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PubMed1980

The effect of penicillamine and 2,3-dimercaptosuccinic acid on urinary excretion and tissue distribution of gold.

In order to study interactions in vivo between Au+ and SH-containing agents, groups of mice were given 35 mumol/kg of radiolabelled [195Au] thiomalate (Myocrisin) intramuscularly. The administration of Myocrisin is known to result in protein-bound gold and free thiomalate (mercaptosuccinate). High doses of dimercaptosuccinate (1 mmol/kg daily) increased the urinary excretion of radiolabelled gold [195Au] for several days. Treatment for 7 days with 1 mmol/kg of penicillamine or dimercaptosuccinate reduced the blood and kidney levels of gold to 30--50% of the controls. The oral administration of penicillamine in high doses, 1--10 mmol/kg, increased significantly the urinary excretion of [195Au] the first day after the Myocrisin injection, but on the subsequent days the radio-metal excretion was unaffected by the treatment. A lower dose level of penicillamine (0.3 mmol/kg daily) gave rise to only a small and insignificant increase in the urinary excretion of gold. The present results indicate that penicillamine at low clinical doses is an inefficient chelator of gold, while high doses (presumably comparable to about 1 200 mg daily in humans) may mobilize certain amounts of the metal deposits.

Animals↗

PubMed1983

Comparison of oral and parenteral gold therapy and placebo in the treatment of rheumatoid arthritis.

Two hundred and eight patients entered a prospective, controlled, double-blind multicenter trial comparing auranofin, gold sodium thiomalate (GST), and placebo. One hundred and sixty-one patients completed at least 20 weeks of therapy. No remissions were seen in the trial. Response to a variety of measures of efficacy was generally modest for both gold treatment groups. There was statistically significant improvement with both gold preparations compared to placebo for the number of tender joints, the joint tenderness score, and physician assessment of disease severity. GST was also significantly better than placebo for the joint swelling score. GST demonstrated statistical improvement in patients with anaemia and thrombocytosis compared to the other treatment groups and both gold preparations were statistically superior to placebo in improvement of an elevated erythrocyte sedimentation rate. Approximately 25% of patients on GST were withdrawn from the study for adverse drug reaction with rash and stomatitis being the predominant reaction. Only 6% of patients on auranofin were withdrawn for untoward drug effect. The two gold preparations were similar in efficacy although auranofin was better tolerated.

Administration, Oral↗

PubMedDate not supplied

Quantitation of gold lymphocyte binding during chrysotherapy.

Carbon rod atomic absorption analysis (CRA) was applied to the quantiation of gold lymphocyte content (GLC) during chrysotherapy. Sensitivity and accuracy of CRA compared favorably with 195Au isotopic scintillation counting, circumventing the limitations and hazards of the latter in clinical applications. Picogram gold quantification of limited sample volume, less than 10 ml blood, e.g., 10(4)-10(5) lymphocytes (5 microliters) containing 5-10 pg was achieved. GLC after IM administration increased significantly in 60% of patients; for the remainder, GLC was observed to be independent of plasma gold content or cumulative dosage. GLC during auranofin administration (6 mg/day p.o.) approached values for IM gold despite significantly lower plasma levels. Unique sensitivity of CRA enables analysis of GLC under therapeutic conditions that could elucidate whether gold alters functional determinants.

Arthritis, Rheumatoid↗

PubMed1979

Distribution of gold in blood following administration of auranofin (SK&F D-39162).

After oral administration of auranofin (SK&F D-39162), a new antiarthritic gold compound, to rats, dogs and humans, a major portion (approximately 50%) of the blood gold content was found to be associated with cellular components. This property is in marked contrast to that reported for gold sodium thiomalate and represents another of the many physical, chemical and pharmacological differences between these therapeutic gold compounds. Although the clinical significance of this property is not presently known, it is recommended that pharmacokinetic studies involving auranofin include the assessment of both blood and serum gold levels.

Animals↗

PubMed1979

Inhibition of pokeweed mitogen-induced immunoglobulin production in humans by gold compounds.

