Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A lupus-like syndrome involving chronic urticaria with cutaneous vasculitis, systemic symptoms, hypocomplementemia with preferential depletion of C1q, and low m.w. (7S) C1q-precipitins has recently been defined. The C1q-precipitin activity (C1q-p) seems to represent a diagnostic marker of the disease, but its chemical nature is not yet clear. We have partially purified and characterized C1q-p from the serum of two patients with this syndrome and compared its activity with the C1q-precipitating activity of aggregated human gamma-globulin (AHGG) anti-C1q antibodies, and several polynucleotides including DNA and polyinosinic acid. C1q-p was found to partition with IgG during precipitation by ammonium sulfate and low ionic strength buffer as well as during column chromatography on DEAE-cellulose and G-200 Sephadex. Like AHGG, but in complete contrast to the polynucleotides, the C1q-precipitating activity of C1q-p was sensitive to pepsin, trypsin, and acidic conditions, but unaffected by DNAse or RNAse; the C1q-precipitating activity of anti-C1q antibody was not diminished by any of these procedures. Thus, C1q-p consists of gamma-migrating protein of low m.w., and its C1q-precipitating activity is indistinguishable from that of AHGG. These results are consistent with the concept that C1q-p is comprised, at least in part, of IgG that binds C1q via the Fc portion of the molecule.
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PMID:Low molecular weight C1q-precipitins in hypocomplementemic vasculitis-urticaria syndrome: partial purification and characterization as immunoglobulin. 2 69

NZB/NZW F1 female mice received levamisole in an attempt to increase suppressor T cell function. Responses varied with dosage of drug and age of mice. When treatment with 25 microgram/gm doses (intermittent or daily) was begun at 12 weeks of age, nephritis was accelerated in spite of transient reduction of anti-DNA antibodies. When treatment was begun at 4 weeks, or when doses of 250 microgram/gm were given, no clinical effects were observed. In the mice with accelerated disease, delayed hypersensitivity and antibody responses to sheep erythrocytes increased; antibody responses to pneumococcal polysaccharide were unaffected. It is possible that some increased immune responses associated with levamisole are undesirable in murine lupus.
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PMID:Alteration of lymphocyte function in NZB/NZW mice. IV. Response to levamisole. 3 81

In blood sera of patients with systemic red lupus there were observed antibodies, which interacted in reaction of indirect hemagglutination and in complement fixation test with DNA of scleromic bacteria and did not react with the other structures of bacterial cell: with Buaven antigen, detergent and capsular polysaccharides. Reaction of indirect hemagglutination of scleromic DNA with the sera was inhibited by DNA preparations of animal origin. The serological activity of DNA from scleromic bacteria depended upon its secondary structure and did not correlate with polymeric state and nucleotide composition of the biopolymer.
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PMID:[Characteristics of the interaction of Klebsiella rhinoscleromatis DNA with the sera from patient with systemic lupus erythematos]. 4 10

Extensive serologic changes occur in systemic lupus erythematosus (SLE) which are probably secondary to unknow primary cause(s). The New Zealand hybrid mouse model most likely has a viral-induced disease and does not show many of the clinical features of the human disease. The best example of human SLE which provides a clue to etiology is the drug-induced type, particularly that due to procainamide. In these patients it is possible to study the development of serologic changes prior to the onset of clinical manifestations, and then observe regression of the clinical and serological changes on withdrawal of the medication. Although there is a rough correlation between the many serologic abnormalities and the clinical picture, enough exceptions exist, so that single tests such as serum complement, anti-DNA antibodies, per cent DNA binding, and others, cannot be used as a sine qua non for management. Care of the patient still remains a clinical problem guided by various laboratory procedures but not dependent on any one. Alkyating agents have a limited role in the treatment of lupus nephropathy and cutaneous vasculitis but azathioprine is probably of no value in SLE.
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PMID:Serologic abnormalities in spontaneous and drug-induced systemic lupus erythematosus. 5 Apr 52

