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At least 181 records · Page 10Linked to original sources
PubMed1996

Three cases of linear lichen planus caused by dental metal compounds.

Three cases of linear lichen planus on the lower extremities unaccompanied by mucous lesions are described. Dental metal compounds were thought to be the precipitating factor in all cases. Skin lesions did not respond to topical steroid ointment or antihistamines. Two cases showed a positive patch test reaction to gold (HAuCl4) and a positive lymphocyte stimulation test to gold compound (Gold sodium thiomalate). One case showed a positive patch test reaction to mercury (HgCl2), but a negative lymphocyte stimulation test. Suspected metal compounds were demonstrated in their dental materials. Removal of gold materials in one case gradually improved the lesions within 6 months with a transient erythematous swelling of the face shortly after removal of the metal. Both of these cases responded to oral disodium chromoglycate therapy. These results suggest that metal compound specific T cells might be responsible for the development of linear lichen planus.

Adult↗
PubMed1999

Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucose.

Gold compounds have long been used in the treatment of rheumatoid arthritis (RA). However, their actions in RA have not been clarified. In this study, we examined the effect of one of the monovalent gold compounds, aurothioglucose (AuTG), on the IL-1-induced production of IL-6, IL-8 and granulocyte macrophage colony stimulating factor (GM-CSF) from rheumatoid synovial fibroblasts (RSF) isolated from three RA patients. IL-6 and IL-8 induction but not GM-CSF induction was inhibited in most of the RSF after pretreatment with AuTG. Since gene expression of these cytokines is known to be under the control of a common transcription factor, NF-kappaB, the effect of AuTG on the cellular localization of NF-kappaB (p65 subunit) and on NF-kappaB-DNA binding was examined. Although AuTG treatment did not prevent NF-kappaB nuclear translocation, AuTG blocked the DNA-binding activity of NF-kappaB when examined in vitro. Morphologically, both metal-specific cell staining using p-dimethylaminobenzylidene rhodamine and transmission electron microscopic examinations demonstrated the accumulation of metal gold in the cytoplama and some organella (mitochondria and lysosomes) of the AuTG-treated RSF. These results indicate that one of the anti-rheumatic actions of AuTG might be through its inhibitory action on NF-kappaB.

Antirheumatic Agents↗
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↗
PubMed1977

Inhibition of lysosomal enzyme release from rat leukocytes by auranofin. A new chrysotherapeutic agent.

Auranofin (SK&F D-39162), a new antiarthritic gold compound reported to be orally effective in animal (adjuvant rat) and human (rheumatoid) arthritic conditions, is a potent in vitro inhibitor of the release of lysosomal enzymes from phagocytizing rat leukocytes. Auranofin, at micromolar concentrations (1-10 microM), produced a dose-dependent reduction in extracellular levels of lysosomal enzyme markers (beta-glucuronidase and lysozyme) which are selectively released from rat leukocytes during phagocytosis of zymosan particles. The reduction in extracellular levels of lysosomal enzymes appears to be caused by inhibition of their selective cellular release, since effective concentrations of auranofin did not produce leukocyte cytotoxicity or inhibition of cell-free lysosomal enzyme activity. Morphologic and biochemical evidence indicated that auranofin also interferes with phagocytosis of zymosan particles. The potent in vitro activity of auranofin appears to result from its unique gold complex, since neither structurally related nongold compounds nor clinically used gold compounds (gold sodium thiomalate and gold thioglucose) were potent inhibitors of lysosomal enzyme release. The results of this investigation suggest that the antiarthritic activity of auranofin may be caused at least in part, by inhibition of lysosomal enzyme release and/or cellular processing of antigens.

Animals↗
PubMed1986

Pharmacology of auranofin: overview and update.

Auranofin, the only approved oral gold complex of value in suppressing rheumatoid arthritis, differs from injectable gold compounds molecularly and pharmacologically. Although comparably efficacious, the side-effect profiles of oral and intramuscular gold differ, and the withdrawal rate for adverse reactions is several-fold lower with auranofin. Considerably less elemental gold is available to the internal milieu with auranofin than with gold sodium thiomalate (3 mg/week vs. 25 mg/week), a difference reflected in lower blood, synovial fluid and tissue gold levels. Approximately 25% of the administered auranofin dose is absorbed orally, and 85% is recovered in feces. Serum gold levels are 300-400 micrograms/dl one week after injectable gold and 60-70 micrograms/dl daily with auranofin (6 mg/d). But, surprisingly, the fraction of gold associated with the red blood cell fraction is higher with auranofin. Blood gold levels do not correlate with clinical response to treatment or frequency or type of adverse reaction, regardless of the gold preparation used. Similar results obtain with penicillamine. Methotrexate blood levels are not related to the development of hepatic fibrosis. The mechanisms of gold action in rheumatoid arthritis are unknown, despite the laboratory definition of multiple antiinflammatory, immunologic and other effects. Sulfhydryl binding activity, an established property of injectable gold compounds and penicillamine of potential importance pharmacodynamically, is limited with auranofin.