The effect of gold compounds on an in vitro model of antibody production was investigated. Peripheral blood mononuclear cells from healthy adult individuals were stimulated with pokeweed mitogen (PWM) and generation of immunoglobulin secreting cells (ISC) was assayed. Addition of gold sodium thiomalate 10 microgram/ml markedly inhibited mitogen-induced ISC production. The suppression of Ig production could not be explained by nonspecific lymphocyte toxicity or interference with the assay system. Inhibition of PWM responsiveness was mediated directly by the gold moiety and was not a function of the thiomalate. Furthermore, it was shown that maximum suppression of ISC generation occurred only when gold was added to cultures within the first 24 hours of incubation. This suggested that gold compounds inhibit an early step in B cell activation and differentiation rather than merely blocking Ig secretion by mature plasma cells.

Antibody-Producing Cells↗

PubMed1989

Molecular distribution of gold(I) in human blood plasma after treatment with the antiarthritic disodium aurothiomalate.

On-line separation and detection of both high- and low-molecular-weight gold species in human blood plasma treated with disodium aurothiomalate were achieved by a technique incorporating a combination of fast protein liquid chromatography with continuous monitoring of absorbance at 254 nm and eluant gold concentration by flame atomic absorption spectroscopy. The fate of gold (40 microM disodium aurothiomalate) in human blood plasma was monitored over a period of 24 h. Results obtained indicated that more than 50% of the gold is associated with a peak identified as albumin after a 5 min incubation period at 37 degrees C, and by 30 min more than 90% is found to be associated with albumin. This novel analytical combination enables the rapid, selective and sensitive determination of gold(I) and its biotransformation products (both protein--and non-protein-bound) in biological fluids.

Adult↗

PubMed1987

Alveolar macrophage gold retention in rheumatoid arthritis.

Alveolar macrophages obtained by bronchoalveolar lavage (BAL) were evaluated by electron dispersive microanalysis (EDX) for the presence of elemental gold. EDX revealed gold in 90% (9/10) of patients with RA who were currently receiving chrysotherapy or who had discontinued chrysotherapy less than 24 months before BAL. All patients who had discontinued chrysotherapy more than 24 months before BAL (range: 3-14 years) were EDX negative (4/4), as were patients with RA who had never received gold therapy (5/5). Seven patients with RA (7/19) had clinical evidence of interstitial lung disease and 12 patients (12/19) had no interstitial lung disease. There was no correlation between chrysotherapy and the development of interstitial lung disease. These results demonstrate that gold is retained for prolonged periods in pulmonary tissue macrophages but do not identify any relationship between gold and chronic rheumatoid lung disease.

Arthritis, Rheumatoid↗

PubMed1977

Gold nephropathy: tissue analysis by X-ray fluorescent spectroscopy.

Three patients developed proteinuria following gold therapy for rheumatoid arthritis. The clinical syndrome was a self-limiting proteinuria with normal renal function. By light and electron microscopic appearances the renal lesion was an epimembranous deposit form of membranous glomerulopathy. Immunofluorescent study showed granular deposits of IgG and C3 complement along glomerular basement membranes. By X-ray fluorescent spectroscopic examination, gold was seen to be present within the proximal convoluted tubular cells but was not identified in the glomerular subepithelial deposits. These findings are consistent with an immune-complex form of glomerulopathy in which gold is neither the antigen nor a hapten in the glomerular deposits, and they suggest the hypothesis that antibodies to tubular epithelial antigens induced by gold therapy may be a causative factor in the renal disease associated with gold therapy in rheumatoid arthritis.

Adult↗

PubMedDate not supplied

[Gold treatment of rheumatoid arthritis].

In basic therapy of Rheumatoid Arthritis gold is preferred. Continued as well as discontinued therapy is used. The effect of gold is of complex nature. Gold is localized in cells of the RES and mesenchyme main in the inflammatory area. The passing acceleration of mesenchyme metabolism possibly shortens the duration of the inflammatory process. Gold further shows effects on cellular and subcellular membranes, on collagen, ACTH-production and on immune reactions. Patients with high activity and slow progression of their disease are especially suitable for chrysotherapy. Low maintenance of gold levels is effective and inhibits toxic-allergical reactions may be in a sort of desensitisation.

Arthritis, Rheumatoid↗

PubMed1983

[Morphology and pathogenesis of glomerular renal lesions in gold nephropathy].

