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)

Assessing disease activity in SLE is often difficult due to the multiple organ systems involved. Three recent disease activity indices (SLAM, BILAG, and SLEDAI) are being increasingly used. Retrospective investigations comparing these indices have not been performed. We compared SLAM, BILAG, and SLEDAI in a retrospective study of 52 patients with SLE. SLAM and BILAG were found to correlate well with one another and with clinicians' evaluations of disease activity (as measured by intensity of immunosuppressive treatment). They correlated less well or insignificantly with laboratory parameters (ESR, anti-ds-DNA-antibodies). If practicability is also considered, SLAM, in particular, appears to be suitable for retrospective evaluation of disease activity in SLE.
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PMID:[Comparison of three indices for the evaluation of disease activity in systemic lupus erythematosus]. 179 57

T cells (CD8+) with specific suppressor activity against anti-dsDNA antibody (16/6 Id+) were generated in vitro. The cells were established from BALB/c-enriched T cells exposed in vitro to silica beads coated with the pathogenic anti-DNA idiotype, 16/6. The idiotype specificity of the suppressor cells was demonstrated by (a) specific induction of a decrease in proliferative response of T helper cell lines specific for the pathogenic idiotype (16/6 Id), when exposed to the idiotype, with no effect on T cell lines with other specificities, e.g., against human IgM or synthetic polypeptide. (b) Effectively suppressing in vitro antibody production of anti-16/6 antibody, employing 16/6-primed B cells and specific helper T cell line. The 16/6 Id-specific Ts cells were found to be MHC restricted. Weekly intravenous injections of 10(7) 16/6 Id-specific Ts cells given to BALB/c mice at different stages of experimental SLE disease prevented the clinical, serological, and pathological manifestations. This effect was characterized by decreased titers of autoantibodies (e.g., anti-DNA, anti-Sm antibodies) in the sera, by abolishment of the proteinuria, leukopenia, and the increased ESR, followed by decreased immunoglobulin deposition in the kidneys. Treating the mice with control IgM-specific T cells did not affect the above parameters. These studies demonstrate the ability to generate Ts cells specific for pathogenic idiotypes. The method might be employed therapeutically to modulate the course of autoimmune conditions.
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PMID:Modulation of SLE induction in naive mice by specific T cells with suppressor activity to pathogenic anti-DNA idiotype. 183 87

Hydralazine caused site-specific DNA damage in the presence of Cu(II), Co(II), Fe(III), or peroxidase/H2O2. The order of inducing effect of metal ions on hydralazine-dependent DNA damage [Cu(II) greater than Co(II) greater than Fe(III)] was related to that of accelerating effect on the O2 consumption rate of hydralazine autoxidation. Catalase completely inhibited DNA damage by hydralazine plus Cu(II), but hydroxyl radical (.OH) scavengers and superoxide dismutase did not. On the other hand, DNA damage by hydralazine plus Fe(III) was inhibited by catalase and .OH scavengers. Hydralazine plus Cu(II) induced piperidine-labile sites predominantly at guanine and some adenine residues, whereas hydralazine plus Fe(III) caused cleavages at every nucleotide. Activation of hydralazine by peroxidase/H2O2 caused guanine-specific modification in DNA. ESR-spin trapping experiment showed that .OH and superoxide are generated during the Fe(III)- or Cu(II)-catalysed autoxidation of hydralazine, respectively, and that nitrogen-centered radical is generated during the Cu(II)- or peroxidase-catalysed oxidation. The generation of nitrogen-centered radical was also supported by HPLC-mass spectrometry. The results suggest that the guanine-specific modification by the enzymatic activation of hydralazine is due to the nitrogen-centered hydralazyl radical or derived active species, whereas .OH participates in DNA damage by hydralazine plus Fe(III). The mechanism of hydralazine plus Cu(II)-induced DNA damage is complex. The possible role of the DNA damage induced by hydralazine in the presence of Cu(II) or peroxidase/H2O2 is discussed in relation to hydralazine-induced lupus, mutation, and cancer.
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PMID:Free radical production and site-specific DNA damage induced by hydralazine in the presence of metal ions or peroxidase/hydrogen peroxide. 184 78

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

The clinical and morphological characteristics of drug-induced lupus (DIL) are not unlike those of systemic lupus erythematosus (SLE). However, DIL is characterised by several distinct features: the two sexes are equally affected; onset occurs in advanced middle-age; the black population is seldom affected. Genetic predisposition seems to influence the onset of disease: subjects affected by DIL are prevalently HLA-DR4 haplotypes with a slow acetylator condition. Modifications in humoral immunity include the presence of anti-nuclear antibodies, denatured anti-DNA antibodies, and antihistone antibodies. Likewise, anti-lymphocytotoxic antibodies, increased ESR and hypocomplementemia are often observed. Little is known about alterations in cellular immunity but the dysregulation of lymphocyte T-helper and T-suppressor activity may be an important feature. Drugs most often leading to DIL include hydralazine, beta-blockers, procainamide and hydantoin. Current pathogenetic theories include a possible immune drug-DNA cross-reaction, the induction of new antigenic structures, an interaction between drugs and immunomodulating cells.
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PMID:[Systemic lupus erythematosus induced by drugs]. 197 6