Administration, Oral↗
PubMed2001

Alteration of the aurophilic interactions in trimeric gold(I) compounds through charge transfer. Behavior of solvoluminescent Au(3)(MeN=COMe)(3) in the presence of electron acceptors.

The ability of the triangular gold(I) complex, Au(3)(MeN=COMe)(3), which as a solid displays the novel property of solvoluminescence (see: Vickery, J. C.; Olmstead, M. M.; Fung, E. Y.; Balch, A. L. Angew.Chem., Int. Ed. Engl. 1997, 36, 1179) to function as an electron donor has been demonstrated through spectroscopic studies and isolation of crystalline adducts with organic acceptor molecules. Four such adducts with nitro-9-fluorenones have been isolated and subject to single-crystal X-ray diffraction study. These are deep yellow [Au(3)(MeN=COMe)(3)].[2,4,7-trinitro-9-fluorenone], red [Au(3)(MeN=COMe)(3)].[2,4,5,7-tetranitro-9-fluorenone], red [Au(3)(MeN=COEt)(3)](2).[2,7-dinitro-9-fluorenone], and red [Au(3)(MeN=COEt)(3)](2).[2,4,7-trinitro-9-fluorenone]. The solid-state structures of [Au(3)(MeN=COMe)(3)].[2,4,7-trinitro-9-fluorenone] and [Au(3)(MeN=COMe)(3)].[2,4,5,7-tetranitro-9-fluorenone] consist of columns in which the planar gold(I) trimers and the nearly planar nitro-9-fluorenones are interleaved with the gold trimers making face-to-face contact with the nitroaromatic portion of the electron acceptor. Thus the organic acceptors disrupt the aurophilic interactions present in crystalline [Au(3)(MeN=COMe)(3)] itself. However, in [Au(3)(MeN=COEt)(3)](2).[2,7-dinitro-9-fluorenone] and [Au(3)(MeN=COEt)(3)](2).[2,4,7-trinitro-9-fluorenone], aurophilic interactions are found which produce dimers, [Au(3)(MeN=COEt)(3)](2), with nearly trigonal prismatic Au(6) cores. These dimers are interleaved with the nitro-9-fluorenone molecules to again form extended columns in which the components make face-to-face contact. Despite the fact that the gold atoms in [Au(3)(MeN=COMe)(3)] and [Au(3)(MeN=COEt)(3)] are in exposed sites and only two-coordinate, there is no evidence of additional coordination of the nitro-9-fluorenones with gold centers in the crystalline adducts.

Journal Article↗
PubMed1977

[Gold therapy in pemphigus].

According to works of Penneys and Eaglstein on the management of pemphigus with gold compounds, the authors report one observation of chronic pemphigus, in which steroid therapy caused severe psychiatric disorders. The use of gold compounds permitted reduction of the dose of steroids and control of the pemphigus.

Female↗
PubMedDate not supplied

[Effect of gold on lymphocyte stimulation by influenza A in chronic polyarthritis].

In vitro stimulation with influenza-A antigens of the peripheral lymphocytes from patients with rheumatoid arthritis is significantly higher than that in those from healthy controls. Stimulation was performed without autologous serum, is dependent on the monocyte function and correlates with disease activity. Gold compounds can inhibit monocyte function and so the lymphocyte stimulation by influenza-A antigens. Cortico-steroids do not do this. Under gold compound treatment, lymphocyte stimulation was markedly reduced in about 70% of cases and was correlated with clinical success.

Adult↗
PubMed1983

Gold therapy in the elderly rheumatoid arthritis patient.

Forty elderly (greater than or equal to 60 years old) and 101 young (less than 60 years old) rheumatoid arthritis patients receiving injectable gold therapy were followed prospectively between April 1971 and April 1982. The mean total gold compound received was 1,392 mg in the young group and 1,861 in the elderly group. Besides age, the only significant difference between the two groups was the increased gold compound received by the elderly. To determine efficacy and toxicity within and between certain age groups, the 141 patients were divided into 4 arbitrary age groups: group A (less than 30 years), group B (30-44 years), group C (45-59 years), and group D (greater than or equal to 60 years). The elderly responded to the gold therapy as well as the young patients did, at any time frame examined after 3 months of therapy. There was no difference in clinical benefit among groups A, B, C, and D. Nine patients in the elderly group and 15 in the young group had therapy discontinued because of no response. This difference was not significant among the groups A, B, C, and D. There was no difference in outcome of individual toxicity between the elderly and the young groups, and no difference in frequency of toxicity between the age groups A, B, C, and D. Serious hematologic toxicity occurred only in patients over 47 years of age, and nephrotic syndrome occurred only in patients over 52. In this study, gold therapy was found to be as clinically beneficial in the elderly as in the young patients, and the toxicity and drug failure rates were not significantly different.

