Levothyroxine sodium
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Addison’s crisis: case report A 34-year-old woman developed Addison’s crisis during treatment with levothyroxine sodium for primary subclinical autoimmune hypothyroidism. The woman, who had been experiencing poor dreamy sleep, difficulty in concentration, fatigue, weakness, lethargy and dizziness from January 2019 (progressive over the last 10 months), presented to a family care clinic for evaluation. On further examination, she was diagnosed with primary subclinical autoimmune hypothyroidism. Laboratory investigations revealed slight elevation in potassium level and decrease in sodium level. She was then treated with oral levothyroxine sodium 50 µg/day and was referred for psychiatric evaluation. The psychiatrist made diagnosis of grief reaction with generalised anxiety disorder and prescribed clonazepam and escitalopram. Over the next 15 days, her symptoms deteriorated, and she discontinued all her medications. After one month, her TSH level was found to be elevated, and she was counselled for hypothyroidism. She was instructed to continue levothyroxine sodium 25µg daily and advised to take follow-up for TSH levels after 30 days. About 25 days prior to the admission in July 2019, her relatives forced her to continue levothyroxine sodium therapy. Thereafter, she had dizziness, severe weakness, worsening of asthenia and abdominal pain associated with persistent vomiting, which required admission. On arrival, her oral temperature was 98.8oF, supine BP was 90/70mm Hg, pulse rate was 120 beats/min and oxygen saturation was 97% at room air. General examination showed moderate dehydration and diffuse hyperpigmentation of the dorsum of the hands, legs and feet. Cardiorespiratory and abdominal examination were non significant except tachycardia. A cortisol therapeutic challenge for Addison’s crisis was positive, and she was diagnosed with Addison’s crisis (worsening of Addison’s disease), which was triggered by levothyroxine sodium use [duration of treatment to reaction onset not stated]. The woman was treated with unspecified IV fluids, broad spectrum antibiotics and supportive measures. After 24h, her dehydration was corrected; however, significant orthostatic hypotension was noted. Laboratory investigations revealed hyperkalaemia, hyponatraemia, hypoglycaemia, low serum cortisol and ACTH levels. Additionally, she developed hypovolaemic shock. Infectious aetiologies were negative. Chest X-ray, 2D-echo, ultrasonogram and abdominal CT scans did not show any abnormal findings. Based on all the findings, she was suspected to have developed adrenocortical crisis. She was treated with hydrocortisone and a significant improvement was noted in her symptoms along with stabilisation of vital signs. An ACTH stimulation test was scheduled at follow-up visit. She was discharged on prednisolone three days later. After 7 days, prednisolone was discontinued for 48h before initiating ACTH stimulation test. She had low serum cortisol level and received tetracosactide [Cosyntropin]. After 60 minutes of administration, cortisol level
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