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)

Paired serum and cerebrospinal fluid specimens from 19 patients with SLE and central nervous system dysfunction were studied with respect to cerebrospinal fluid IgG index (a measure of intrathecal IgG synthesis), isoelectric focusing using immunoperoxidase staining techniques to detect oligoclonal IgG, and determination of the cerebrospinal fluid/serum albumin quotient (Q albumin) as a measure of blood-brain barrier integrity. Twenty-five patients without neurologic disease and 70 patients with a variety of non-SLE neurologic disorders were also studied for comparison. Of most interest was the observation that 42 percent of the patients with SLE had cerebrospinal fluid oligoclonal IgG, usually in association with elevation of the cerebrospinal fluid IgG index. In addition, two of the cerebrospinal fluid specimens that exhibited oligoclonal IgG also had increased titers of alpha-interferon. Q albumin was normal (under 9.0) in 12 of 13 patients with SLE, who had seizure, psychosis, or cranial neuropathy as principal central nervous system manifestations (mean +/- SD = 5.3 +/- 2.4), but was significantly elevated (mean +/- SD = 27.4 +/- 18.8, p less than 0.001) in five of six patients with diffuse, major central nervous system injury, for example, encephalopathy with coma, transverse myelopathy, paraparesis. Blood-brain barrier impairment was not correlated either with presence of circulating immune complexes or with other clinical or serologic evidence for extra-central nervous system disease activity. Taken together, the data suggest that, within the limitations of the techniques used, impairment of the blood-brain barrier in SLE may be secondary to the central nervous system lesion, rather than a result of systemic immune complex injury. In addition, substantial evidence is provided for an ongoing humoral immune response within the central nervous system in this disorder, which, in certain patients, may be associated with the production of intrathecal alpha-interferon.
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PMID:Intrathecal IgG synthesis and blood-brain barrier impairment in patients with systemic lupus erythematosus and central nervous system dysfunction. 683 7

A 34-year-old man had polar extremes of B cell dysfunction: systemic lupus erythematosus evolving into common variable hypogammaglobulinemia. He presented in 1974 with seizures and six other criteria for systemic lupus erythematosus; his antinuclear antibody titer was 1:1024 and IgG level, 2870 mg/dL. After 5 months of immunosuppressive treatment, a 79% decrease in serum IgG and 95% decrease in IgA levels occurred and manifestations of systemic lupus erythematosus disappeared. Six years later, he developed panhypogammaglobulinemia, had recurrent sinopulmonary infections, and showed nodular lymphoid hyperplasia on rectal biopsy. For comparison, serum immunoglobulin concentrations were measured serially in 13 other patients with systemic lupus erythematosus. Three developed severe depressions of these levels, two with IgG levels less than 300 mg/dL and one with an IgA level of 8 mg/dL. These decreases were transient, related to treatment, and not associated with infections. Daily high-dose prednisone therapy (60 mg/d) rather than treatment with cytotoxic drugs correlated with decreased immunoglobulin concentrations.
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PMID:Transition from systemic lupus erythematosus to common variable hypogammaglobulinemia. 685 20

The premise that chronic antigenic stimulation may be involved in lymphoproliferative disorders was considered in a patient with angioimmunoblastic lymphadenopathy who had received diphenylhydantoin (DPH) for seizure. This patient had clinical features overlapping with systemic lupus erythematosus (SLE) and serum antibody directed against DPH. It was proposed that the syndrome was caused by chronic antigenic stimulation with DPH.
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PMID:Angioimmunoblastic lymphadenopathy in a patient taking diphenylhydantoin. 697 73

Nervous system involvement in systemic lupus erythematosus is frequent. Psychiatric manifestations, seizures, headaches are most often observed. Movement disorders, hemiparesis, aseptic meningitis occur more rarely. Myelitis is exceptional as is peripheral nerve involvement. CT Scan shows cerebral atrophy and sometimes hemorrhages or ischemic lesions. Pathological examination usually demonstrates cortical microinfarcts, hemorrhage and meningitis, but lesions are not always found. In these case the cause of the neuropsychiatric disorder is unknown: a transitory vascular or immune mechanism has been proposed. Corticotherapy is effective in the majority of cases, but can be occasionally responsible for an exacerbation of neuropsychiatric symptoms.
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PMID:[Neuropsychiatric disorders in systemic lupus erythematosus: a general review (author's transl)]. 702 67

