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Biomedical subjects

M Tirosh

Publications and source records attributed to M Tirosh.

25 records · Page 2Linked to original sources
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

Value of serum digoxin concentration measurement in the control of digoxin therapy in atrial fibrillation.

The association between steady-state serum digoxin concentrations and control of ventricular response rate (VRR) was studied in 53 consecutive patients with atrial fibrillation. Decreases in VRR were significantly correlated with serum digoxin (rs = -0.22, P less than 0.05). Clinical responses were appropriate to serum digoxin concentrations in 37 patients (69.8%) and were inappropriate in 16 (30.2%) (P less than 0.05). Complicating clinical factors were present in all eight patients with inappropriate responses to therapeutic serum digoxin (0.5 to 2.0 ng/ml) (P = 0.046), but were also found in many patients with appropriate responses and thus could not serve to differentiate between the two categories. Digitalis intoxication occurred in one of the three patients with a concentration of serum digoxin greater than 2 ng/ml (P = 0.056). In 30% of our patients with atrial fibrillation, monitoring of serum digoxin was of value in identifying inappropriate therapeutic responses indistinguishable by clinical means and in defining the subgroup of refractory cases, which allows the prevention of digitalis intoxication.

Atrial Fibrillation↗
PubMedDate not supplied

The Arjenyattah epidemic. A mass phenomenon: spread and triggering factors.

A massive epidemic of psychogenic aetiology occurred in three districts of the West Bank over two weeks in March-April, 1983. It affected 949 individuals, 727 (77%) of them adolescent females. The symptoms were not accompanied by positive physical signs or by laboratory findings. The epidemiological pattern was pathognomonic of that of a psychogenic disorder. The initial trigger was probably the odour of H2S escaping from a faulty latrine in the schoolyard of the first affected school. Subsequent spread of the disease was due to psychological and extra-medical factors, including publicity by the mass media. Spread was stopped immediately after closure of schools.

Abdomen↗
PubMedDate not supplied

Acute pyridostigmine overdose: a report of nine cases.

Pyridostigmine is known as a pre-treatment drug against intoxication with organophosphorus nerve agents. During the Persian Gulf war, we encountered a cluster of nine cases of pyridostigmine self-poisoning, of which three presented with mixed drug poisoning. The clinical and laboratory features of pyridostigmine toxicity are presented. Doses ranged between 390 and 900 mg. Pyridostigmine ingestion resulted in mild to moderate cholinergic symptoms such as abdominal cramps, diarrhea, emesis, nausea, hypersalivation, urinary incontinence, fasciculations, muscle weakness and blurred vision. No central nervous system manifestations were evident. The symptoms developed within several minutes and lasted up to 24 h. All patients underwent gastric emptying followed by administration of activated charcoal. Atropine (1-8 mg) was required in only three patients. Measurement of serum cholinesterase inhibition was found to be a reliable and sensitive diagnostic tool in pyridostigmine poisoning. No clear correlation was found between the extent of cholinesterase inhibition and the incidence or severity of the cholinergic signs. The clinical recovery was faster than the spontaneous recovery of the enzyme. Pyridostigmine intoxication is self-limited and well tolerated by young healthy adults.

Adolescent↗