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Biomedical subjects

Y Shnaps

Publications and source records attributed to Y Shnaps.

10 recordsLinked to original sources
PubMed1982

Methyldopa poisoning.

A case of methyldopa overdose, confirmed by quantitative blood analysis, is presented. The clinical manifestations were coma, hypothermia, hypotension, bradycardia, and dry mouth. This combination of clinical findings, previously considered characteristic of phenothiazines or tricyclic antidepressants poisoning, should also raise the suspicion of methyldopa overdose. Methyldopa is a commonly used antihypertensive agent. Surprisingly, reports on overdose are exceedingly rare [1, 2]. We have recently treated a case of methyldopa overdose in which the presenting signs resembled those of psychotropic drug poisoning.

Adult↗
PubMed1981

Iron poisoning.

Explore the source record for details and available documents.

Humans↗
PubMed1981

The chemically abused child.

The case of an 18-month-old child poisoned by her mother with chlorpromazine is described. Fifteen other cases of child poisoning have been previously reported. In all of these cases the assailant was the mother (who in 11 cases was described as mentally disturbed); in 14 cases the presenting sign was a change in the level of the child's consciousness; and in ten cases the agent was a psychotropic drug. These poisonings were always well planned and manipulative, usually of long duration (1 1/2 to 48 months), and often continued during hospitalization, but lacked homicidal intent. Three children died. It is suggested that this subgroup of child abuse be more rigidly defined and possibly be named "the chemically abused child." A higher degree of suspicion and alertness to this problem would increase the number of cases identified and the number of children who receive professional care.

Child Abuse↗
PubMed1980

Colchicine kinetics in patients with familial Mediterranean fever.

Serum colchicine levels were determined by radioimmunoassay after a 1-mg bolus injected intravenously in 4 patients with familial Mediterranean fever and in 6 normal subjects. Mean elimination half-life (t1/2) (+/- SEM) was 157 +/- 20 min in the patients and 65 +/- 15 min in the normal subjects (p less than 0.005). Total clearance was 239 +/- 50 ml/min in the patients and 601 +/- 155 ml/min in the normal subjects (p less than 0.05). Volume of distribution (Vdarea) was 76 +/- 16 and 49 +/- 91 and did not differ significantly. In 8 patients receiving colchicine prophylactically with good clinical response, serum colchicine ranged from 0.3 to 2.4 ng/ml after daily doses of 1 mg orally. In 2 responding patients 2-mg doses orally induced levels from 4 to 10 ng/ml, and in one (a nonresponder) a 3-mg dose induced levels of 7.5 to 13 ng/ml. Of 3 patients receiving 2 mg daily with unsatisfactory clinical responses, serum levels were not detectable in one and in the low range of 1.5 to 5.4 ng/ml in the others. It is suggested that lack of response to colchicine orally in some nonresponders could result from inadequate absorption or altered disposition of colchicine.

Adult↗
PubMed1980

Inadequacy of reported intake in assessing the potential hepatotoxicity of acetaminophen overdose.

No evidence of liver damage was found in a series of 22 patients with acute acetaminophen overdose, 13 of whom reported ingesting doses of 10 to 25 g, which is within the accepted hepatotoxic range. Serum acetaminophen concentrations did not exceed 160 micrograms/ml, an amount well below the minimal hepatotoxic level. Moreover, mean serum concentrations of acetaminophen in patients reporting the ingestion of less than 10 g [74 +/- 48 (SD) micrograms/ml) were similar. Throughout the study, no correlation was found between serum concentrations and the reported dose ingested. Poor bioavailability of local acetaminophen formulations was ruled out as a factor in the dose-concentration discrepancy by comparison with a British formulation ingested by four volunteers. We conclude that information regarding dose ingestion given by patients admitted to hospital for self-poisoning is inaccurate and often exaggerated. Management of acute acetaminophen overdose must be based on serum concentrations of acetaminophen and not on the reported dose.

Acetaminophen↗
PubMed1979

Acute triclofos poisoning in a preterm infant.

A preterm infant with accidental triclofos sodium poisoning is described. He developed deep coma, severe hypothermia, mild by hypotension and lack of the primitive and deep tendon reflexes. During recovery, the primitive reflexes were the last to appear. The natural course of triclofos poisoning, and its influence on the immature central nervous system of the preterm infant are discussed.

Central Nervous System↗