Levothyroxine sodium

Abstract

Various toxicities: case report A 63-year-old man developed hyponatraemia, hypoglycaemia and hypotension secondary to worsening of pre-existing central adrenal insufficiency during treatment with levothyroxine sodium for hypothyroidism [dosage and route not stated; time to reaction onset not clearly stated]. The man was hospitalised with severe hyponatraemia manifesting as tiredness, generalised weakness and fatigue, progressing over last 6 months. He reported nausea and lack of appetite for last 6 weeks and a recent onset of mild intermittent confusion with occasional slurring of speech. He had a history of traumatic brain injury resulting in left orbital fracture. He also had subdural haematoma which was currently resolved. Ten days prior to current admission, he had presented to his general practitioner and was noted to have low serum sodium. He had been advised fluid restriction. However, his symptoms had worsened over the next few days leading to current hospitalisation. Few days prior, he had started receiving levothyroxine sodium [levothyroxine] for a new diagnosis of hypothyroidism. During current admission, his serum sodium, blood glucose and plasma osmolality were low and urine sodium and urine osmolality were elevated. Initially, a provisional diagnosis of syndrome of inappropriate antidiuresis was considered. Further fluid restriction was advised. However, on day 2 of admission, he developed abnormal body movements, which were involuntary, wide, repetitive and flailing involving all limbs consistent with bilateral ballism. During this event, he was mildly confused, but was aware and embarrassed of involuntary movements. A finger prick test revealed severe hypoglycaemia. The man was treated with glucose. Subsequently, his abnormal movements resolved. Over the next few hours, he developed hypotension. Further investigation revealed significantly low early morning cortisol and a low adrenocorticotropic hormone, consistent with underlying, previously undiagnosed central adrenal insufficiency. The central adrenal insufficiency was considered to have developed due to prior traumatic brain injury. Levothyroxine sodium therapy was suspected to have led to worsening of preexisting central adrenal insufficiency. His complete pituitary hormone profile was indicative of hypopituitarism. He was treated with IV hydrocortisone and unspecified IV fluids. His clinical condition improved over the next 48 hours. His blood pressure and serum sodium level normalised. Hydrocortisone dose was tapered and switched to a maintenance oral dose. Levothyroxine sodium dose was optimised. He was discharged on day 7. During follow up after 2 months, he had no symptoms and his clinical investigations were within normal range.