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)

After immunization with A/New Jersey/76 and A/Victoria/75 influenza vaccines, 11 patients with systemic lupud erythematosus were serially evaluated for changes in disease activity, serologic abnormalities, and their capability to generate specific antibodies. One patient, with active disease, developed a diffuse, proliferative glomerulonephritis. None of the other patients or control subjects had significant local or systemic side effects. Significant levels of antibodies were generated to A/New Jersey/76 in eight of the 11 patients and in seven of eight control subjects and to A/Victoria/75 in seven of 11 patients and five of eight control subjects. The geometric mean responses of both total and IgG antibodies to each viral antigen were no different in patients with systemic lupus erythematosus than in control subjects. In patients with stable systemic lupus erythematosus, immunization with killed influenza viral vaccine appears to be safe and effective.
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PMID:Clinical and antibody responses after influenza immunization in systemic lupus erythematosus. 30 56

Two recently described murine strains, MRL/1 and BXSB, develop a lupus-like syndrome resulting in a 50% mortality by the fifth month of age. Comparison of the immunopathological and virological characteristics of these mice with those of the NZB/NZW F1 mouse reveals several pathogenetic common denominators but no obvious common etiologic factors. In all three kinds of mice, the lupus-like syndrome consists of a fatal immune complex type glomerulonephritis and complete or near complete thymic cortical atrophy plus lymphoid hyperplasia that varies in degree among the three kinds of mice. The nephritic glomeruli contain a concentration of antinuclear antibodies plus varying amounts of stainable gp70. This syndrome is consistently correlated with abnormally elevated serum IgG levels, antinuclear antibodies, anti ds- and ssDNA antibodies, and circulating immune complexes, as well as depressed serum hemolytic complement. Features that differ among the three kinds of mice include: H2 type, anti-lymphocyte antibody, cryoglobulins, T-B cell ratios, sex incidence of disease, vasculitis, and oncornaviral flora. The serum gp70 levels in the three mice also differ considerably, but all are within the range of gp70 levels found in some immunologically normal strains.
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PMID:Etiology and pathogenesis of a spontaneous lupus-like syndrome in mice. 30 93

MRL/1 and BXSB male mice have a systemic lupus erythematosus (SLE)-like disease similar to but more acute than that occurring in NZB X W mice. The common elements of lymphoid hyperplasia, B-cell hyperactivity, autoantibodies, circulating immune complex (IC), complement consumption, IC glomerulonephritis with gp70 deposition, and thymic atrophy were found in all three kinds of SLE mice. On the basis of these common elements, SLE seen in these mice can be considered a single disease in the same sense that human SLE is one disease. The differences in the SLE expressed in the different mice are no greater than those found in an unselected series of humans with SLE. However, the significant quantitative and qualitative variations in abnormal immunologic expression suggest that different constellations of factors, genetic and/or pathophysiologic, may operate in the three murine strains and that each constellation is capable of leading, via its particular abnormal immunologic consequences, to the activation of common immunopathologic effector mechanisms that cause quite similar SLE-like syndromes. From an experimental point of view, the availability of several inbred murine strains of commonplace histocompatibility types that express an SLE-like syndrome makes possible innumerable manipulations which should help to elucidate the nature and cause(s) of this disorder.
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PMID:Spontaneous murine lupus-like syndromes. Clinical and immunopathological manifestations in several strains. 30 11

This report describes a previously unrecognized animal model of SLE, the PN mouse. Although outbred PN mice were studied originally as models of polyarteritis nodosa, their inbred descendants have autoimmune disease which closely resembles SLE. In the current study, positive indirect immunofluorescence tests for ANA appeared when the mice were 5 months old, and 80% of mice were ANA-positive at 10 months of age. Anti-DNA were detected in sera from newborn mice and from 53% of mice under 2 months of age. Seventy-six percent of PN mice developed anti-DNA at the age of 10 months. Glomerular deposits of IgG, IgM, IgA, and complement appeared at 2 to 4 weeks of age, and examination of renal tissue by electron microscopy showed basement membrane thickening and dense intramembranous deposits. Neoplasms arose in 14% of PN mice. Female mice died earlier than male mice, and the most common causes of death were glomerulonephritis and arteritis. It was concluded that the serologic and histologic characteristics of disease in PN mice resembled SLE.
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PMID:Palmerston North mice, a new animal model of systemic lupus erythematosus. 31 Aug 56

Herein we present our experience with 16 children in whom the diagnosis of SLE was established between May 1974 and April 1978. In eleven of them renal biopsy was performed. Five had family history of immunologic disease. Only one patient had history of anticonvulsant drug intake. The clinical picture resembles adult SLE, where the most frequent symptoms were arthritis, fever and dermatosis. Three patients showed focal proliferative glomerulonephritis; another 3, increased mesangial cellularity; 3 more presented diffuse proliferative glomerulonephritis and another one had membranous glomerulonephritis. LE cells, antinuclear antibodies, anti-DNA were present in various combinations in all patients. Treatment with an average dose of 22.8 mg/day of prednisone, plus immunosuppressive therapy in 9 patients, has allowed a 36 months survival in 13 patients. Progressive renal involvement and tuberculosis were the cause of death in 3 cases. Our results are compared with those in the literature.
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PMID:[Systemic lupus erythematosus in pediatrics]. 31 44

