[Argyria: new physio-pathological and therapeutic hypothesis]. / Argirìa: nuove ipotesi fisio-patologiche e terapeutiche.

The authors describe a case of sistemic argyria. They suggest a common physiopatologic mechanism with Wilson disease and they consider the utilization of penicillamine as a ligand for the silver, since there are not other available valid treatments.

Argyria and convulsive seizures caused by ingestion of silver in a patient with schizophrenia.

The case study of a schizophrenic patient with argyria which resulted from the chronic and excessive ingestion of antismoking pills contain silver, is presented. Convulsive seizures developed after the patient had been addicted to the pills for 40 years. An extremely high concentration of silver was detected in serum. This case provides support for the hypothesis that silver may cause convulsive seizures as a result of systemic poisoning.

Hypoactivity in silver exposed mice.

The functional implications of the presence of silver in the central nervous system are unknown. Since silver is present in the environment and since systemic silver poisoning leads to intraneuronal accumulations of the metal we have evaluated the possible effects of silver on the open field behaviour of mice. Argyric mice have been compared with controls in three experiments, one including long term administration of 0.015% silver nitrate in the drinking water and two in which the reactions of male and female mice to shock doses of silver lactate have been studied. In all experiments the silver treated mice were hypoactive. We suggest that this hypoactivity is due to an influence of silver upon the functional status of the CNS.

Acute toxicity of some silver salts of sulfonamides in mice and the efficacy of penicillamine in silver.

The silver salt of 2-metanilamido-5-chloropyrimidine (AgMCP) and the sodium, amminosilver and trimethylphosphite-silver salts of 3',5'-dichlorobenzenesulfonanilide (NaDBS, AgNH3DBS and AgP(OCH3)3DBS were synthesized as possible antibiotic of antiparasitic drugs. All the organosilver compounds were extremely water-insoluble. For animal studies these, and other reference compounds, were given as fine suspensions in an Emulphor-safflower oil mixture. The ip LD50's in mice in mmol/kg were: 1.67 for NaDBS, 0.22 for silver acetate (AgAc), 0.15 for AgP(OCH3)3DBS, 0.13 for AgMCP and 0.10 for AgNH3DBS. When given by mouth, 15 mmol AgAc/kg produced a high mortality, but none of the organosilver compounds caused death in maximal doses (1.9 to 2.6 mmol/kg) that could be given based on considerations of total volume and stability of the suspension. All the silver compounds, including AgAc, produced a similar toxic syndrome with initial hyperexcitability, ataxia, central nervous depression, labored breathing, loss of righting reflex and death. Most deaths occurred between 12 and 24 hours after dosing. In contrast, animals given NaDBS often died within 3 hours although the major signs were very similar to those produced by the silver compounds. When given ip as a single dose 30 minutes after AgAc, D-penicillamine was effective in reducing mortality, but it had no effect on the mortality of the organosilver compounds. Histological studies revealed similar patterns of silver deposition, especially in the liver and kidneys, at 6, 18 and 24 hours after the organosilver compounds and after AgAc. We conclude that the presence of silver contributes significantly to the acute toxicity of these sulfonamides although they may dissociate free silver less readily than does AgAc.