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)

Red lunulae are associated with rheumatoid arthritis, systemic lupus erythematosus, alopecia areata, cardiac failure, hepatic cirrhosis, lymphogranuloma venereum, psoriasis, carbon monoxide poisoning, twenty-nail dystrophy, and reticulosarcoma. We examined four patients with red lunulae. Three had chronic obstructive pulmonary disease. Two of these three were alcohol abusers and were without any of the conditions previously associated with red lunulae. Two of the four also had palmar erythema. Histopathologic examination of the red lunula in one of the four cases did not show signs of neovascularization. We report our findings in these patients, which suggest that red lunulae result from increased arteriolar blood flow, a vasodilatory capacitance phenomenon, or changes in the optical properties of the overlying nail so that normal blood vessels become more apparent.
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PMID:Red lunulae revisited: a clinical and histopathologic examination. 264 22

The pulmonary function of 70 nonsmoking patients with systemic lupus erythematosus (SLE) was evaluated, and the results were compared with those of 70 age- and sex-matched, nonsmoking healthy individuals. Isolated reduction of carbon monoxide diffusing lung capacity (DCO), usually subclinical, was the most commonly detected functional abnormality in the SLE population, whereas it was absent in the comparison group. Isolated small airways disease (SAD) was observed in a relatively high percentage of patients, but not significantly different from that in the healthy people. Restrictive and obstructive patterns were very unusual in the SLE people and absent in the members of the comparison group. Finally, normal lung function was seen in the majority of the latter, but only in one third of the lupus patients. Subclinical respiratory dysfunction, most commonly expressed as diminished DCO, is a common feature of SLE.
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PMID:Pulmonary function of nonsmoking patients with systemic lupus erythematosus. 339 9

The safety and efficacy of captopril therapy in children with severe and refractory hypertension has been evaluated in a collaborative international study which enrolled a group of 73 patients, 15 years of age or younger. Most patients had hypertension associated with renal disease or vascular abnormalities. Captopril was administered for periods of less than 3 months to more than 1 year. A significant decrease in both systolic and diastolic blood pressures was produced by the administration of captopril, usually in conjunction with other antihypertensive agents (most commonly diuretics and/or beta-blockers). Systolic blood pressures were normalized in 62% and 53% and diastolic blood pressures in 56% and 45% of reported patients after the second and sixth months of captopril therapy, respectively. The response to captopril was sustained over a 12-month period. Adverse reactions were reported in 49% of the 73 patients; 48% of patients had experienced adverse reactions to other antihypertensive agents prior to entering the study. The reactions most frequently observed during captopril therapy were hypotension, vomiting, postural symptoms, anemia, rash, and anorexia. Leukopenia was reported in six patients, all of whom had renal impairment. Two of these patients had received concomitant therapy with immunosuppressants, and one had systemic lupus erythematosus. Captopril was discontinued in two of these six children. Statistically significant increases in mean serum urea nitrogen and potassium concentrations and decreases in mean serum CO2 levels were observed during the course of therapy. These effects could not be exclusively attributed to captopril administration as the study population received multidrug therapy and had significant intrinsic disease. Captopril was demonstrated to be an effective and safe drug for the treatment of children with severe hypertension.
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PMID:Efficacy and safety of captopril in the treatment of severe childhood hypertension: report of the International Collaborative Study Group. 388 18

We have previously demonstrated that procainamide is oxidized to a reactive metabolite. We speculated that this reactive metabolite might be a hydroxylamine and further that it might be responsible for the syndrome of procainamide-induced lupus. We now report that procainamide is metabolized to a hydroxylamine by rat and human hepatic microsomes. The extent of this metabolic oxidation was quantitated by HPLC after conversion of the hydroxylamine to the more stable nitro derivative of procainamide. Formation of the hydroxylamine required NADPH, active microsomes, and oxygen and was inhibited by carbon monoxide, SKF 525-A, and cimetidine. Formation of the hydroxylamine was also studied as a function of time, microsomal protein concentration, and procainamide concentration.
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PMID:Metabolism of procainamide to a hydroxylamine by rat and human hepatic microsomes. 614 17