Biopsies of apparently normal skin were obtained from 30 unselected patients with systemic lupus erythematosus. The immunoglobulin class distribution of the immune deposits at the dermal-epidermal junction was determined in order to assess associated disease patterns and to investigate the possibility that the immunoglobulin classes in the skin were an indication of the classes of serum anti-native DNA antibodies. Biopsy specimens containing IgG deposits were obtained from 10 patients with more active disease and a greater incidence of glomerulonephritis than those patients with only IgM deposits or negative biopsies. However, in this unselected group of patients the immunoglobulin class of the immune deposits did not necessarily indicate the class of serum anti-native DNA antibodies. Therefore biopsy of clinically uninvolved skin will not always identify SLE patients with an immunological restriction to IgM antibody production.
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PMID:Immunoglobulin classes in skin basement membrane in systemic lupus erythematosus: clinical significance and comparison with classes of serum anti-DNA antibodies. 31 9

Eighteen patients with systemic lupus erythematosus (SLE) and proliferative glomerulonephritis, underwent serial serum determinations of C3, C4, and native DNA binding capacity, as well as repeat renal biopsy 7 to 48 months (median 25 months) following initial biopsy. Highly significant correlations were found between serum C3 levels and renal histologic changes (P less than 0.0001), and between serum C3 levels and DNA binding capacity (P less than 0.03). Histologic deterioration correlated with depressed C3 levels, while improvement was associated with normalization of C3 levels. No correlation between renal histologic changes and either serum C4 levels or DNA binding capacity was found. The data suggest that the serum level of C3 is the best index of activity of lupus nephritis.
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PMID:The significance of serial measurements of serum complement C3 and C4 components and DNA binding capacity in patients with lupus nephritis. 31 52

Detailed immunopathologic studies of early or silent renal alterations in systemic lupus erythematosus have been sparse. The renal biopsies of 16 lupus patients with normal renal function, including 8 with hematuria and/or proteinuria of recent onset, and 8 without clinically detectable renal disease were investigated by light, immunofluorescence, and electron microscopy. Immunoglobulins, complement components, and electron-dense deposits were detected in glomeruli of all patients, regardless of morphologic appearance or lack of clinical evidence of renal involvement. Features of membranous glomerulonepritis were observed in 4 patients with substantial proteinuria. In the remaining 12 patients, including 3 with hematuria and 4 with slight proteinuria, either minimal glomerular alterations or features of mesangial proliferative glomerulonephritis were seen. Transformation of the original disease was demonstrated in 3 of 3 patients rebiopsied within 2 years. The significance of these findings is discussed in relation to a) the spectrum of clinical and immunopathologic alterations in lupus nephritis and b) transformation of the original disease.
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PMID:Immunopathology of early and clinically silent lupus nephropathy. 32 2

The complement system may be activated by two pathways, the classical and the alternate. To evaluate their respective participation in different forms of glomerulonephritis, the plasma values of C3, C4, C3PA, C1q and properdin were determined in 70 patients. In systemic lupus erythematosus (LED), acute poststreptococcal glomerulonephritis (AGN) and septicemia the classical pathway appears to be mainly involved, whereas the amplification loop and the alternate pathway seem to be of secondary importance. By contrast, in membranoproliferative glomerulonephritis (MPGN) the alternate pathway plays a major role. However, the present data suggest that activation of the classical pathway may often be involved as well. In minimal change glomerulonephritis no signs indicating involvement of the complement system were apparent. Follow-up observation demonstrated a correlation between decreases in plasma complement concentrations and the clinical severity of the primary disease in LED, AGN and septicemia, but not in MPGN.
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PMID:[Activation of the complement system in different forms of glomerulonephritis]. 33 69

Six patients with glomerulonephritis were found to have granular deposits of complement and/or immunoglobulins at the dermalepidermal junction of normal skin. No patient had extrarenal clinical manifestations of systemic lupus erythematosus (SLE). The only serologic test suggestive of SLE was a positive antinuclear antibody (ANA) reaction; results of complement and antinative deoxyribonucleic acid (DNA)-antibody tests were repeatedly normal. The patients with glomerulonephritis had a favorable initial response to therapy with prednisone with or without azathioprine. These patients may represent a variant of SLE in which the diagnosis can only be established by a direct immunofluorescence test of normal skin. Alternatively, they may constitute a separate new clinical entity. Because of the favorable response to therapy, we suggest that skin immunofluorescence be performed in patients who present with unexplained glomerulonephritis and a positive ANA.
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PMID:Diagnosis of lupus nephritis by skin immunofluorescence, in the absence of extrarenal manifestations of systemic lupus erythematosus. 33 49


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