Forty-five patients with histologically proved cutaneous leukocytoclastic vasculitis were studied with regard to the clinical features, laboratory findings and etiology. There were 12 males and 33 females, with an age range of 13 to 64 years. The most common skin lesions were palpable purpura which appeared mostly on the lower part of the legs. Renal involvement was the most common systemic manifestation, which occurred in 45 per cent of the patients. Abdominal pain occurred in 42 per cent of the male patients while none of the female patients had this symptom. Arthralgia occurred in 20 per cent of the patients. The most common laboratory abnormalities were elevation of ESR, which was significantly more common in females than in males (P = 0.047). The possible etiology of leukocytoclastic vasculitis was identified in 5 patients, these included streptococcal infection in 2 patients, in the other patients the possible causes were penicillin hypersensitivity, systemic lupus erythematosus and livedoid vasculitis, respectively.
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PMID:Cutaneous leukocytoclastic vasculitis: clinical and laboratory features of 45 patients seen in Ramathibodi Hospital. 221 16

The incidence and latency period of collagen vascular disease (CVD) were surveyed prospectively in patients originally diagnosed as idiopathic interstitial pneumonia (IIP). We also examined whether there were differences between IIP and CVD preceded by interstitial pneumonia. Background information, extrapulmonary symptoms, smoking history, laboratory findings, prognosis (Kaplan-Meier estimates), respiratory functions, and radiological findings were compared. The subjects consisted of 68 patients of whom 13 (19%) developed CVD (RA; 5 cases, DMPM; 5 cases, SLE; 1 case, Sjoegren syndrome; 1 case, Overlap syndrome; 1 case). The latency period for development of CVD was 24.9 +/- 39.2 (mean +/- SD) months. IIP patients who developed CVD were predominantly female and were younger than those without CVD (p less than 0.05). These patients also had faster ESR, higher CPK values, and a higher incidence of arthralgia, joint deformity and clubbed fingers (p less than 0.05). Abnormal shadows around costo-phrenic angles were seen more frequently in patients with CVD (p less than 0.05). These results suggest that quite a number of patients with IIP develop CVD. The clinical course of these patients should be followed by keeping these clinical findings in mind.
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PMID:[A prospective study of idiopathic interstitial pneumonia and collagen vascular disease preceded by interstitial pneumonia]. 226 27

We have previously demonstrated the pathogenicity of the common anti-DNA idiotype designated 16/6 Id. Immunization of naive mice with the 16/6 Id induced SLE-like disease characterized by serological (e.g. anti-dsDNA and anti-Sm auto-antibodies), clinical (increased ESR, leucopenia and proteinuria), and pathological (16/6 Id deposition in kidneys) parameters. To elucidate further the role of the 16/6 Id in SLE induction the following studies were carried out: BALB/c mice were immunized with SA-1, a human anti-DNA monoclonal antibody carrying the 16/6 Id; TB-68, a mouse monoclonal anti-tuberculosis (TB) glycolipid, which binds dsDNA and carries the 16/6 Id; TB-72, a mouse monoclonal anti-TB glycolipid that binds DNA and does not harbour the 16/6 Id; and 4B4, a human anti-Sm antibody that carries the 16/6 Id. SLE was induced in BALB/c mice only when immunized with SA-1, TB-68, and 4B4, namely antibodies with diverse binding capacities albeit having the 16/6 Id. Our studies further support previous evidence on the pathogenic role attributed to the 16/6 Id in SLE, and suggest that SLE is most probably an idiotype-induced disease.
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PMID:The importance of the pathogenic 16/6 idiotype in the induction of SLE in naive mice. 240 76

A female newborn of SLE mother developed transient typical discoid-like lupus skin lesions over her face soon after birth and had severe relapse with generalized spreading following an episode of upper respiratory tract infection at 50 days of age. Blood picture showed anemia, transient thrombocytopenia and high ESR. Cardiac echo disclosed small ASD with minimal TR. Both EKG and 24 hrs EKG monitor presented normal findings. Serological studies at the early relapse stage of this disease showed increased serum ANA, IgA and IgM level with normal IgG and decrease of C3 and C4. Both Ro(SSA) and La(SSB) antibody systems were positive in mother but only positive for La(SSB) antibody system in this baby. The alpha-anticardiolipin antibody was negative. We suggest that the Ro(SSA) and/or La(SSB) antibody systems may play a role in the pathogenesis of neonatal lupus erythematosus.
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PMID:Neonatal lupus erythematosus: report of one case. 263 97

Sixty-two cases of systemic lupus erythematous (SLE) treated with Tab. Gentiana macrophylla complex 5 tablets three times per day or 10 tablets twice per day and prednisone 10-30 mg per day were reported. As controls, 19 cases of SLE were treated with prednisone alone at the same time. The results showed complete remission in 86.46% (50/62) cases in the observation group and 31.57% (6/19) cases in the control group. Eight cases of SLE treated with Tab. Gentiana m. complex alone also achieved complete remission in 6 cases and improvement in 2. There was very significant statistical difference between the two groups (P less than 0.001). The Tab. Gentiana m. complex was more effective on the improvement of nephropathy, arthralgia, erythema and restoration of ESR, LE cells and CH50, C3 than prednisone alone. No apparent side effects of Tab. Gentiana m. complex were found in this observation.
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PMID:[Observation on the treatment of systemic lupus erythematous with a Gentiana macrophylla complex tablet and a minimal dose of prednisone]. 273


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