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)

Evidence has gradually accumulated that DNA antibodies play a pathogenic role in SLE in combination with DNA, as DNA: anti-DNA complexes, but until recently there was no direct assay for such complexes. By measuring DNA binding before and after DN'ase digestion, an indication of the amount of DNA complexes in biological fluids was obtained. This assay was used to examine sera from patients with SLE or non-SLE nephritis. DNA:anti-DNA complexes were detectable only in the circulation of patients with SLE, almost invariably with active nephritis. When a large series (50) of SLE patients were serially examined, similar results were found. Significant amounts of DNA:anti-DNA complexes were found in the circulation only during active CNS and/or renal lupus. Persistence of the complexes was associated with treatment resistance and increased morbidity and mortality. In addition, DNA:anti-DNA complexes were found in the CSF of a patient with CNS lupus.
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PMID:Clinical studies on the significance of DNA:anti-DNA complexes in the systemic circulation and cerebrospinal fluid (CSF) of patients with systemic lupus erythematosus. 80 29

CNS involvement is a rare manifestation of collagen disease. But in three patients with lupus erythematosus (L.E.) the disease was from its onset characterized by CNS signs: epileptic seizures, cerebellar ataxia, and organic psychosis. The combination of epilepsy or organic psychosis with inflammatory joint disease should make one consider L.E. in the differential diagnosis, even if there is no close time relationship between the occurrence of these signs. Muscle biopsy, EEG recordings and CSF examinations may be of diagnostic value in addition to serological and immunological studies.
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PMID:[Early CNS manifestations in lupus erythematosus (author's transl)]. 118 35

The active vitamin D metabolite 1,25-dihydroxyvitamin D3 [1,25-D3] is thought to promote many of its actions through interaction with a specific intracellular receptor. The discovery of such receptors in monocytes and activated lymphocytes has led investigators to evaluate the role of the hormone on the immune system. The sterol inhibits lymphocyte proliferation and immunoglobulin production in a dose-dependent fashion. At a molecular level, 1,25-D3 inhibits the accumulation of mRNA for IL-2, IFN-gamma, and GM-CSF. At a cellular level, the hormone interferes with T helper cell (Th) function, reducing Th-induction of immunoglobulin production by B cells and inhibiting the passive transfer of cellular immunity by Th-clones in vivo. The sterol promotes suppressor cell activity and inhibits the generation of cytotoxic and NK cells. Class II antigen expression on lymphocytes and monocytes is also affected by the hormone. When given in vivo, 1,25-D3 has been particularly effective in the prevention of autoimmune diseases such as experimental autoimmune encephalomyelitis and murine lupus but its efficacy has been limited by its hypercalcemic effect. Synthetic vitamin D3 analogues showing excellent 1,25-D3-receptor binding but less pronounced hypercalcemic effects in vivo have recently enhanced the immunosuppressive properties of the hormone in autoimmunity and transplantation.
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PMID:Immunomodulatory role of 1,25-dihydroxyvitamin D3. 164 50

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

Interactions of the ligand/receptor pair LFA-1(CD11a/CD18) and ICAM-1(CD54) initiate and control the cell-cell interactions of leukocytes and interactions of leukocytes with parenchymal cells in all phases of the immune response. Induction of the intercellular adhesion molecule 1 (ICAM-1) on the surface of epidermal keratinocytes has been proposed as an important regulator of contact-dependent aspects of cutaneous inflammation. Ultraviolet radiation (UVR) also modifies cutaneous inflammation, producing both up- and down-regulation of contact hypersensitivity. We have found that UVR has a biphasic effect on the induction of keratinocyte CD54. Using immunofluorescence and FACS techniques to quantitate cell-surface CD54 staining, we have shown that UVR (100 mJ/cm2 of UVB) significantly (p less than 0.01) inhibits keratinocyte CD54 induction by gamma interferon 24 h after irradiation. However, at 48, 72, and 96 h after UVR (10 to 100 mJ/cm2), CD54 expression is significantly induced (p less than 0.01 to p less than 0.001) to levels even greater than are induced by gamma interferon (20 U/ml). In addition, at 48, 72, or 96 h following UVR (30-100 mJ/cm2), the gamma-interferon-induced CD54 expression on human keratinocytes is also strongly (p less than 0.05 to p less than 0.001) enhanced. In this cell-culture system, gamma interferon and TNF-alpha are both strong CD54 inducers and are synergistic, but GM-CSF, TFG-beta, and IL-1 have no direct CD54-inducing effects. Thus the effects of UVR on CD54 induction are biphasic, producing inhibition at 24 h and induction at 48, 72, and 96 h. This effect on CD54 may contribute to the biphasic effects of UVR on delayed hypersensitivity in vivo. The early inhibition of ICAM-1 by UVR may also contribute to the therapeutic effects of UVR. We also speculate that the late induction of ICAM-1 by UVR might be an important step in the induction of photosensitive diseases such as lupus erythematosus.
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PMID:Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes. 197 76