Histological, immunofluorescent and electron microscopical investigations on the glomerular renal lesions in gold-induced nephropathy were performed by analyzing biopsy materials from 9 patients with rheumatoid arthritis treated by Sanocrysin (gold sodium thiosulfate). The morphological and immunofluorescent main changes consisted in the characteristic pattern of immune complex nephritis as membranous glomerulonephritis on the one hand (4 cases) and as mesangioproliferative glomerulonephritis (4 cases) on the other hand; in one case there could be demonstrated a focal proliferative glomerulonephritis similar to that observed as visceral manifestation of rheumatoid arthritis in the kidney. These different types of glomerular alterations in gold nephropathy evidently are related to th duration and immunological activity of the main disease and to the individual immune reactivity of the body as a whole determined by this, and not at all, by the combination of gold additionally with other antiinflammatory, especially antirheumatic drugs. The possible pathogenesis of nephropathy is discussed with special regard to definite effects of gold on the immune system.

Adult↗

PubMed1984

[Mechanism of action of gold compounds].

The mechanisms of action of gold salts are still poorly understood. While Auranofin (AF) has a direct anti-inflammatory action in animal models, Myochrysin (MC) has not. Both gold compounds inhibit various enzymes. Among these, lysosomal enzymes are of particular interest. Gold is known to accumulate in the lysosomes, and gold salts modulate certain macrophage functions in the immune system. The role of organic gold salt ligands containing, like D-penicillamine, a thiol group is still unclear. Positive data characterizing responders versus nonresponders are not yet available. As in other clinically heterogeneous diseases, medical action has mainly been based on clinical empiricism which, although resting on false premises, has helped to find a comparatively efficacious treatment. In fact, the proposals for further studies to shed light on the mode of action presented here may equally be ill conceived. However, these studies would at least expand our understanding of rheumatoid arthritis and thus be beneficial in the long run.

Animals↗

PubMed1981

A mechanism of action of gold sodium thiomalate in diseases characterized by a proliferative synovitis: reversible changes in collagen production in cultured human synovial cells.

These studies, conducted on early passage synovial cell mono-layers (derived from explant cultures of tissue obtained from patients with rheumatoid arthritis), have established that gold sodium thiomalate (GST) exposure results in dose-dependent changes in cell proliferation and protein synthesis as a consequence of the cellular accumulation of gold. The amount of gold found in the cell layer is correlated with the degree of inhibition of [3H]thymidine incorporation. Gold remains in the cell layer of treated cells after they have been subcultured twice in the absence of GST. Exposure of cells to a concentration of GST of 100 muM for 4 days results in 50% inhibition of [3H]thymidine incorporation. This antiproliferative effect is reversible at concentrations of 10 muM GST or less. Only partial recovery is observed after exposure to higher concentrations of GST which may be related to retained gold. The amount of collagen and noncollagen protein synthesized per cell increases at concentrations of GST of 10 muM and below but decreases with concentrations above 10 muM. A dose-dependent decrease in protein synthesized per flask and a decrease in the commitment to synthesize collagen relative to total protein synthesis follows exposure to GST in excess of 10 muM for 20 days which recovers partially after synovial cells are grown in GST-free medium for 10 days. An observed decrease in the percentage of type III collagen synthesized by synovial cells after GST exposure was not observed in cells grown in GST-free medium for 5 days after exposure, indicating that this effect of collagen synthesis is reversible. The reversible biochemical changes resulting from the exposure of cultured human synovial cells to GST are discussed as a mechanism of action of this drug on the proliferative synovitis that characterizes diseases such as rheumatoid arthritis.

Anti-Inflammatory Agents↗

PubMed1982

Pharmacokinetics of gold sodium thiomalate.

Two normal males participated in a study designed to examine the disposition of gold given intravenously and intramuscularly as gold sodium thiomalate. Blood samples were collected for 30 days, urine and feces for ten. A triphasic decay pattern in plasma gold concentrations was observed. Terminal log-linear phases corresponded to a mean disposition half-life of 12.5 days. Absolute bioavailability of IM gold sodium thiomalate appears to be variable with one subject having complete absorption and the other absorbing 64% of the administered IM dose. The major route of elimination of an IV dose of gold sodium thiomalate is urinary excretion, with a mean of 35% of the dose found in the urine in ten days. Fecal elimination accounts for an additional 9.4% of the IV dose excreted in ten days, probably as a result of biliary secretion.

Adult↗

PubMedDate not supplied

Stopfgold: a new direct filling gold.

A new direct gold material that is considerably different from other direct golds has been available since 1989. The advantages of this material are that the final restoration exhibits greater density than other forms of granular gold and has a 50% increase in shear strength when compared to gold foil. Clinical experience with the use of this new restorative material has been encouraging. Further clinical and laboratory research comparing this material with the other types of direct gold is anticipated.

