Endocrine Abstracts

Introduction: Autoimmune thyroiditis can occasionally be associated with a transient hyperthyroid phase which is followed by a hypothyroid state. Thyrotoxicosis is thought to be caused by thyroid cell destruction with release of preformed thyroid hormones into the circulation.

Case: An 18-year-old Asian male was admitted to hospital 7with a four week history of lethargy, weight loss, palpitations and excessive sweating. He had tachycardia, sweating, tremors, no palpable goitre but mild tenderness in the region of the thyroid gland. TSH was undetectable and free T4 was 97 pmol/l (12–22 pmol/l). Anti thyroid peroxidase antibody was >600 IU/ml (0–34). Haemoglobin was 10 g/dl, total white cell count 1.32 with a neutrophil count of 0.8, and a platelet count of 137. His CRP was 187 mg/l.

He was commenced on propranolol, prednisolone 30 mg and carbimazole 20 mg and he showed rapid clinical improvement with a normal full blood count after 4 days. Prednisolone was stopped and he was discharged on carbimazole and propranolol.

He was readmitted 3 weeks later with a sore throat and a white cell count of 0.8, neutrophil count of 0.04 and platelet count of 119. His TSH was 14.8 mU/l with a free T4 of 5.7. Neutropenic sepsis secondary to carbimazole was diagnosed and carbimazole and propranolol were stopped. Two weeks later he was still neutropenic with a white cell count of 1.53, neutrophil count of 0.6 and platelet count of 86, and clinically hypothyroid with a TSH of 52.7 and a free T4 of 10.4. He was commenced on thyroxine.

Discussion: Hashimoto’s disease of acute onset may present as a painless, non goitrous thyroiditis, with initial hyperthyroid features and later developing hypothyroidism. Differentiation from painless subacute thyroiditis may be difficult. Thyrotoxicosis induced neutropenia is recognised but pancytopenia in such a case poses a diagnostic and therapeutic challenge.