Endocrine Abstracts

Graves’ disease is a leading cause of hyperthyroidism, typically confirmed by a concordant biochemical and clinical profile. This case demonstrates the diagnostic complexity created by double assay interference affecting both TSH and free T4 measurements. A 38-year-old woman presented with anxiety, tremor and sweating. Examination revealed a small goitre; her identical twin had isolated ACTH deficiency. Initial thyroid function tests on a Roche platform were discordant, showing markedly elevated free T4 (63 pmol/l) with a normal TSH (1.04 mIU/l). Repeat results remained inconsistent. Given the strong clinical suspicion of hyperthyroidism, samples were reanalysed using an Abbott assay, confirming a hyperthyroid state (free T4 37.5 pmol/l, TSH <0.01 mIU/l). TSH receptor antibodies were strongly positive (22.6 IU/l), confirming Graves’ disease. Dynamic pituitary testing identified isolated ACTH deficiency, likely secondary to longstanding inhaled corticosteroid therapy for asthma. Hydrocortisone was commenced but discontinued after significant weight gain; she now uses hydrocortisone only during intercurrent illness. Therapeutic management was further complicated by delayed turnaround of Abbott assay results (3–4 weeks), necessitating a ‘block and replace’ regimen guided by clinical rather than biochemical assessment. Nineteen months after diagnosis, she underwent radioactive iodine ablation, subsequently developing hypothyroidism requiring levothyroxine therapy. Post-radioiodine testing showed complete resolution of the Roche assay interference. This case highlights the impact of dual assay interference on the diagnosis and management of Graves’ disease, and the need to consider assay artefact when biochemical data conflict with clinical findings.