DNA transcripts of infectious RNA viruses were found to be integrated in the DNA of chronically-infected tissue cultures. DNA sequences homologous to RNA of measles virus were found in tissues affected with systemic lupus erythemotosus. These data open up a new class of virus-cell interaction that may be a result of cooperation between infectious and oncogenic viruses.
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PMID:Integration of viral genomes. 5 75

The serum of a female suffering from Lupus erythematosus visceralis was investigated by complement fixation for the reaction with native and denatured DNA's of various base composition. The reaction with native DNA is independent on the (G+C)-content of the DNA. It is apparent that the responsible antibodies react with determinants of the helical conformation, which are identical in the various DNA-molecules. Quantitative differences are found with denatured DNA's. The strongest complement fixation is observed with (G+C)-rich denatured DNA. The reaction with denatured DNA is only partially inhibited by DNA digest. These antibodies obviously react with sequential determinants containing bases. Therefore, they are induced by a different mechanism of sensitization.
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PMID:[The reactivity of lupus erythematosus serum with native and denatured DNA of various origins]. 5 75

A 63-year-old man developed an asymptomatic pleural effusion following the administration of 500 gm of procainamide hydrochloride over a six-month period. The diagnosis was initially suggested by the finding of lupus erythematosus cells in the pleural fluid. Lupus erythematosus cells and antinuclear antibodies appeared in the blood two months later and remained for a period of six months. The diagnosis was corroborated by the presence of antibodies to denatured DNA, but not to native DNA.
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PMID:Lupus erythematosus cells in pleural effusion: the initial manifestation of procainamide-induced lupus erythematosus. 7 76

Systemic lupus erythematosus (SLE) is not a rare disease. There are several common clinical signs which should alert the physician to a possible diagnosis of SLE and which should condition him to look for specific clinical and laboratory findings. In addition to simple screening tests, useful procedures include a search for antinuclear antibodies, lupus erythematosus (LE) cells, anti-DNA antibodies and low serum complement. Management is determined by the type of course encountered but most patients will do well under the care of their family physician.
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PMID:Diagnosis and management of systemic lupus erythematosus. 7 45

In the course of a prospective study of 165 patients with SLE a subgroup of eight patients with active SLE yet with persistently negative tests for ANF and LE cells was identified. These patients were characterized by a photosensitive skin rash with a negative lupus band test, a high incidence of arthritis, mild form of renal disease, and a positive family history for connective tissue disease. Antibodies to DNA and cytoplasmic antigens were detected in a few.
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PMID:Systemic lupus erythematosus with negative LE cells and antinuclear factor. 7 82

Circulating antibodies against certain nuclear acidic protein antigens have been shown to have diagnostic and prognostic importance in connective tissue disease. We describe a new precipitin system found in the sera of patients with systemic lupus erythematosus. The antigen, called MA, was prepared from calf thymus nuclei, and was shown to be distinct from other nuclear acidic protein antigens by physicochemical and immunologic techniques. MA antibodies were detected in the serum of 12 of 66 lupus patients and in none of 554 sera from normal controls or patients with other rheumatic diseases. Lupus patients having MA antibodies had more severe disease than did lupus patients with Sm or native DNA antibodies, manifested by recalcitrant skin rashes and a significantly greater incidence of hypocomplementemia, serious renal disease, hypertension, hepatosplenomegaly, lymphadenopathy, and neurological disease (P values range from 0.025 to 0.005). The presence of circulating MA antigen was demonstrated in three lupus patients immediately before a flare of nephritis. These data suggest that MA is a nuclear acidic protein antigen that may identify a subset of lupus patients with very severe disease. The presence of the antigen in the circulation before clinical flares suggests a possible biologic role for the MA system in an immune complex nephritis.
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PMID:Characterization of a distinct nuclear acidic protein antigen (MA) and clinical findings in systemic lupus erythematosus patients with MA antibodies. 8 19


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