In 2 radioimmunoassays in use to detect antibodies to dsDNA, the Farr assay and the PEG assay, we observed inhibitory effects of normal human serum (NHS) on the DNA binding by SLE sera. This was found to be due by the fact that, during incubation at 37 degrees C, CO2, introduced in the incubation mixture by the serum, evaporates from the mixture. This results in increase in pH to values well above pH 8.0, which in turn leads to a decreased DNA binding by antibody. When SLE sera are tested at low dilution, this phenomenon may lead to false negative results. Proper pH control, by the use of buffers with a greater buffering capacity than PBS, completely prevented the observed inhibitory effects. However, under these conditions NHS bound significant amounts of DNA in both assays. The non-specific DNA binding by NHS was found to be heat-stable, but could be eliminated either by aerosil treatment of the sera or by addition of dextran sulphate to the incubation mixture. Lipoproteins and, to a lesser extent, the complement component C1q appear responsible for this non-specific binding. To avoid false negative results with SLE sera as well as non-specific binding by NHS, we propose the use of stronger buffers in combination with added dextran sulphate to the incubation mixture in both the Farr assay and the PEG assay.
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PMID:Influence of pH on the detection of low- and high-avidity anti-dsDNA. 618 61

We have reviewed the alveolar hemorrhage (AH) syndromes, defined as immune or idiopathic disorders associated with diffuse microvascular hemorrhage into the acinar portion of the lung. The disorders that are most often associated with AH include antibasement membrane antibodies (ABMA) disease, idiopathic pulmonary hemosiderosis, systemic lupus erythematosus, systemic vasculitides, and idiopathic rapidly progressive glomerulonephritis. An approach to the recognition, diagnosis, and treatment of the AH syndromes has been outlined and several illustrative case studies have been presented. Recognition of AH is not usually difficult, but does require a high index of suspicion, since many disease processes may give rise to hemoptysis with infiltrates on chest roentgenogram. Recognition of AH is aided by careful clinical and laboratory assessment for evidence of extrapulmonary disease; simple hematologic studies such as sequential hemoglobins and iron studies; and measurement of carbon monoxide uptake by the lungs. Early recognition of AH may decrease the likelihood of respiratory failure and end-stage renal disease. The specific etiology of AH is usually determined by clinical examination, serologic assay for ABMA, and percutaneous renal biopsy by immunofluorescence. Open-lung biopsy is required in a minority of cases. High-dose pulse methylprednisolone appears to effectively control AH of diverse etiology. Combined plasma exchange and immunosuppression controls AH in ABMA disease and is the treatment of choice in this disorder. Cyclophosphamide is used for Wegener's granulomatosis, and sometimes in systemic necrotizing vasculitis, in an attempt to prevent irreversible damage to the kidneys.
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PMID:Alveolar hemorrhage syndromes: diffuse microvascular lung hemorrhage in immune and idiopathic disorders. 639 80

The effects of corticosteroid administration to eight patients with severe thoracic systemic lupus erythematosus (SLE) were assessed in a prospective study over a mean period of 26 months by serial measurements of respiratory function, ESR, and a clinical score. Initial assessment of respiratory function showed severe restrictive ventilatory defects and impairment of carbon monoxide uptake not wholly attributable to the small lung volumes. ESR and clinical score showed high correlation coefficients with FEV1 in all patients, with VC and TLC in seven patients, and with TLCO in four patients, indicating that changes of respiratory function were reflecting the activity of the disease. This study shows that in patients with severe thoracic SLE it is valid to use serial measurements of respiratory function to assess the response to treatment and that pronounced and sustained improvement of respiratory function can be expected.
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PMID:Severe thoracic systemic lupus erythematosus. 659 14

