Clinical toxicology
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The authors have observed 59 cases of bismuth encephalopathy between 1972 and 1979. Eight female patients in this group showed osteoarticular lesions confined exclusively to the thoracic vertebrae and the humerus. ⋯ Intraspongy microfractures due to the intense and repeated myoclonia could explain osteonecrosis. It has been suggested that bismuth facilitates the modification of the bony tissue; however, the evidence remains inconclusive as there are few anomalies of phosphocalcic metabolism.
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Clinical toxicology · Oct 1981
Epidemiological aspects of poisoning in children observed over a 10-year period.
During 10 years of activity at our Service, we collected 1867 cases of poisoning in children. Our observations concern only subjects hospitalized at our Institute and do not include phone call consultations. Our experience confirmed a higher number of poisonings among males. ⋯ The time of the day when most accidental poisonings occurred ranged from 10:00 AM to 12:00 noon and from 6:00 to 8:00 PM. Most poisonings took place in the kitchen. The colors preferred by children are white and pink.
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Clinical toxicology · Sep 1981
Case ReportsThe metabolism of arsenic in humans acutely intoxicated by As2O3. Its significance for the duration of BAL therapy.
The urinary excretion of inorganic arsenic and of its less toxic metabolites [monomethylarsonic acid (MMA) and dimethylarsinic acid (DM)] has been followed-up in five cases of acute oral intoxication by As2O3. In addition to supportive therapy all patients were given BAL. ⋯ The time at which the majority of arsenic is excreted as its organic metabolites depends on the severity of the intoxication but in all the cases, more than 95% of th excreted arsenic is in the organic form after 9 d, the dimethylated derivative being preponderant. Speciation of arsenicals in urine might be useful to determine the duration of BAL treatment.
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Clinical toxicology · Jun 1981
Case ReportsAcute yellow phosphorus poisoning from pesticide pastes.
Ten cases of ingestion of yellow phosphorus rat poison, including four cases that occurred during the past 3 years, are reported. Comparison of these cases with 82 others from the literature showed that ingestion of yellow phosphorus paste often results in clinical findings that are different from those described for acute yellow phosphorus poisoning in current toxicology texts. The time lag between swallowing of the poison and onset of symptoms varied from a few minutes to 24 h. ⋯ Initial symptoms were referable to the gastrointestinal tract, central nervous system, or both. Mortality rates were 23% for patients who had early symptoms of vomiting or abdominal pain; 73% for those where the first manifestation of intoxication was restlessness, irritability, drowsiness, stupor, or coma; and 47% for patients who had a combination of these GI and CNS symptoms initially. Applying standard diagnostic criteria for yellow phosphorus poisoning to patients who have consumed yellow phosphorus pastes may result in serious diagnostic errors.