Dental Restoration, Permanent↗

PubMed1987

A clinical evaluation of gold-plated tubes for middle-ear ventilation.

Gold-plated tympanostomy tubes have been recently marketed as possessing qualities making them ideal for middle-ear ventilation. The performance of these tubes was compared with that of similarly designed Teflon tubes in a controlled, prospective study. Twenty-eight children underwent bilateral myringotomy and tube placement. One ear was randomly chosen for intubation with a gold-plated tube, and a Teflon tube was inserted into the other ear. Patients were examined monthly for 12 months and evaluated for otorrhea, tube occlusion, and early tube extrusion. Although the incidence of otorrhea and tube occlusion were higher for the gold-plated tube, these differences were not statistically significant. The gold-plated tube had a significantly higher rate of early extrusion than the Teflon tube. Based on these findings, there appears to be no advantage to using gold-plated tubes for middle-ear ventilation.

Child↗

PubMed1979

Gold nephropathy in juvenile rheumatoid arthritis.

A 2-year-old girl was treated with gold salts for juvenile rheumatoid arthritis. Treatment had to be discontinued when persistent proteinuria was detected. As this case report indicates, close monitoring of the urine is mandatory during treatment with gold salts to detect early signs of toxicity: hematuria followed by casts and then proteinuria as therapy is continued. Histologic examination with electron microscopy will help to differentiate the different forms of gold toxicity. When the findings are consistent with gold-induced renal involvement, therapy should be discontinued. The gold nephropathy usually resolves in time, with no permanent renal damage.

Arthritis, Juvenile↗

PubMed1992

Protein-gold transport in the endocytic complex of trophotaenial absorptive cells in the embryos of a goodeid teleost.

This paper reports adsorptive endocytosis of exogenous proteins by the trophotaenial absorptive cells (TACs) in the viviparous goodeid teleost, Ameca splendens. In vitro incubations were performed with gold conjugated to bovine serum albumin (Au-BSA), human transferrin (Au-HTf), fetuin (Au-Fet), and asialofetuin (Au-ASFet). Localization of gold label on the TAC surface was nearly exclusive to patches of an amorphous coat associated with part of the intermicrovillous plasma membrane. On addition of excess BSA, HTf, Fet, or ASFet to incubation media containing, respectively, Au-BSA, Au-HTf, Au-Fet, or Au-ASFet, the density of gold particles adsorbed on the TAC surface decreased drastically. Moreover, attachment of the four protein-gold complexes to the same plasma membrane sites was suggested by reciprocal inhibitory effects. Further proteins such as hemoglobin, myoglobin, and cytochrome c were as well potent inhibitors of Au-BSA and Au-HTf binding and uptake. Binding of TACs of native BSA or HTf was visualized by immunogold labeling. The interactions between proteins and binding sites required both the presence of Ca2+ and appropriate pH greater than 6.6. Analyses of the concentration-dependent BSA and HTf binding curves, plotted from morphometric data, resulted in apparent dissociation constants, Kds, of approximately 5 x 10(-7) M and 4 x 10(-7) M, respectively. Following binding at the TAC surface and internalization via clathrin-coated pits and vesicles the several ligands were routed along the lysosomal pathway with transit through the endosomal compartment. Prolonged incubation periods led to massive intracellular accumulation of tracer proteins. The effects of NH4Cl (10 mM) treatment on TACs included enormous cytoplasmic vacuolation, a reversible loss of protein binding sites on the plasma membrane, and a block in the transport of protein-gold complexes to lysosomes.

Absorption↗

PubMed1979

Gold-induced changes in the morphology and functional capabilities of human monocytes.

The capacity of gold compounds to induce morphologic changes and alterations in the functional activity of human mononuclear phagocytes (M phi) in vitro was examined. Human peripheral blood mononuclear cells were incubated with gold sodium thiomalate (25 microgram/ml) for 96 hours. As a result, M phi developed electron dense precipitates within phagolysosomes, as well as marked dilatation of these organelles. Gold incubation also altered a number of M phi functions. While viability and adherence were unaffected, the capacity to spread on surfaces was diminished. Pinocytosis of soluble proteins and phagocytosis of opsonized sheep erythrocytes were impaired, but Fc mediated particle binding was not. These data indicate that gold can alter certain functional activities of M phi and support the idea that the major action of gold in rheumatoid arthritis results from its capacity to alter M phi function.

Cell Adhesion↗