Endocrine Abstracts

An 88-year old female was referred to the Endocrine clinic for abnormal thyroid function tests. She had been complaining of intermittent palpitations, being generally unwell, with low mood and some degree of weight loss (3 kg within the last 6 months). Her past medical history includes: osteoporosis, atrial fibrillation, poor mobility and falls. There is no family history of thyroid disease. She is currently on Duloxetine, AdCal-D3 and Alendronic acid. On examination, her heart rate was 78/min and irregularly, irregular. She was normotensive and did not display any overt clinical features of hyperthyroidism – no tremors, no palmar erythema, no proximal myopathy, no features of thyroid eye disease and no goitre.

Investigations: The most recent thyroid function tests showed a TSH level of 0.1 mU/l (normal range: 0.27–4.20 mU/l), Free T4 of 21.3 pmol/l (normal range: 11–25 pmol/l), TRAb <0.9 U/l and TPO <9 U/ml. Her TSH levels have been persistently low (0.02–0.43 mU/l) but has never been completely suppressed. She also had a normal Free T4 for the last 3 years (0.02–0.43 pmol/l).

Management: Radio Iodine therapy was arranged and low dose Bisoprolol was started for symptomatic atrial fibrillation.

Discussion: Subclinical hyperthyroidism (SH) is a mild form of hyperthyroidism. It is characterised by elevated levels of TSH with normal thyroid hormone levels. SH can either be exogenous or endogenous. Example of exogenous subclinical hyperthyroidism would be secondary to levothyroxine and of endogenous subclinical hyperthyroidism would be multinodular goitre or Graves’ disease. Diagnosis of SH is dependent upon ruling out pituitary/hypothalamic disease, drug effects, non-thyroid illness and exogenous thyroid hormone use. Multi-nodular goitre of the thyroid is the most common cause of SH followed by Graves’ disease. Treatment for SH is recommended when TSH levels are persistently lower than 0.1 mU/l in individuals over 65 years of age; in patients with cardiac risk factors, heart disease or osteoporosis; in post-menopausal women who are not on oestrogen or bisphosphonates; and in patients with hyperthyroid symptoms. Treatment for SH is based on the aetiology of the thyroid dysfunction and follows the same principles as for the treatment of overt, clinical hyperthyroidism.¹

Reference: 1. Ross DS, Burch HB, Cooper DS, Greelee MC, Laurberg P, Maia AL et al. 2016 American thyroid association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, Thyroid, 2016; 26(10): 1343-1421.