The Treatment of Gold Dermatitides

Ragan, Charles

doi:10.1001/jama.1947.02880110018005

Cited by 36 publications

(9 citation statements)

References 10 publications

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“…Relapse in Rheumatoid Arthritis.-It has already been noted that Ragan and Boots (1947) found that four of their five cases showed an increase in the symptoms of rheumatoid arthritis within one month of treatment with BAL. In the present series six cases have been followed up for periods of one to six months and only one of these showed any relapse.…”

Section: Discussionmentioning

confidence: 91%

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Bal in the Treatment of Gold Toxicity

MacLeod

1948

Annals of the Rheumatic Diseases

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Section: Discussionmentioning

confidence: 91%

“…Among the first papers on the use of BAL in toxic reactions due to gold was that of Ragan and Boots (1947). Before using the drug in human subjects suffering from gold toxicity these authors carried out an important preliminary experiment.…”

mentioning

confidence: 99%

Bal in the Treatment of Gold Toxicity

MacLeod

1948

Annals of the Rheumatic Diseases

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“…It has been reported that BAL reacts with gold (Brown et al 1979) and is used as an antidote for gold intoxication (Cohen et al 1947;Lockie et al 1947;Ragan and Boots 1947). However, DMPS appears to be more advantageous as an antidote against gold toxicity than BAL because of the lesser toxicity of DMPS (Gabard et al 1980).…”

Section: Discussionmentioning

confidence: 99%

“…The adverse reactions in these cases have been treated by various procedures. 2,3-Dimercaptopropanol (BAL) has been used to prevent the development of toxic side effects (Cohen et al 1947;Lockie et al 1947;Ragan and Boots 1947;England and Smith 1972). Gabard (1980) reported that orally administered sodium 2,3-dimercaptopropane sulphonate (DMPS) reduced the concentration of gold in rats treated with AuroDetoxin and increased the urinary excretion of the metal.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of chelating agents against renal toxicity of gold sodium thiomalate in rats

et al. 1991

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The protective effects of various chelating agents such as D-penicillamine (D-PEN), 2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercaptopropane sulphonate (DMPS), and N-(2-mercapto-2-methylpropanoyl)-L-cysteine (bucillamine), on the renal damage induced by gold sodium thiomalate (AuTM) in rats were studied. Rats were injected i.v. with AuTM at doses of 0.026, 0.066, 0.132, and 0.198 mmol/kg. Urinary excretion of protein, aspartate aminotransferase (AST), and glucose in rats injected with AuTM significantly increased compared to the control levels within 1 day after the injection and thereafter decreased nearly to the control levels at 3 or 7 days. Gold was excreted rapidly during the first day after AuTM injection and excreted gradually thereafter. The concentrations of gold in the kidney and liver at 1 or 7 days after AuTM administration were approximately dose dependent. Treatment with D-PEN, DMSA, DMPS, and bucillamine (1.2 mmol/kg) significantly prevented increases in the urinary excretion of protein, AST, and glucose and the BUN level after AuTM (0.026 mmol/kg) injection. The injection of the chelating agents after AuTM administration showed that D-PEN, DMSA, and DMPS enhanced mainly the urinary excretion of gold and that bucillamine enhanced mainly the fecal excretion of the metal. These chelating agents significantly decreased the gold concentrations in the kidney and liver. The findings suggest that the chelating agents tested can ameliorate the renal damage induced by AuTM.

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“…However, there is a relatively high rate of toxic side-effects, mainly disturbances of the haemapoietic system, dermatitis and nephrosis (Eberl, 1974;Schattenkirchner, 1977). In severe cases, 2,3-dimercaptopropanol (British Anti-Lewisite, BAL) has been employed to counter the development of these toxic effects (Cohen, Goldman & Dubbs, 1947;Lockie, Norcross & George, 1947;Ragan & Boots, 1947;Meyer, 1963;Witzgall, 1967). More recently, D-penicillamine, which is better tolerated than BAL, has been tried (Bluhm, Sigler, Ensign & Sharp, 1962;Eyring & Engleman, 1963).…”

Section: Introductionmentioning

confidence: 99%

Removal of Internally Deposited Gold by 2,3‐dimercaptopropane Sodium Sulphonate (Dimaval)

Gabard

1980

British J Pharmacology

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Orally administered 2,3‐dimercaptopropane sodium sulphonate (DMPS, Dimaval) reduced the concentration of gold in rats treated with Auro‐Detoxin and increased the urinary excretion of the metal. In a long‐term experiment, DMPS decreased significantly the concentration of gold in the kidneys and in the skin and increased it in plasma. DMPS appears to be of interest as a possible antidote to gold, which could replace the more toxic 2,3‐dimercaptopropanol (BAL).

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The Treatment of Gold Dermatitides

Cited by 36 publications

References 10 publications

Bal in the Treatment of Gold Toxicity

Bal in the Treatment of Gold Toxicity

Protective effects of chelating agents against renal toxicity of gold sodium thiomalate in rats

Removal of Internally Deposited Gold by 2,3‐dimercaptopropane Sodium Sulphonate (Dimaval)

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