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Results for “Organogold Compounds”

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At least 253 records · Page 14Linked to original sources
PubMed1990

Disease-modifying anti-rheumatic drug therapy. An expensive therapy despite inexpensive drugs.

In a study of the costs for drug therapy, 81 patients with rheumatoid arthritis taking parenteral gold, penicillamine or chloroquine were included. The patients were assessed for costs, directly and indirectly caused by the therapy, during a 12-week period. The three therapy groups were comparable in terms of number of patients, sex, age and duration of disease. There were substantial differences in costs for therapy between the three disease-modifying anti-rheumatic drugs. Treatment with parenteral gold gave the highest cost, 2.2 times that of chloroquine and 1.4 times the cost of penicillamine. The cost for the antirheumatic drug constituted a minor part of the total cost (4.4-15.4%). The need for patient visits for treatment and safety controls was a major factor in the overall cost.

Adult↗
PubMed1995

Plasma viscosity in the monitoring of therapy in rheumatoid arthritis patients.

Plasma viscosity (PV) was compared with erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and clinical measures in the monitoring of parenteral gold therapy in a longitudinal study of 40 consecutive rheumatoid arthritis (RA) patients. Significant correlations with the combined clinical variables were only found for differences in PV and not for the other laboratory tests. PV but not ESR or CRP discriminated significantly between active and inactive disease. The sensitivity and specificity for PV above the normal range as a sign of disease activity was 89% and 73%, respectively, which was superior compared with ESR and CRP. The advantages of PV over CRP and ESR justify wider use of this test and warrant further studies of PV in the monitoring of other therapies in RA patients.

Adult↗
PubMed1998

Dealing with drug-induced thrombocytopenia.

Unpredictable and potentially life-threatening, immune thrombocytopenia can occur with any drug, at times even after long, uneventful use. Heparin is the most common cause; although the fall in platelet count tends to be modest, these cases are particularly dangerous because of associated thrombosis. Much has been learned about heparin-induced disease, but complex issues remain.

Algorithms↗
PubMed2001

The balance between CD45RChigh and CD45RClow CD4 T cells in rats is intrinsic to bone marrow-derived cells and is genetically controlled.

The level of CD45RC expression differentiates rat CD4 T cells in two subpopulations, CD45RC(high) and CD45RC(low), that have different cytokine profiles and functions. Interestingly, Lewis (LEW) and Brown Norway (BN) rats, two strains that differ in their ability to mount type 1 and type 2 immune responses and in their susceptibility to autoimmune diseases, exhibit distinct CD45RC(high)/CD45RC(low) CD4 T cell ratios. The CD45RC(high) subpopulation predominates in LEW rats, and the CD45RC(low) subpopulation in BN rats. In this study, we found that the antiinflammatory cytokines, IL-4, IL-10, and IL-13, are exclusively produced by the CD45RC(low) CD4 T cells. Using bone marrow chimeras, we showed that the difference in the CD45RC(high)/CD45RC(low) CD4 T cell ratio between naive LEW and BN rats is intrinsic to hemopoietic cells. Furthermore, a genome-wide search for loci controlling the balance between T cell subpopulations was conducted in a (LEW x BN) F(2) intercross. Genome scanning identified one quantitative trait locus on chromosome 9 (approximately 17 centiMorgan (cM); log of the odds ratio (LOD) score 3.9). In addition, two regions on chromosomes 10 (approximately 28 cM; LOD score 3.1) and 20 (approximately 40 cM; LOD ratio score 3) that contain, respectively, a cytokine gene cluster and the MHC region were suggestive for linkage. Interestingly, overlapping regions on these chromosomes have been implicated in the susceptibility to various immune-mediated disorders. The identification and functional characterization of genes in these regions controlling the CD45RC(high)/CD45RC(low) Th cell subpopulations may shed light on key regulatory mechanisms of pathogenic immune responses.

Aging↗
PubMed2004

Studies of congenic lines in the Brown Norway rat model of Th2-mediated immunopathological disorders show that the aurothiopropanol sulfonate-induced immunological disorder (Aiid3) locus on chromosome 9 plays a major role compared to Aiid2 on chromosome 10.

