Disease relevance of Monomercaptosuccinic acid

• Two patients had diffuse, reversible pulmonary injury possibly owing to gold sodium thiomalate treatment: a 32-year-old woman with chronic inflammatory arthritis compatible with seronegative rheumatoid arthritis and a 32-year-old man with shoulder arthralgia [1].
• Three patients with Felty syndrome were treated with gold sodium thiomalate [2].
• A 56-yr-old woman with long-standing rheumatoid arthritis exhibited jaundice, pruritus and abdominal discomfort after 8 yr of periodic gold sodium thiomalate injections amounting to a cumulative dose in excess of 2.5 gm [3].
• Acute myocardial infarction following gold sodium thiomalate induced vasomotor (nitritoid) reaction [4].
• Gold sodium thiomalate (GST) has been used for treatment of patients with bronchial asthma [5].

High impact information on Monomercaptosuccinic acid

• Decreased spleen size and increased neutrophils in patients with Felty syndrome. Effects of gold sodium thiomalate therapy [2].
• Gold sodium thiomalate inhibited cytokine (TNF, IL-1, IL-4)-stimulated expression of vascular cell adhesion molecule-1 and E-selectin but not intercellular adhesion molecule-1 on endothelial cells [6].
• Gold sodium thiomalate also suppressed TNF-stimulated increases in vascular cell adhesion molecule-1 and E-selectin mRNA levels but had no effect on intercellular adhesion molecule-1 mRNA [6].
• We have investigated the effect of the antirheumatic drug gold sodium thiomalate on adhesion molecule protein and mRNA expression in cultured human endothelial cells [6].
• Immunomodulatory effects of therapeutic gold compounds. Gold sodium thiomalate inhibits the activity of T cell protein kinase C [7].

Chemical compound and disease context of Monomercaptosuccinic acid

• We therefore decided to assess the prevalence of H. pylori and peptic ulcers in rheumatoid patients being treated with gold sodium thiomalate (GST) plus NSAID, sulfasalazine plus NSAID, or NSAID only [8].
• 6. Of the slow acting anti-rheumatic drugs examined, only gold sodium thiomalate (GSTM) and dapsone significantly decreased cartilage loss, with an accompanying modest decrease in granuloma formation [9].
• Seventy-two consecutive patients with pauciarticular and polyarticular juvenile rheumatoid arthritis (JRA) were randomized into a parallel 50-week open, controlled, comparative trial of hydroxychloroquine (HC), gold sodium thiomalate (GSTM) and D-penicillamine (PEN) [10].
• Proteinuria was clinically closely associated with the use of antirheumatic drugs in 9 out of 13 cases (6 with gold sodium thiomalate, 2 with D-penicillamine and 1 with auranofin) suggesting that antirheumatic drugs are important contributors to proteinuria in these patients [11].
• Protective effects of chelating agents against renal toxicity of gold sodium thiomalate in rats [12].

Biological context of Monomercaptosuccinic acid

• Auranofin was more effective than gold sodium thiomalate in suppressing inflammation and stimulating cell-mediated immunity [13].
• It is speculated that down-regulation of adhesion molecules might be one of the novel mechanisms of action of gold sodium thiomalate [14].
• Treatment of adult mice with gold sodium thiomalate made the normally non-lethal Semliki Forest virus and Sindbis virus infections lethal and increased the virulence of Langat and West Nile viruses [15].
• Heme metabolism in the fetoplacental unit and neonatal livers during lactation: effect of gold sodium thiomalate [16].
• Gold sodium thiomalate and aspirin at high concentrations also produced significant (P less than 0.01 and P less than 0.05) inhibition of chemotaxis as assayed by the leukotactic index procedure [17].

Anatomical context of Monomercaptosuccinic acid

• We have, therefore, studied the effects of gold sodium thiomalate (GST), auranofin, and gold chloride on the proliferation of human umbilical vein EC [18].
• Peripheral lymphocyte depletion in gold sodium thiomalate-treated rheumatoid arthritis patients [19].
• Effects of gold sodium thiomalate on functional correlates of human monocyte maturation [20].
• We cultured phytohemagglutinin- or anti-CD3 antibody-activated normal peripheral blood mononuclear cells (PBMC), as well as the erythroleukemic K562 cell line, in the presence of gold sodium thiomalate or auranofin [21].
• The effects of gold sodium thiomalate (GST) on the production of specific collagenase by thioglycolate-elicited macrophages was investigated [22].

Associations of Monomercaptosuccinic acid with other chemical compounds

• Effects of gold sodium thiomalate on interferon stimulation of C2 synthesis and HLA-DR expression by human monocytes [23].
• We studied the effects of gold sodium thiomalate (GST) and a new antirheumatic drug, tenidap sodium ([Z]-5-chloro-2,3-dihydro-3-[hydroxy-2-thienylmethylene]-2-oxo-1H- indole-1-carboxamide, sodium salt), previously known as CP-66,248-2, in a model system of macrophage differentiation using a myelomonocytic cell line [24].
• A comparison of placebo, auranofin, and parenteral gold sodium thiomalate therapy in 209 patients with active rheumatoid arthritis was performed in a 21-week prospective, controlled, double-blind multicenter trial [25].
• OBJECTIVE: To compare the radiographic outcomes after 36 months in patients with early erosive rheumatoid arthritis (RA) who were treated with methotrexate (MTX) or gold sodium thiomalate (GSTM) [26].
• Normal human neutrophils were treated with therapeutic concentrations of aspirin, gold sodium thiomalate, D-penicillamine, and azathioprine [17].

Gene context of Monomercaptosuccinic acid

• None of the DMARDs or DEX inhibited bFGF production when given alone, but a combination of SASP and GST inhibited the production of bFGF in cultured synoviocytes [27].
• RESULTS: BUC and GST inhibited VEGF production even when given alone, and a combination of BUC, GST and MTX with DEX also inhibited VEGF production [27].
• We have studied the in vitro effects of gold sodium thiomalate (GST) and auranofin (Auf) on the production of interleukin 1 (IL1) expressed as thymocyte co-stimulatory activity (TCSA), and interleukin 1 beta (IL1 beta) as modulated by interferon gamma (IFN gamma) [28].
• OBJECTIVE: Gold sodium thiomalate (GST) is a drug commonly used for the treatment of rheumatoid arthritis (RA) [29].
• Of three disease-modifying drugs tested, dexamethasone and gold sodium thiomalate (GST) inhibited the production of IL-8 and MCP-1, while methotrexate (MTX) was inactive [30].

Analytical, diagnostic and therapeutic context of Monomercaptosuccinic acid

• We assessed the effects of administration of gold sodium thiomalate on the clinical and immunologic manifestations of type II collagen-induced arthritis in rats [31].
• Following a standard 50 mg intramuscular injection of gold sodium thiomalate, plasma gold levels rise sharply, peak between 400 and 800 micrograms/dl in approximately two hours, then decline to approximately 300 micrograms/dl by seven days [32].
• The new oral gold compound auranofin differs pharmacokinetically from the existing injectable gold compounds such as gold sodium thiomalate [32].
• After perfusion for two hours with 2 mM auranofin the jejunal mucosa showed severe injury by light and scanning electronmicroscopy while myochrysine had no apparent effect [33].
• In pharmacokinetic studies, the daily oral administration of SK&F D-39162 to normal rats produced greater stability of blood gold levels and less kidney gold accumulation than parenterally administered gold sodium thiomalate [34].

References