Fernando and Chir 1st reported an association between chorea and oral contraceptives (OCs) in 1966. Differential diagnosis of chorea, in addition to Sydenham chorea, include Wilson disease; encephalitis; Huntington chorea; drug intoxication; benign familial chorea; pregnancy; systemic lupus erythematosus; Henoch-Schonlein purpura; polycythemia vera; hypocalcemia; hyperthyroidism; carbon monoxide poisoning; cerebral infarction, and; intracranial tumor. Chorea can also occur as an untoward side-effect of OC therapy, as shown by the case report of a 20-year old white woman. Chorea associated with OC therapy occur unilateraly but has also been bilateral in 37% of reported cases. 8 of 24 reported cases (33%) had a prior history of rheumatic fever - mean age of patient was 22 years (range, 16 to 40 years). The time between initiation of OC therapy and appearance of choreiform movements can vary from 6 days to 9 months, with a mean of 3 months. Time between discontinuation of OC therapy and cessation of symptoms vary from 3 days to 3 months, with a mean of 5 weeks. Speculations by various authors on the pathogenesis of chorea are described.
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PMID:Chorea associated with oral contraceptive therapy. 739 41

We examined the relationship between peripheral blood and bronchoalveolar lavage (BAL) lymphocyte phenotypes and lung function in 19 patients with SLE, and evaluated their association with disease activity. Lung function assessment showed a mildly restrictive pattern with frequent impairment of transfer factor for carbon monoxide (T1,co) and diffusing capacity of the alveolocapillary membrane (Dm), of late-expiratory airflow rates and with a high prevalence of increased airway resistance. T1,co, Kco and Dm correlated inversely with the numbers of CD8+ cells and CD56+/CD16+/CD3- (NK) cells in BAL. Oxygen radical production, both by stimulated and unstimulated BAL cells and blood polymorphonuclear leucocytes (PMN) was significantly increased in SLE. In comparison with healthy controls, patients with SLE had a lower percentage of CD19+ B cells in the BAL versus an increased percentage of these cells in peripheral blood. HLA-DR expression on CD4+ and CD8+ lung lymphocytes was markedly increased in SLE. Current SLE disease activity was not associated with changes in BAL or peripheral blood lymphocyte phenotypes. Our data suggest that an ongoing cell-mediated immune response is present in the lungs in SLE, particularly involving activated CD8+ T cells and CD56+/CD16+/CD3- NK cells. It is associated with up-regulated local production of oxygen radicals and with impaired pulmonary diffusing capacity. This inflammatory process seems to be independent of general SLE disease activity.
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PMID:Bronchoalveolar lavage cell analysis and lung function impairment in patients with systemic lupus erythematosus (SLE). 840 94

Anti-nucleolin antibodies have been detected in patients with systemic connective tissue diseases (SCTD) including systemic sclerosis (SSc) and systemic lupus erythematosus (SLE). In vivo bound autoantibodies to nucleoli of epidermal keratinocytes have been demonstrated in skin from patients with SCTD. In this study, monoclonal antibody to nucleolin (D-3) was used to determine the distribution of nucleolin in different culture cells including HEp-2, HepG2, HRCC, Molt-4 and Wil2 cells. Nucleolin was found to be present on the surface of HEp-2 and HepG2 cells, but not on the surface of HRCC and lymphoblastoid (Molt-4 and Wil2) cells; in contrast, nucleolin was detected in the nucleoli of all permeabilized cells examined. In immunoprecipitation, using extracts from 32P-labeled HEp-2 cells as antigenic source, cell membrane as well as nuclear nucleolins were found to be phosphorylated with a molecular weight of 105 kDa. Viable HEp-2 and HepG2 cells were cocultured with IgG fraction of D-3 in a CO2 incubator for 1 to 24 h, and then permeabilized with acetone followed by immunofluorescence staining with FITC-labeled goat anti-mouse IgG antibodies. Nucleolar staining was observed in cells after 10 h or longer of coculture. These data indicated that D-3 antibody reacted with cell membrane nucleolin and subsequently gain access into cells in a process related to pinocytosis.
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PMID:Internalization of anti-nucleolin antibody into viable HEp-2 cells. 911 28


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