Brown Norway (BN) rats treated with aurothiopropanol-sulfonate (Atps) constitute a model of Th2-mediated immunological disorders associated with elevated IgE responses and renal IgG deposits. Using F(2) offspring between Atps-susceptible BN and Atps-resistant Lewis rats, we had previously mapped three quantitative trait loci on chromosomes 9, 10, and 20 for which BN alleles increased susceptibility to Atps-induced immunological disorders (Aiid). In this study we have used congenic lines for the latter two quantitative trait loci, formerly called Atps2 and Atps3 and now named Aiid2 (chromosome 10) and Aiid3 (chromosome 9), for fine mapping and characterization of their impact on Atps-triggered reactions. In Aiid2 congenic lines, the gene(s) controlling part of the IgE response to Atps was mapped to an approximately 7-cM region, which includes the IL-4 cytokine gene cluster. Two congenic lines in which the introgressed segments shared only a portion of this 7-cM region, showed an intermediate IgE response, indicating the involvement of several genes within this region. Results from BN rats congenic for the Lewis Aiid3 locus, which we mapped to a 1.2-cM interval, showed a stronger effect of this region. In this congenic line, the Atps-triggered IgE response was 10-fold lower than in the BN parental strain, and glomerular IgG deposits were either absent or dramatically reduced. Further genetic and functional dissections of these loci should provide insights into pathways that lead to Th2-adverse reactions.

Animals↗
PubMed1991

Effect of parenterally administered gold therapy on the course of adult rheumatoid arthritis.

OBJECTIVE: To describe the course of rheumatoid arthritis over 5 years in adults and to evaluate the effect of parenterally administered gold salts on that course. DESIGN: A prospective observational study of adults with rheumatoid arthritis. Data derived from annual interviews with patients from 1983 to 1988 and from physician surveys in 1983 and 1987. SETTING: Rheumatology practices in the community. PATIENTS: The study began in 1982 with 822 adults who had rheumatoid arthritis and were under the care of rheumatologists. INTERVENTIONS: Those selected by rheumatologists in the management of their patients. MEASUREMENTS: Information describing sociodemographic and clinical characteristics, course, and therapy was collected from patients and verified by physician reports. Functional status, measured by the Health Assessment Questionnaire, and the number of painful joints were used as outcome variables. Outcome variables were adjusted for age, sex, disease duration, baseline values of the outcome variable, and the use of four disease-remittive agents other than gold. MAIN RESULTS: Multivariate repeated-measures analysis of variance showed no change in the course of rheumatoid arthritis over 5 years. The use of parenteral gold for at least 2 consecutive years at the start of the observation period produced, on average, no change in the course over 5 years in the two outcome variables. CONCLUSION: In our study of a community-based population of adults with rheumatoid arthritis who were under the care of community rheumatologists, we found that there was, on average, no statistically significant change in function or number of painful joints between 1983 and 1988. Patients receiving parenteral gold therapy for at least 2 consecutive years did not show a statistically significant difference in outcome when compared with those not receiving such therapy.

Antirheumatic Agents↗
PubMed1993

Low-dose prednisone induces rapid reversible axial bone loss in patients with rheumatoid arthritis. A randomized, controlled study.

OBJECTIVE: To determine the effects of a short course of a low dose of a glucocorticoid agent on bone mass. DESIGN: Double-blind, placebo-controlled, randomized study. SETTING: Outpatient clinic of a university hospital. PATIENTS: Forty patients with active rheumatoid arthritis. INTERVENTION: All patients started receiving intramuscular gold salts. In addition, they were randomly allocated to receive either prednisone or placebo. The initial dose was 10 mg/d, which was tapered between weeks 12 and 20. Thereafter, patients were followed for an additional 24 weeks. MEASUREMENTS: Lumbar bone mineral density was measured with dual-energy, quantitative computed tomography in a trabecular and a cortical region of interest. RESULTS: Despite favorable effects on disease activity and functional capacity, trabecular bone mineral density decreased in the prednisone-treated patients between baseline and week 20 (mean change, -8.2%; 95% CI, -12.7% to -3.7%; P = 0.001). Little change was found in the placebo-treated patients (P > 0.2), and the prednisone group had a greater mean bone loss than the placebo group (9.5%; CI, 3.4% to 15.6%; P = 0.003). After discontinuation of prednisone, an increase was found in trabecular bone mineral density between weeks 20 and 44 (mean change, 5.3%; CI, 0.7% to 9.9%; P = 0.03). Little change was found after withdrawal of placebo (P > 0.2). The mean improvement in the prednisone group was 6.8% (CI, 0.8% to 12.8%; P = 0.03) greater than for placebo. In both treatment groups, cortical bone mineral density did not change markedly in either period (P > or = 0.2). CONCLUSIONS: Low doses of glucocorticoid agents cause marked vertebral trabecular bone loss in the initial months of therapy in patients with active rheumatoid arthritis. After discontinuation of treatment, this bone loss seems to be (partially) reversible.

Analysis of Variance↗