Liothyronine/levothyroxine sodium/liothyronine overdose
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Thyrotoxicosis following administration of liothyronine or levothyroxine-sodium/liothyronine in an overdose due to compounding errors: 3 case reports In a case series, three patients [1 man and 2 women] aged 20–44 years were described, who developed thyrotoxicosis following administration of liothyronine or levothyroxine-sodium/liothyronine in an overdose due to compounding errors. Case 1: A 20-year-old man presented to his primary care physician with several weeks’ history of fatigue and generalised malaise. Extensive investigations, including thyroid function tests, were unremarkable. He was prescribed compounded oral liothyronine 10µg capsules twice a day. Shortly after the ingestion of the second dose, he experienced severe anxiety, palpitations, agitation and shortness of breath and presented to a local emergency department. En route to the emergency department, he was informed by the compounding pharmacy that the capsule might contain an excessive amount of liothyronine due to a compounding error. In the emergency department, his physical exam was significant for irritability, tachycardia and fine tremor. The thyroid gland was not enlarged to palpation. An EKG showed sinus tachycardia without evidence of ischaemic changes. His initial TSH was mildly suppressed. He was given an unspecified β-blocker for symptomatic relief and discharged home. He was instructed not to continue with the compounded medication. However, he continued to experience thyrotoxic symptoms that prompted multiple emergency department visits in the following weeks. During these visits, multiple thyroid function tests were done which showed a decrease in TSH level. Additionally, EKG and echocardiogram showed regional ischaemic changes (elevations of troponin, creatine kinase (CK), and CK-MB isozyme). At that time, one of the remaining liothyronine capsules was sent out to an independent laboratory for analysis, which revealed that it contained 10794.4µg of liothyronine, more than 1000-fold higher than intended. His thyroid function and regional ischaemic changes normalised 8 months after the incident without thyroid hormone treatment, and no further intervention was indicated. Case 2: A 30-year-old woman, who had been diagnosed with subclinical hypothyroidism, had been treated with levothyroxinesodium [levothyroxine]. Subsequently, she was prescribed desiccated thyroid and later switched to liothyronine [triiodothyronine; Cytomel] with eventual improvement in her energy level. Two years later, she was switched to compounded liothyronine 15µg controlled-release capsules twice per day. She presented to the emergency department with a 3-day history of nausea, vomiting, abdominal pain and severe headache. She had a normal thyroid function 2 months before the onset of her symptoms. She was discharged with improvement on narcotics [specific drug not stated]. Laboratory results were unremarkable although thyroid function was not checked. She was documented to be taking ’thyroid supplements’ without elaboration. She continued to take the comp
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