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)

The 25,000 dalton protein of Mason-Pfizer monkey virus (MPMV) was isolated by gel filtration chromatography. In agreement with results from other laboratories, antisera to type-C and the non-type-C bovine leukemia and equine infectious anemia viruses did not precipitate 125I-labelled MPMV p25. In addition, these viruses did not cross-react in a competition radioimmunoassay for MPMV p25. Twenty-one human tissues (15 breast carcinomas, 2 normal breasts, 3 acute myelogenous leukemias and 1 sarcoma) were fractionated by detergent solubilization, ammonium sulfate precipitation, and DE-52 anion exchange chromatography. These methods were shown to be highly effective for purification of MPMV p25. Under assay conditions which minimized incubation damage to the 125I-MPMV p25, all tissues failed to react in the competition radioimmunoassay (RIAT). Two hundred and two human sera or plasma specimens, including those from patients with breast cancer and 33 age-matched controls, from 50 patients with hematologic malignancies, from 12 patients with amyotrophic lateral sclerosis, and from 14 patients with systemic lupus erythematosis, were examined for antibodies to MPMV p25. With the exception of two multiple myeloma plasma which produced artifactual false positive reactions based on hypergammaglobulinemia, a known complication of salt precipitation radioimmunoassays, the remainder of the specimens were negative for evidence of MPMV p25 antibodies.
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PMID:Radioimmunoassay for the major structural protein of Mason-Pfizer monkey virus: Attempts to detect the presence of antigen or antibody in humans. 40 48

Two modified polynucleotides having the Z-DNA conformation (poly [dG-dC] dien Pt and poly [dG-br5dC] . poly [dG-br5dC]) have been used for determination of antibodies to Z-DNA. Such antibodies were found in sera of patients with systemic lupus erythematosus and with Crohn's disease. They were scarcely observed in polyradiculoneuritis and in amyotrophic lateral sclerosis. In Crohn's disease sera, no antibodies to B-DNA were ever found but presence of two different families of antibodies to Z-DNA was demonstrated.
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PMID:Presence of Z-DNA specific antibodies in Crohn's disease, polyradiculoneuritis and amyotrophic lateral sclerosis. 633 95

Increasing numbers of patients are being recognized with neurological abnormalities associated with the immunochemical changes of plasma cell disease. To illustrate the wide spectrum of clinical disorders that can be found, I discuss in detail 5 patients: 2 with neuropathy, 3 with amyotrophic lateral sclerosis (ALS), all of whom had serum monoclonal paraproteinemia. In addition, I report in tabular form 6 patients with paraproteinemia and the following clinical presentations: 1) systemic lupus with polyneuropathy and severe cerebritis, 2) myasthenia gravis with thymoma, 3) polymyositis, 4) polymyositis, arthritis and Grave's disease, 5) relapsing polyneuritis (one of the original patients diagnosed by Austin) and 6) ALS, dystonia and parkinsonism. Major improvements in clinical condition occurred sometimes, but not always, coincident with reductions in the levels of the paraprotein using prednisone, cyclophosphamide, chlorambucil and plasma exchange treatments even in some of the patients who had the clinical appearance of ALS. Patients with neuromuscular diseases should be routinely screened with serum immunoelectrophoresis for monoclonal gammopathy. If a monoclonal gammopathy is found and if the disease is serious, then those patients should be treated as if they had an autoimmune disorder.
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PMID:Neuropathy and motor neuron syndromes associated with plasma cell disease. 647 86

Sera from patients with multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), subacute sclerosing panencephalitis (SSPE), and myasthenia gravis (MG) were assayed for immune complexes. Three techniques were used: a modified Raji cell assay, the 125I-Clq polyethyleneglycol assay, and a solid-phase clq assay. Immune complex levels were elevated in sera of some patients with MS, ALS, and SSPE, but the elevations were modest when compared with active systemic lupus erythematosus (SLE). In some cases, abnormalities were detected in only one assay system; in other cases, abnormalities were detected by two or three assay systems. In MS, immune complex elevations correlated with active disease and with decreased suppressor cell activity. Of two ALS patients with antecedent poliomyelitis, one had markedly increased levels of immune complexes in two assays. In MG, levels of immune complexes did not differ from those of controls.
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PMID:Circulating immune complexes in neurologic disease. 719 88