Both stroke and transient cerebral ischaemic attacks occurring in younger patients may be due to systemic lupus erythematosus. Other clinical features of the disease may be absent. Initially the ESR may be normal, as may serological tests. Seizures may occur at or near the time of the vascular events. Systemic lupus erythematosus may be the cause of an asymptomatic cerebral infarct or multi-infarct dementia.
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PMID:Stroke as an early manifestation of systemic lupus erythematosus. 711 20

Left homonymous hemianopia, hemiparesis, left-body clonic seizures, and progressive deterioration of consciousness complicated the clinical course of a 57-year-old woman with systemic lupus erythematosus (SLE). Autopsy documented the presence of multiple brain infarcts and cerebral arterial emboli that originated from the verrucae of Libman-Sacks endocarditis. Clinicians and pathologists should consider this unusual vascular mechanism of cerebral injury in patients with SLE who develop strokes.
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PMID:Cerebral embolism in Libman-Sacks endocarditis. 718 54

A 20-year-old patient with biologically-confirmed lupus developed a perirenal abscess following puncture biopsy of the kidney. Postoperative treatment included metronidazole at a mean dose of 2.5 g daily for 68 days (total dose : 165 g). Generalised convulsive seizures occurred on four occasions, associated with paresthesia of the four limbs, but without loss of motor or reflex activity, though some distal hypoesthesia was detected. An acute lupus attack was eliminated, the convulsive seizures not recurring after discontinuation of treatment, and the paresthesias diminishing progressively over a period of three months. Electrical investigations showed lack of motor anomalies but a marked reduction in sensory conduction. This is the 13th reported case of polyneuritis due to metronidazole, the 4th case of convulsive seizures, and the first case in which both manifestations occurred. The plasma concentration curve after oral administration of 1 g of the product to this patient demonstrated that the product was not being metabolised in a pathological manner.
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PMID:[Convulsive seizures and polyneuritis in a patient with lupus treated with metronidazole (author's transl)]. 731 7

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16

A high incidence of autoantibody against the neutral glycolipid "asialo GM1" was observed in sera from patients with systemic lupus erythematosus (SLE) with neurological disorders, using an immunoflocculation test. The sera from 14 out of 17 cases of SLE with neurological disorders showed antibody activity against asialo GM1 but not against the following glycolipids: asialo GM2 GM1, and galactocerebroside. In another 87 cases of SLE without any history of seizures, as well as 61 cases of other autoimmune diseases (rheumatoid arthritis, progressive systemic sclerosis, mixed connective tissue disease, etc.) and 20 cases of various neurological diseases (epilepsy, multiple sclerosis, etc.), no antibody could be detected. In general, the antibody titer was high several months, even years, before and/or after the seizure, though the titer was low at the time that patients showed definite neurological symptoms. Immunochemical characterization with Sephadex G-200 chromatogrphy and protein A-Sepharose CL-4B affinity column indicated that the antiasialo GM1 was probably an autoantibody belonging to the immunoglobulin G class. The above results suggest that this newly found autoantibody plays a role in the pathogenesis of neurological disorders accompanying SLE.
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PMID:Antiglycolipid autoantibody detected in the sera from systemic lupus erythematosus patients. 744 Jul 25

The validity of the hypothesis that some of the neuropsychiatric manifestations of systemic lupus erythematosus (SLE) are mediated by the direct effects of antibody binding to neuronal cell membranes is dependent on the demonstration of antineuronal activity within the central nervous system of patients with active central nervous system disease. Using a radiolabelled staphylococcal protein A assay, we tested cerebrospinal fluid from 27 patients with SLE and central nervous system manifestations, and cerebrospinal fluid from 18 additional patients with SLE but free of central nervous system disease for antibody reactive with the cultured human neuronal cell line SK-N-SH. Cerebrospinal fluid from 20 of 27 patients with active lupus central nervous system disease had increased immunoglobulin G (IgG) antineuronal activity compared with cerebrospinal fluid from two of 18 patients with SLE without central nervous system disease. Ninety percent of the patients with psychosis, organic brain syndrome or generalized seizures had increased IgG antineuronal activity as compared with only 25 percent of the patients who presented with hemiparesis or with chorea/hemiballismus. Antineuronal activity per microgram of IgG was concentrated eightfold in the cerebrospinal fluid of patients with active central nervous system disease as compared with the serum activity. Patients with or without active central nervous system disease did not differ significantly in the amount of serum antineuronal binding activity. The results are consistent with the hypothesis that the more diffuse central nervous system manifestations of SLE are a direct result of the interaction of antibody with neuronal cell membranes.
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PMID:Cerebrospinal fluid antibodies to neuronal cells: association with neuropsychiatric manifestations of systemic lupus erythematosus. 746 11


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