A 31 year old woman presented to the emergency department after 3 days of diarrhoea and vomiting. She was 18 months post partum and had lost 19 kg in two months. She described sweats, tremor and palpitations which had been attributed to recent emotional stress. There was no history of ingestion of iodinous compounds or family history of thyroid dysfunction. On examination the patient was tremulous, pale, cachexic, and tachycardic. There was a smooth goitre with no retrosternal extension or localised lymphadenopathy.
There was no abnormality in electrolytes, transaminase levels, or full blood count. Beta-HCG was <2, Glucose 5.1, CRP 82, Albumin 29, and INR 1.7. Chest radiography and plain abdominal film were normal. ECG revealed a narrow complex tachycardia with ventricular rate 156. Profuse, watery diarrhoea revealed no pathogenic bacteria on culture.
The patient was admitted to the ward, but within 12 hours deteriorated, with pyrexia, hypotension and severe narrow complex tachycardia of 220. Thyroid function tests revealed TSH <0.05, T4 >77. Thyroid autoantibodies were positive (TPO 831). Initial management involved propylthiouracil, dexamethasone, modified release propranolol and intravenous fluids. Further tests revealed normal electrolytes, cortisol 1551, CRP 156. The patient subsequently developed cardiac arrest which she did not survive.
Post mortem finding revealed lymphocytic thyroiditis and thymic hyperplasia. However, there was also widespread sarcoidosis involving heart, lungs, spleen. Within the heart there was chronic focal interstitial inflammation with a histiocytic reaction.
Autoimmune endocrine dysfunction is associated with sarcoidosis. Up to 4% of sarcoid patients have thyroid involvement at autopsy. True thyrotoxic crisis carries a mortality of 10-75% and is often precipitated by physiological stress on a background of underlying hyperthyroidism. In this case symptoms of hyperthyroidism went unrecognised for many months. Despite active treatment, underlying cardiac sarcoidosis is likely to have worsened the prognosis of thyrotoxic crisis.
24 - 26 Mar 2003
British Endocrine Societies