We report the case of a 48-year-old woman diagnosed as having systemic lupus erythematosus who developed a neurological disorder that finally resulted in amyotrophic lateral sclerosis. Although neurological disturbances caused by systemic lupus erythematosus are protean, there are no reported cases of amyotrophic lateral sclerosis associating with lupus disease. This association and the suspected autoimmune mechanism of pathogenesis in amyotrophic lateral sclerosis suggest that this might not be a simple coincidence but perhaps a causal relationship.
Lupus 1993 Apr
PMID:Amyotrophic lateral sclerosis in a patient with systemic lupus erythematosus. 833 35

Based on the review of the literature, therapeutic PP has a definite role in the treatment of patients with GBS, CIDP, polyneuropathies associated with MGUS, MG, and LEMS (table). PP may have a role in treating patients with Refsum's disease, acquired neuromyotonia, stiff-man syndrome, cryoglobulinemic polyneuropathy, CNS-SLE, ADEM, and MS, but these decisions should be made on a case-by-case basis. PP has no role in treating patients with ALS or paraneoplastic syndromes with circulating autoantibodies.
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PMID:Assessment of plasmapheresis. Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. 879 93

In an attempt to identify unique disease-related autoantibodies, the serum from an ataxia and sensory neuropathy patient was used as a probe to isolate a 2.5-kd cDNA from a HeLa expression library. The nucleotide sequence was 99% identical to MPP1, a cell-cycle-related nuclear protein phosphorylated during mitosis. Expression of the cDNA in an in vitro translation system yielded a recombinant protein that migrated in SDS-PAGE at approximately 97 kd. This protein was immunoprecipitated by the prototype human serum, by an immune guinea pig anti-MPP1 serum, but not by normal human serum or preimmune guinea pig serum. Western blot analysis of HeLa cell proteins showed that the prototype human serum and immune guinea pig antiserum recognized an approximately 225-kd protein, suggesting that the isolated clone contained a partial cDNA. By indirect immunofluorescence, the affinity-purified antibody and a guinea pig antiserum reacted with nuclei of interphase HEp-2 cells and the cytoplasm of certain neuronal cells. Sera from 10 of 25 unselected patients with ataxia, 1 of 30 patients with peripheral neuropathy, 1 of 50 multiple sclerosis patients, 0 of 20 amyotrophic lateral sclerosis, 0 of 10 children with postviral ataxia, 0 of 10 systemic lupus erythematosus patients, 0 of 3 patients with hereditary cerebellar ataxia, 0 of 8 with ataxia telangiectasia, and 0 of 30 age- and gender-matched controls immunoprecipitated the recombinant MPP1 protein. None of the patients with anti-MPP1 antibodies had evidence of malignancy. This is the first report of MPP1 as a target autoantigen in patients with idiopathic ataxia.
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PMID:Autoantibodies from patients with idiopathic ataxia bind to M-phase phosphoprotein-1 (MPP1). 1069 67

Since the Persian Gulf War ended in 1991, veterans have reported diverse, unexplained symptoms. Some have wondered if their development of systemic lupus erythematosus, amyotrophic lateral sclerosis, or fibromyalgia might be related to Gulf War service. The authors used Cox proportional hazard modeling to determine whether regular, active-duty service personnel deployed to the Persian Gulf War (n = 551,841) were at increased risk of postwar hospitalization with the three conditions compared with nondeployed Gulf War era service personnel (n = 1,478,704). All hospitalizations in Department of Defense facilities from October 1, 1988, through July 31, 1997, were examined. With removal of personnel diagnosed with any of the three diseases before August 1, 1991, and adjustment for multiple covariates, Gulf War veterans were not at increased risk of postwar hospitalization due to systemic lupus erythematosus (risk ratio (RR) = 0.94, 95% confidence interval (CI): 0.65, 1.35). Because of the small number of cases and wide confidence limits, the data regarding amyotrophic lateral sclerosis were inconclusive. Gulf War veterans were slightly at risk of postwar hospitalization for fibromyalgia (RR = 1.23, 95% Cl: 1.05, 1.43); however, this risk difference was probably due to the Gulf War veteran clinical evaluation program beginning in 1994. These data do not support Gulf War service and disease associations.
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PMID:Is systemic lupus erythematosus, amyotrophic lateral sclerosis, or fibromyalgia associated with Persian Gulf War service? An examination of Department of Defense hospitalization data. 1087 28

