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Aurothiomalate, sodium

C4H5O4S 70-49-5) see Erythromycin monopropionate mercaptosuccinate Sodium aurothiomalate thionyl bromide... [Pg.2446]

Hurst, N.P., Bell, A.L. and Nuki, G. (1986). Studies on the effect of D-pencillamine and sodium aurothiomalate therapy on superoxide anion production by monocytes from patients with rheumatoid arthritis evidence for in vivo stimulation of monocytes. Ann. Rheum. Dis. 45, 37-43. [Pg.258]

Treatment of RA patients with various drugs was shown to affect free radical production by phagocytic cells. It was found that the therapy with gold compounds [252] and piroxicam [237] diminished superoxide production in RA patients. Surprisingly, Hurst et al. [253] reported that successful therapy with penicillamine or sodium aurothiomalate is accompanied by an increase in superoxide production and serum thiol levels. The mechanism of this phenomenon is unknown. Mur et al. [254] demonstrated that antirheumatic medication of RA patients caused reducing cytokine priming of superoxide generation. [Pg.933]

The first-line agents in the treatment of rheumatoid arthritis are non-steroidal anti-inflammatory drugs such as diclofenac. Diclofenac and indometacin, another NSAID, tend to have similar activity hov/ever, indometacin has a higher incidence of side-effects and therefore diclofenac is more appropriate for initial treatment. Sodium aurothiomalate is classified as a disease-modifying antirheumatic drug and is used as a second-line treatment in rheumatoid arthritis, but has been superseded by methotrexate, administered v/eekly. Paracetamol is often indicated in the management of osteoarthritis. Local intra-articular injections of dexamethasone may be administered for the relief of soft-tissue inflammatory conditions. [Pg.293]

Synonyms sodium aurothiomalate mercaptobutanedioic acid monogold (1+) sodium salt Myochrysine Mycocrisin Shiosol... [Pg.329]

Dimensional structures of small molecules that exhibit IL-1 modulating activities. They are tenidap, ciprofloxacin, 3-Deazaadenosine, (SK F 86002), E5110, DMARDs (Chloroquine, Auranofin, Sodium aurothiomalate and Dexamethasone) tiaprofenic acid, dexamethasone, tricyclic-ylidene-acetic acid and its derivative, Probucol, eicosapentenoic acid + docosahexenoic, pentoxifylline, Denbufylline, and Romazarit (Ro-31-3948). [Pg.422]

Antinflammatory DMARDs such as chloroquine, auranofin, sodium aurothiomalate, and dexamethasone have been shown to inhibit IL-1 synthesis [89]. Analogs of these compounds have exhibited potent inhibition of IL-1 a- induced cartilage resorption [90]. Elevated collagenase and proteoglycanase levels caused by IL-1 in human cartilage were found to be reduced by tiapro-... [Pg.425]

This technique is a histochemical procedure to evaluate die hyahuonidase activity of spermatozoa. Using this technique, Waibel el al. evaluated the inhibition of mouse testicular hyaluronidase by sodium aurothiomalate [147]. Hirayama et al. [Pg.176]

Sodium Aurothiomalate The treatment of adverse effects is symptomatic. Therapy is withdrawn and a chelating agent such as dimercaprol may be used. [Pg.344]

The complexes sodium aurothiomalate and sodium aurothioglucose provide effective therapy for rheumatoid arthritis but can produce unpleasant and toxic reactions because of the relatively large doses used (up to 250jumol (50 mg) per week). The resultant high concentrations of Au in plasma of patients receiving chrysotherapy may be measured easily by solvent extraction and FAAS. The main advantages of ETA—AAS are the direct analysis and the sensitivity to measure the various Au containing species in body fluids. [Pg.364]

Nitritoid reactions have been reported rarely in patients receiving therapy with injectable gold (sodium aurothiomalate) and concomitant ACE inhibitor therapy, Symptoms may include facial flushing, nausea, vomiting and hypotension. Be aware,... [Pg.6]

ACE INHIBITORS GOLD (SODIUM AUROTHIOMALATE) Cases of 1 BP Additive vasodilating effects Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (lightheadedness, dizziness on standing, etc.). If reaction occurs, consider changing to alternative gold formulation or stopping ACE inhibitor... [Pg.50]

SODIUM ARSONILATE see ARA500 SODIUM-l-ASCORBATE see ARN125 SODIUM ASCORBATE (FCC) see ARN125 SODIUM AUROTHIOMALATE see GJCOOO SODIUM AZIDE see SFAOOO SODIUM, AZOTURE de (FRENCH) see SFAOOO... [Pg.1880]

Gold salts modify a variety of cellular and humoral immune responses their mode of action is not understood but may relate to the formation of aurocyanide in areas of inflammation. Sodium aurothiomalate by deep i.m. injection or auranofin by mouth are available but oral gold is less effective and is rarely used as initial therapy. [Pg.292]

Sodium aurothiomalate is water-soluble and is given intramuscularly as an aqueous solution. Aurothioglucose is water-soluble and is given intramuscularly in either an aqueous solution or an oily suspension. Sodium aurothio-propanol sulfonate, aurotioprol, and aurothiosulfate have similar actions and uses to those of sodium aurothiomalate. They are given by intramuscular injection. [Pg.1520]

In rheumatoid arthritis the most commonly used gold salts are sodium aurothiomalate and aurothioglucose (3). There is some reason to believe that adverse effects are less frequent with the suspensions (of aurothioglucose or aurothiosulfate) than with the more rapidly absorbed solution (of sodium gold thiomalate) (SEDA-16, 233) (4). [Pg.1520]

Apart from the nitritoid cardiovascular reaction, which is unique to sodium aurothiomalate, and possible differences between slowly and rapidly absorbed gold salts in the relative frequency of adverse effects, the general pattern of adverse reactions is similar for all parenteral gold salts. [Pg.1521]


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