Care Centre, Government General Hospital, 59 children were analysed. There was no case with onset before the age of 5 years. There were 49 females and 110 males (M:F = 1:4.9). The initial manifestations were fever (67%), arthritis (61%), skin rash (59%) and lymphadenopathy (27.1%). There was no case of Raynaud's phenomenon. Only 10.1% of patients presented with thrombocytopenic purpura. In the cumulative clinical features, arthritis in 86.6%, fever in 79.8%, skin rash in 69.4%, lymphadenopathy in 61% and hepatosplenomegaly in 39.9% were observed. Renal involvement was seen in 49.1%, neuropsychiatric manifestations in 27.1%, pleuropulmonary in 22% and cardiac manifestations in 10.2%. Anaemia was seen in 50.8%, leukopenia in 18.4%, thrombocytopenia in 11.8%, ANA in 100%, anti-dsDNA in 92.3%, anti-Sm in 34.7%, anti-SSA in 38.5%, anti-SSB in 15.4%, ACL in 30.8%, low C3 in 50% and false positive VDRL in 3.3%. Death occurred in 8 children, 3 due to infection, 2 due to renal causes, 1 due to cardiac and 2 due to central nervous system involvement.
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PMID:Childhood systemic lupus erythematosus in south India. 795 96


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