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)

Many sera from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) inhibit lymphocyte-dependent antibody cytotoxicity (LDAC). RA synovial fluids also inhibit LDAC. RA serum inhibition was present in high molecular weight and 5S serum fractions, whereas in SLE it was confined to 7S fractions. A correlation between rheumatoid factor activity and LDAC inhibition was noted, and there was some evidence for inhibition of SLE serum acting on effector cells. Inhibition in RA synovial fluid was found in both high molecular weight and very low molecular weight fractions (less than 4S.)
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PMID:Serum and synovial fluid inhibitors of antibody-mediated lymphocytotoxicity in rheumatoid arthritis and systemic lupus erythematosus. 5 39

To study the role of genetically determined immune responsiveness in the pathogenesis of systemic amyloidosis complicating rheumatoid arthritis the HLA antigens were identified in 26 patients with rheumatoid arthritis complicated by secondary amyloidosis, in 44 patients with rheumatoid arthritis, and in 11 patients with secondary amyloidosis of non-rheumatoid origin. Subjects with ankylosing spondylitis, sacroiliitis without peripheral polyarthritis, Reiter's disease, reactive arthritis, erosive osteoarthritis, psoriatic arthropathy, systemic lupus erythematosus or arthritis associated with a gastrointestinal involvement were excluded from the study. Patients with amyloidosis secondary to rheumatoid arthritis had a high frequency of the HLA specificity B27 and of the haplotype likely to bear A2, B27. The association with B27 was closest in the group of male patients with amyloidosis whose rheumatoid arthritis had begun at an early age and who lacked demonstrable rheumatoid factor in serum. These patients may represent a genetically determined subentity of rheumatoid arthritis.
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PMID:HLA-B27 in rheumatoid arthritis and amyloidosis. 6 5

Evidence for the presence of immune complexes in blood, synovial fluid, and tisues of patients with rheumatoid arthritis (RA) includes low complement levels in blood and effusions, deposition of immunoreactants in tissues and vessel walls, precipitate formation after addition of monoclonal rheumatoid factor (mRF) to serum or synovial fluid. To quantitate immune complex-like material in RA patients, we developed a radioimmunoassay based on inhibition by test samples of the interaction of (125I)aggregated IgG (agg IgG) and mRF coupled to cellulose. This method could measure immune complexes of human antibody with hemocyanine prepared in vitro. The assay was not influenced by presence of polyclonal RF in test samples, nor by freezing and thawing. Normal levels of immune complex-like material in serum were less than 25 mug agg IgG EQ/ML. 12 of 51 RA sera examined (26%) contained more than 25 mug/ml. The presence of this material in RA sera was found to correlate with severity of disease, as measured by anatomical stage and functional class. There was an inverse correlation of the material with serum C4 level. Rheumatoid synovial fluids generally contained higher levels than serum, and five of 23 contained very much higher levels. The frequency of elevated levels of immune complex-like material in sera of patients with systemic lupus erythematosus (2 of 29) and with miscellaneous vasculitides (2 of 21 was much lower than in RA, suggesting that mRF exhibits a specificity for only certain kinds of immune complexes. The reason for this apparent specificity may explain such distinctive features of RA as the high frequency of polyclonal RF, the lack of immune complex nephritis, and the generally normal levels of serum complement.
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PMID:Immune complexes in sera and synovial fluids of patients with rheumatoid arthritis. Radioimmunoassay with monocylonal rheumatoid factor. 12 89

Five patients with systemic lupus erythematosus (SLE), four of whom died with colonic perforations, are reported. Perforation of the colon constituted the most frequent cause of death among 107 patients with SLE admitted to the Rheumatic Disease Unit during a three year period. All five patients with colonic perforation had clinical and laboratory manifestations of active SLE in addition to the abdominal syndrome. Most striking was evidence of active arteritis in all patients with either central nervous system involvement and/or peripheral arteritis, in addition to that found in the gastrointestinal tract. Hyperglobulinemia and rheumatoid factor as well as antinuclear antibodies were present at some time in all patients. The abdominal syndrome was characterized by the insidious onset of lower quadrant pain which was intermittent and colicky. Although direct abdominal tenderness was eventually present in all patients, rebound tenderness and hypoactive bowel sounds were variable and abdominal rigidity occurred only in one patient and late in the course. The differential diagnosis of abdominal pain in SLE is reviewed and possible mechanisms for the production of colonic perforations are discussed. It is suggested that the presence of rheumatoid factors in conjunction with circulating immune complexes may be the pathogenetic mechanism via the production of a mesenteric arteritis.
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PMID:Colonic perforations in systemic lupus erythematosus. 12 39

Seventeen patients with characteristic disseminated gonococcal arthritis-dermatitis syndrome were studied for the presence of immune complexes, and circulating gonococcal antigen and antibody. The two immune complex techniques, monoclonal rheumatoid factor assay and cryoglobulin survey, did not reveal any consistent abnormalities. Complement levels (CH50, C'3, C'4) were not consistent with peripheral consumption except in 2 patients with coinciding systemic lupus erythematosus. Gonococcal antibody was detected in 47% of patients when they presented with the syndrome. However, gonococcal antigen was not found in either serum or synovial fluid. These results do not support the hypothesis that circulating immune complexes are involved in the pathogenesis of disseminated gonococcal arthritis-dermatitis syndrome.
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PMID:Survey for immune complexes in disseminated gonococcal arthritis-dermatitis syndrome. 15 44