Determination of antineuronal antibodies was carried out by a solid phase radioimmunoassay, in which the neuronal cells SK-N-SH were cultured as the target antigens, the positive rate in sera and CSF of neuropsychiatric SLE patients being 85% and 77.8% respectively, all with quite high level of antibodies. Although 66.7% sera of SLE patients without CNS involvement were also positive for the antibodies, yet the antibody levels of them were distinctly lower, and only 3 of them showed weak positive reactions in their CSF. It was shown that 90% of neuropsychiatric SLE patients with diffuse CNS manifestations had increased antineuronal antibodies, compared with only 20% in cases with local CNS involvements. The antibody levels both in sera and CSF decreased remarkably following the patients' recovery from the neuropsychiatric attack. It is concluded that the antineuronal antibodies might play a role in the pathogenesis of neuropsychiatric lupus and the determination of them in CSF might be useful in the diagnosis and differential diagnosis of neuropsychiatric lupus.
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PMID:[Antineuronal antibodies and neuropsychiatric systemic lupus erythematosus]. 220 46

By means of a questionnaire, we have determined the combination of clinical features and laboratory tests which rheumatologists, nephrologists, immunologists, and neurologists in New South Wales consider most helpful in discriminating between central nervous system (CNS) involvement due to systemic lupus erythematosus (SLE) and that due to other causes. There was a uniformity of views amongst the four specialties in terms of the likelihood that a given clinical presentation was due to active CNS lupus. The clinical presentation made little difference to the interpretation of laboratory data. CNS abnormalities (EEG, CT, and CSF), as well as the finding of serum DNA antibody of 95%, influenced decision-making, although the other serological tests had little impact. There was disagreement amongst physicians as to whether a given test abnormality (e.g. focal CT scan abnormality) supported or rejected the diagnosis of active CNS lupus. This study indicates that physicians interpret test results selectively in their assessment of patients with SLE who develop CNS symptoms.
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PMID:An evaluation of the role of laboratory investigations in establishing a diagnosis of central nervous system lupus. 336 32

A 19-year old female with catatonia associated with multi-system involvement with systemic lupus erythematosus is described. There was no evidence of CNS involvement (negative CT scan, normal EEG, normal ice-caloric response, and normal CSF findings). The patient improved on large doses of steroids. It is suggested that cerebral lupus should be considered in the differential diagnosis of catatonia even in the absence of radiological and focal neurological signs when the active disease is present.
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PMID:Lupus catatonia: a case report. 365 61

A middle-aged woman had five discrete episodes of herpes zoster. The first attack consisted of uncomplicated herpes zoster ophthalmicus. The subsequent four episodes involved thoracic, cervical, and finally sacral dermatomes and were complicated by myelitis or encephalomyelitis. During the most recent attack, while she was receiving corticosteroids, varicella-zoster virus was cultured from the CSF. In addition, the patient had strong evidence of systemic lupus erythematosus, with a history of Raynaud's phenomenon, migratory arthralgia, and unexplained anemia before the first attack of zoster with subsequent development of a positive lupus cell preparation and elevated antinuclear antibody levels.
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PMID:Recurrent herpes zoster encephalitis. A complication of systemic lupus erythematosus. 625 12

Three cases of cerebral vascularitis are reported. This affection does not occur frequently and is often unrecognized. It can be isolated or associated with disease such as sarcoidosis, Behcet's disease, or collagen disorders (lupus erythematosus, mixed connective tissue diseases). Diagnosis is made from the evolution with transient remission, the inflammatory nature of the CSF, and the presence of segmentary narrowing on arteriography. In case of doubt an exploratory operation with biopsy is necessary. The most likely etiology is an auto-immune disturbance, and cortico-therapy has greatly improved the prognosis.
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PMID:[Diffuse corticoid-sensitive cerebral arteritis (author's transl)]. 742 45


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