In previous studies we observed that human umbilical cord blood (HUCB) could have a protective effect on the onset of disease and time of death in MRL Lpr/Lpr mice which have an autoimmune disease that may be considered similar to human lupus. We believed a temporary xenograph may have occurred in these animals with the disease process delayed and the life span markedly increased. When HUCB is stored at 4 degrees C in gas permeable bags, there is a decrease of the cell reaction in mixed lymphocyte cultures. The blood, however, maintains a significant number of cells capable of producing replatable colonies. This study attempted to determine the effect of HUCB on SOD1 mice (transgenic B6SJL-TgN(SOD1-G93A)1GUR), which have a mutation of the human transgene, (CuZn superoxide dismutase gene SOD1) that has been associated with amyotrophic lateral sclerosis. We previously developed evidence that the survival of lethally irradiated mice was related to the number of human mononuclear cells administered. In the present study, we decided to investigate the effect of a relatively large dose of human mononuclear cord blood cells on SOD1 mice subjected to a sublethal dose of irradiation preceded by antikiller sera (rabbit anti-asialo). The SOD1 mice show evidence of paralysis at 4 to 5 months. The average expected lifetime of these mice is reported to be 130 days (Jackson Laboratory). In this experiment, there were 23 mice. Two mice died before the onset of paralysis. The remainder were divided into three groups: group I: control group of 4 untreated mice; group II: an experimental group of 6 mice treated with antikiller sera, 800 cGy irradiation plus 5 x 10(6) congenic bone marrow mononuclear cells; group III: another experimental group of 11 mice treated with antikiller sera, 800 cGy irradiation plus 34.2-35.6 x 10(6) HUCB mononuclear cells, previously stored for 17-20 days at 4 degrees C in gas permeable bags. The results were as follows: the average age at death was: (I) 127 days for the untreated control group, (II) 138 days for the group that received 800 cGy of irradiation and congenic bone marrow (BM) and (III) 148 days for the group that received irradiation and HUCB. (P < 0.001 HUCB vs control, p < 0.01 HUCB vs BM). The longest surviving mouse in each group was 131, 153, and 182 days old respectively. In summary, large doses of HUCB mononuclear cells produced considerable delay in the onset of symptoms and death of SOD1 mice. These preliminary results may not only indicate that amyotrophic lateral sclerosis is an autoimmune disease, but may also indicate a possible treatment for a devastating disease and possibly others.
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PMID:Human umbilical cord blood effect on sod mice (amyotrophic lateral sclerosis). 1089 29

A 61-year-old woman with a history of photosensitive dermatitis and recurrent mouth ulcers presented with progressive weakness typical of amyotrophic lateral sclerosis (ALS), and subsequently underwent extensive neurologic and rheumatologic testing. We investigated whether ALS-like motor neuron disease associated with a positive antinuclear antibody (ANA) is really ALS or rather neuropsychiatric systemic lupus erythematosus (NPSLE). On neurologic evaluation, she had prominent bulbar involvement with dysarthria and dysphagia associated with profound lingual fasciculations and a denervating pattern on electromyogram. MRI showed no evidence of cerebral ischemia. Laboratory studies revealed a positive ANA (1:2560 titer), positive antiphospholipid antibodies (GPL and MPL), circulating lupus anticoagulant, and depressed C3 and C4. Repeat MRI studies at 4 and 11 mo revealed an evolving infarct in the paramedian pons consistent with the presence of NPSLE. Therapy was initiated with corticosteroids and intravenous cyclophosphamide, and the neurologic condition did not improve, but also did not progress inexorably as would be expected with ALS. NPSLE, presumably through the mechanism of ischemic vasculopathy, may present as motor neuron disease clinically indistinguishable from ALS.
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PMID:Neuropsychiatric systemic lupus erythematosus presenting as amyotrophic lateral sclerosis. 1190 83


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