ABSTRACT
Exposure to thyroid products is common, but acute poisonings in adults are rare. Most cases of severe toxicity are related to prolonged, repeated exposure (either inadvertent or deliberate abuse). There are a few reports of toxicity in children following large (greater than 10 mg) single ingestions. Expect significant toxicity in children and adults who have ingested more than 2 to 4 mg of levothyroxine. However, in comorbid elderly patients, the threshold may be lower. In this paper we present acute overdose of levothyroxine in nine adult patients (aged 21-44 years; mean--30.5 years); ingested doses were from 1.2 mg to 15 mg (mean--6.5 mg). Only in three cases (ingested doses were 5.6; 8.0 and 15 mg) minor and mild clinical symptoms were observed and pharmacological treatment was necessary. No severe symptoms were observed in our group. Asymptomatic clinical course in patients who ingested more than 3 mg of levothyroxine probably was related to coingestion of benzodiazepins, beta-blockers, ACE inhibitors and ethanol. Serum free triiodothyronine (T3) level of 20 pg/ml (normal, 4.1 pg/ml) was reported following an overdose of 15 mg levothyroxine in day five. Normalization was observed in day eleven.
Subject(s)
Drug Overdose/etiology , Thyroxine/poisoning , Acute Disease , Adult , Drug Interactions , Drug Overdose/drug therapy , Female , Humans , Male , Young AdultABSTRACT
UNLABELLED: The aim of the study was to evaluate carbohydrate metabolism in patients hospitalised because of acute intoxication with xenobiotics. MATERIAL AND METHODS: An analysis of 3628 patients (1553 females and 2075 males; age: 40.6 +/- 15.9 y) hospitalized at the Ward of Toxicology and Environmental Diseases because of acute poisoning in 2004-2006 was done. The patients with diabetes mellitus diagnosed prior to hospitalisation were excluded from the analysis. The blood ethanol concentration was measured, medication drugs and/or psychoactive substance screening test were performed in all patients on admission. Fasting glucose level on admission and control level on second or third day of hospitalisation were determined. Risk ratio of hyperglycaemia according to toxic agent was assessed using multiple regression model considering age, gender, and the patient education. RESULTS: In 18.2% (398 males and 254 females) of the patients the blood glucose level on admission was > or = 7.8 mmol/l; in u 3.6% (78 males and 50 females) > or = 11.1 mmol/l. In 24 (0.6%) of the patients glycaemia on admission was < or = 3.5 mmol/l. Control fasting glucose level of > or = 7.0 mmol/l was determined in 115 males and 76 female patients. 42% elevation in risk of hyperglycaemia was noted in acute carbon monoxide poisoning (OR = 1.42; 95% PU: 1.11-1.82). In ethanol intoxicated patients 12% drop in risk of hyperglycaemia was noted (OR = 0.88; 95% PU: 0.72-1.07). Benzodiazepine poisoning diminished risk of hyperglycaemia in 36% (OR=0.64; 95%PU: 0.48-0.84). Risk of hyperglycaemia in poisoning by medicines co-ingested with ethanol was always lower compared to poisoning with the single agent. CONCLUSION: A higher risk of hyperglycaemia was related to acute carbon monoxide poisoning whereas lower risk of hyperglycaemia was attributed to benzodiazepines and alcohol. A frequency of hypoglycaemia in the group of poisoned patients was much more lower compared to hyperglycaemia.
