Fatality from potassium gold cyanide poisoning.

While potassium cyanide poisoning has been well described, the toxicity of potassium gold cyanide is less well understood. This case describes an 84-year-old man who presented after an intentional ingestion of 0.5-1 teaspoons of potassium gold cyanide. Despite antidotal therapy, the patient rapidly developed severe lactic acidosis, multiorgan dysfunction and ultimately expired. While the patient's clinical findings were consistent with acute cyanide poisoning, a serum cyanide level was below the toxic threshold. Previous reports have suggested that gold toxicity may also contribute to the effects of potassium gold cyanide, and may have played a role in the patient's rapid decline. In addition to treatment of cyanide toxicity, management of acute gold toxicity should also be considered in potassium gold cyanide ingestion.

Japanese medaka exposed to gold nanoparticles: Only embryonic exposure generates irreversible hatching failure, developmental failure, and mortality of sac-fry.

This study evaluated irreversible toxicity effects of gold nanoparticles (AuNPs) during the short-term (only embryonic stage) and long-term (both embryo and sac-fry stages) exposures of Japanese ricefish, Oryzias latipes (medaka) embryos and sac-fry. Embryos and sac-fry exposed to AuNPs at 8 and 15days post-fertilization exhibited mortality, developmental failure, and abnormal appearance, and sac-fry additionally exhibited hatching failure and abnormal behavior. Embryos damaged by AuNPs during the embryonic stages failed to hatch and died, despite being raised under AuNP-free conditions after embryonic exposure. This study demonstrates that AuNPs have irreversible effects on O. latipes embryos and sac-fry, including the embryonic stages, regardless of the length of exposure. This result may be critical for predicting the potential continuous effects of AuNPs when the exposure duration of fish is short but includes the embryonic stages. To the best of our knowledge, this is the first study to test the toxicity of AuNP exposure on the embryos and sac-fry of O. latipes.

Hematologic effects of heavy metal poisoning.

Heavy metal poisoning can cause a variety of hematologic disorders. Exposure to heavy metals is ubiquitous in the industrial environment and must be considered in the differential diagnosis of many types of anemia. The heavy metals most commonly associated with hematologic toxicity are arsenic and its derivative arsine, copper, gold, lead, and zinc. A few distinctive clinical features characterize the hematologic manifestations of many occult heavy metal poisonings. These features have a limited differential diagnosis. A knowledge of these clinical features can assist the astute clinician in making the correct diagnosis.

Aurothioglucose overdosage in five patients with rheumatoid arthritis.

Five patients with active seronegative, rheumatoid arthritis, HLA-DR3 negative, received inadvertently 250 to 500 mg of aurothioglucose instead of their usual weekly dose, during standard remission-inducing chrysotherapy. Subsequently a rapid and sustained clinical remission appeared in all five patients.

Acute poisoning with gold cyanide.

A case of deliberate ingestion of an electroplating solution containing gold cyanide is described. Despite the use of an antidote, and supportive treatment for cyanide poisoning, the patient died after 13 hours. Sublethal cyanide and high red blood cell gold levels suggest acute gold toxicity as the most likely cause of death. Evidence for this is discussed and recommendations are made for the treatment of cyanide poisoning.

Should acute gold overdose be invariably treated?

Acute gold overload is rare and its clinical and pathophysiological consequences are not well delineated. Consequently the therapeutic approach has not been formulated. We describe 2 patients with rheumatoid arthritis in whom an acute gold overload was inadvertently administered. Their subsequent course, without specific treatment, was benign and uneventful. We suggest that with similar cases a conservative approach of watchful expectancy be adopted.

Antidotes for gold (sodium bis[thiosulfato]gold[I]) intoxication in mice.

Eight compounds were examined to determine their relative efficacy as antidotes in acute gold intoxication in mice after the intraperitoneal injection of 200 mg/kg of Na3 [Au(S2O3)2] X 2H2O. Of the compounds examined, 2,3 dimercaptosuccinic acid was the most effective antidote. It was noted that with D-penicillamine those animals which did not survive died sooner (in a matter of hours) than the corresponding control animals which had received no antidote (about 3 days). In subsequent experiments in which Na3 [Au(S2O3)2] X 2H2O was administered at the lower level of 140 mg/kg, 2,3 dimercaptosuccinic acid showed itself to be capable of reducing kidney gold levels by a factor of about 5 and liver gold levels by a factor of approximately 2.

Gold toxicity presenting as peripheral neuropathy.

A patient with rheumatoid arthritis developed gold induced peripheral neuropathy after 255 mgs of aurothioglucose. This neuropathy is characterized by weakness and numbness of the hands and feet in association with hyperalgesia of the palmar surface of the hands. The absence of vasculitis permits differentiation of gold neuropathy from the neuritis associated with rheumatoid arthritis or systemic lupus erythematosus. Treatment consists in cessation of gold and possibly the use of dimercaprol; recovery is slow but generally complete.

Penicillamine in metal poisoning.

Penicillamine is used to treat heavy metal poisonings because it forms complexes in vitro with several toxic metals, including lead, cadmium, mercury, and gold. Urinary excretion of lead is immediately, markedly increased by penicillamine, but this is not true for the urinary excretion of cadmium, mercury, and gold. There is evidence that cadmium is shifted from 1 binding site to another in vivo; this may also be true of mercury and gold. Whether the effects of such possible shifts are beneficial or adverse is unknown.

Inhibition of adenosine triphosphatases by gold.

Inhibition of adenosine triphosphatase (ATPase) by chlorauric acid (Au3+) and gold sodium thiomalate (Au+) was studied in dog brain and kidney and in human kidney enzyme preparations. Au3+ indiscriminately affected ouabain-sensitive (Na+ + K+-dependent) ATPase and ouabain-insensitive (Mg2+-dependent) ATPase with concentrations for 50% inhibition (I50) approximately 10(-6) M. The I50 of Au3+ for Na+ + K+ ATPase was several-fold higher in homogenates than in microsomal fractions. The enzyme was protected by bovine serum albumin. Although Au3+ and Au+ were equipotent against Mg2+ ATPase, Au+ inhibited Na+ + K+ ATPase 2 to 3 times more effectively than did Au3+. The inhibitory action of Au3+ (but not Au+) was potentiated by ascorbic acid, suggesting reduction of Au3+ to Au+ by ascorbic acid. The fractional inhibition of Na+ + K+ ATPase by Au3+ or Au+ was not affected by changing concentrations of NaCl, KCl, MgCl2, ATP, and MgATP. Decreasing pH from 8.0 to 6.8 enhanced both Au+ and Au3+ inhibition. We conclude that gold is one of the most potent nonspecific of Na+ + K+ ATPase, with characteristics differing from other metallic inhibitors of this enzyme system.