Adolescent↗
PubMed1984

Problems of antiarthritic therapy in the elderly.

Rheumatic diseases are prevalent in the elderly population, resulting in high morbidity caused mainly by lack of mobility. Consequently, the use of antirheumatic drugs in older persons is extensive. This review outlines some of the hazards encountered in the use of antirheumatic drugs in the elderly. Analgesics such as propoxyphene and acetaminophen are useful adjuncts to the treatment of arthritic pain, but propoxyphene has been associated with respiratory depression, and renal clearance of acetaminophen is reduced in elderly subjects. Salicylates may cause deafness, and like the other nonsteroidal anti-inflammatory drugs, may cause salt and water retention resulting in congestive cardiac failure. Phenylbutazone should not be used because of the risk of blood dyscrasia, and indomethacin has been reported as interfering with the antihypertensive effect of beta-blockers. Chloroquine levels may be raised in patients with impaired renal function, and there is increased risk of retinal damage with the drug in elderly subjects. Injectable gold compounds and penicillamine are not contraindicated in the elderly, because they are just as efficacious as in younger persons for the treatment of rheumatoid arthritis. Toxicity due to gold compound is not increased in the elderly, but skin rashes and abnormalities of taste do occur more commonly in elderly patients treated with penicillamine. Corticosteroids do not affect disease progression and therefore should be used only in acute severe disease for short periods of time. As in the younger population, treatment of gout in the elderly is dependent on renal function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗
PubMed1997

Molecular Aggregation of Annular Dinuclear Gold(I) Compounds Containing Bridging Diphosphine and Dithiolate Ligands.

A series of annular dinuclear Au(I) complexes containing diphosphine (R(2)P(CH(2))(n)()PR(2); R = Me, n = 1, dmpm; R = Me, n = 2, dmpe; R = Ph, n = 1, dppm; R = Ph, n = 2, dppe) and dithiolate (dtc = S(2)CNEt(2)(-), i-mnt = S(2)C(2)(CN)(2)(2)(-)) ligands were synthesized: [Au(2)(P-P)(S-S)]X (S-S = dtc: P-P = dmpm, X = Cl, 1; P-P = dppm, X = PF(6), 2; P-P = dppe, X = PF(6), 3; P-P = PPh(3), X = PF(6), 4) and [Au(2)(P-P)(S-S)] (S-S = i-mnt: P-P = dmpm,5; P-P = dppm, 6; P-P = dmpe, 7; P-P = dppe, 8). Crystal structures of two complexes are reported. Pertinent crystallographic data: [Au(2)(dmpm)(i-mnt)] (5), space group Fdd2, with a = 19.574(3) Å, b = 48.220(11) Å, and c = 15.273(2) Å, R = 0.0542; [Au(2)(dppe)(i-mnt)] (8), space group P2(1)/n, with a = 11.793(2) Å, b = 19.607(2) Å, and c = 15.349(2) Å, R = 0.0448. Each molecule has two gold atoms bridged by a dithiolate ligand on one side and a diphosphine ligand on the other side, thus forming an eight- or nine-membered ring digold complex. The tendency of the digold(I) compounds to aggregate through an intermolecular Au-Au interaction depends on the ligands. Among the structures determined, complex 5 forms a polymeric chain and compound 8 is monomeric. Molecular aggregation also occurs in solution. Concentration-dependent absorption spectra of Au-dtc compounds suggest that an equilibrium between the monomer and dimer exists. Equilibrium constants corresponding to the intermolecular Au-Au interaction range from 38 to 137 M(-)(1) with DeltaH values of approximately 15 kcal/mol and DeltaS values of approximately -35 to approximately -46 cal/(K mol). Concentration dependence of emission spectra of annular compounds in acetonitrile also supports association in solution. Emissions at approximately 400-440 nm assignable to spin-allowed metal-centered transitions from monomeric Au(2) at lower concentrations and dimeric Au(4) at higher concentrations are observed. Compounds 1-3 and 5-8 in the glass state having spin-forbidden dithiolate ligand to gold charge transfer ((3)LMCT) transitions give emission bands at approximately 550 nm. Compound 4 has a S --> Au (3)LMCT transition at 500 nm. (31)P variable-temperature NMR experiments were performed for 1-3. The dynamic process is attributed to molecular aggregation through an intermolecular Au-Au interaction in solution. The activation energies are approximately 9 kcal/mol for 1 and 2.

Journal Article↗