Glomerular deposits of immunoglobulin A (IgA) (and immunoglobulin G [IgG]) has been described in IgA-nephropathy (Berger's disease), in anaphylactoid purpura, and systemic lupus erythematosus. The pathogenesis of mesangial IgA deposits in these disease states is unclear. Circulating immune complexes have been speculated to be involved although their existence in blood in IgA nephropathies have never been reported. We describe a 53-year-old man who presented with a petechial rash in lower extremities accompanied by painful swelling of left ankle and wrist. Polyclonal elevation of IgA and IgG in serum was found, along with cryoglobulins containing IgA and IgG (rheumatoid factor positive). After two years, hematuria, mild proteinuria, and active urinary sediment developed and renal biopsy revealed focal proliferative changes. Immunofluorescence revealed predominantly mesangial deposits of IgA and IgG but no IgM nor complement. This experience suggests that circulating complexes consisting of IgA and IgG may lead to renal lesions presenting clinically and histologically in a way similar to that commonly seen in IgA nephropathies.
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PMID:Case report: mesangial IgA-IgG deposition in mixed cryoglobulinemia. 15 12

Warts were found in 25 out of 56 patients with definite or probable systemic lupus erythematosus (SLE) but in only 19 out of 160 control patients. Warts were particularly prevalent in elderly patients with SLE. The corticosteroid and antimalarial drugs used to treat SLE did not influence the frequency of warts. Wart-virus antibodies were found significantly less often in patients with SLE than in controls: antibodies were detected in 23 out of 51 patients and in 40 out of 54 controls. Ihe findings suggest that some deficiency in the immune mechanisms of patients with SLE predisposes them to develop warts. There was an inverse correlation among the patients with SLE between the occurrence of warts and rheumatoid factor activity. This suggests that rheumatoid factor may interfere with resistance to warts.
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PMID:Warts and wart virus antibodies in patients with systemic lupus erythematosus. 18 13

The present epidemiological study concerned and evaluation of the level of measles antibodies (hemagglutination inhibition (HI) assay) and para-influenza-1 (Sendai) antibodies (complement fixation (CF) test) in serum of 107 control individuals (38 women), 176 multiple sclerosis (MS) patients (93 women), 717 relatives to MS patients (361 women), 9 patients with systemic lupus erythematosus (SLE) (all women), 46 relatives to SLE patients (28 women), 57 patients with rheumatoid arthritis (RA) (37 women), and 143 relatives to RA patients (85 women). In MS and their relatives the HI titer value was significantly raised and the CF titer only insignificantly increased. In SLE the HI titers were insignificantly raised but the CF values significantly decreased. In RA HI values were insignificatly raised, but the CF values were significantly decreased among females lacking rheumatoid factor in serum. In the individuals under study, HI values did not correlate with CF values. In MS two groups of patients could be treated, i.e. one group with raised HI values and one with normal distribution of titers. The data obtained are discussed in light of the theory, that all three disease entities may be "Slow Virus Diseases".
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PMID:An epidemiological study on paramyxovirus antibody titers in multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. 20 37

Peripheral blood polymorphonuclear leucocytes (PMN) and cryoglobulins were isolated from patients with systemic lupus erythematosus (SLE). Fluorescent inclusions were found in PMN. Normal donor PMN were incubated with the sera and cryoglobulins from SLE patients. In most cases inclusions were observed after incubation. The high incidence of anti-IgG activity in phagocytosed cryoglobulins confirms the importance of the rheumatoid factor in phagocytosis of immune complexes. It is concluded that phagocytosis of cryoglobulins supports the suggestion that cryoglobulins are a subpopulation of immune complexes.
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PMID:Polymorphonuclear leucocyte fluorescence and cryoglobulin phagocytosis in systemic lupus erythematosus. 22 18

Of 22 children with congenital complete heart block (CCHB) available for study, 14 (63.6%) were born to 11 mothers with clinical or laboratory evidence of connective tissue disease, primarily lupus erythematosus (LE). Seven mothers had both clinical and laboratory evidence of disease while four had only positive laboratory studies including fluorescent antinuclear antibody, rheumatoid factor, and depressed complement levels. In adults with systemic LE, pathologic changes in the collagen surrounding the conduction system have led to the fibrosis and death from heart block. Antinuclear antibodies of the IgG class cross the placental barrier and newborn infants have been reported with transient skin lesions of lupus. Placental transmission of such antibodies may affect the fetal cardiac conduction system, surrounding collagen, and myocardium, leading in some cases to CCHB. This is probably one important etiologic factor in CCHB even though the mother is asymptomatic during her pregnancy.
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PMID:Congenital heart block in newborns of mothers with connective tissue disease. 30 Oct 70


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