EU2019 Clinical Update Additional Cases (14 abstracts)
University College London Hospitals NHS Foundation Trust, London, UK.
We report a 42-year-old female who was known to have autoimmune hypothyroidism for nearly 20 years with positive antiTPO antibodies. She was well controlled on levothyroxine including three antenatal periods when she required a slightly higher dose of 125 mcg daily. No significant past medical history and denies use of herbal/over the counter medications. In early 2017, the patient started to experience nonspecific symptoms of lethargy and tiredness. Her thyroid state was managed in the community. Initially, her tests showed suppressed TSH and raised FT4 (see table). Her replacement therapy was adjusted by GP and had to reduce her dose to 25 mcg on alternate days to maintain levels within the desired biochemical range until September 2017 when the GP decided to stop treatment and was referred to the specialised endocrine clinic given her persistent thyrotoxic state. At this stage, she became profoundly hypothyroid with TSH 97.8 mIU/l and >100 mIU/l in November 2017 and January 2018 respectively. Upon clinical review in the endocrine clinic and given her fluctuating thyroid status, a provisional diagnosis of thyroiditis was made and a small dose of levothyroxine was restarted. US thyroid scan revealed hypervascular gland suggestive of active inflammatory thyroiditis.
Case Resolution: Interestingly the patient reports no change in her symptoms during TSH fluctuation but clinically she had fine tremor which was consistent with thyrotoxicosis. Further investigations revealed elevated TRAB antibodies at 9.1 u/l and Thyroid 99m pertechnetate scan is consistent with Graves. Carbimazole has been started to control her symptoms.
Learning point: There are two distinct thyroid syndromes most commonly caused by autoimmune aetiology, Hashimotos thyroiditis and Graves disease. The latest is induced by TRAB antibodies. There are two types of these antibodies cause two different clinical conditions. The first stimulates the thyroid (TSAb) causes Graves thyrotoxicosis and the second type blocks thyrotropin action (TBAb) occasionally responsible for hypothyroidism. There are few case reports of switching between TBAb and TSAb (or vice versa) with complete variation in clinical status. The process of changing antibodies action is not fully understood as yet. We believe this lady has been TRAB positive even she was hypothyroid but it was never checked. Extreme fluctuation of thyroid status with small variations in levothyroxine dose in previously well controlled compliant patients should alert physicians to the possibility of switching stimulatory and inhibitory antibodies status.