ECE2023 Eposter Presentations Thyroid (128 abstracts)
1University of Southampton, Faculty of Medicine, Southampton, United Kingdom, 2University Hospital Southampton NHS Foundation Trust, Diabetes & Endocrinology, Southampton, United Kingdom
Introduction: We present a series of 10 cases of GD presenting with seemingly unrelated symptoms with limited features of thyrotoxicosis, where control of thyroid function tests (TFTs) led to complete normalisation of presenting symptoms. In all cases patients were shown to have Graves disease with thyroid antibodies.
Case series review: 1. 82F with symptomatic hypercalcaemia and thymic hyperplasia on CT. Calcium normalised with standard therapy and remained within range with normalisation of TFTs. Hyperthyroidism could cause hypercalcaemia due to increased osteoclastic activity.
2. 37F with visual blurring due to bilateral papilloedema. Brain MRI excluded tumour and lumbar puncture excluded idiopathic intracranial hypertension. No thyroid eye disease or orbitopathy on MRI. TFTs and papilloedema improved spontaneously, where papilloedema mimicking brain tumour pseudotumor cerebri has been reported with GD.
3. 32M with severe headaches and photophobia. MRI head and venogram confirmed extensive cerebral venous sinus thrombosis. Enlarged thymus and splenomegaly on CT. Thymic hyperplasia and splenomegaly resolved with carbimazole. 4. 51F debilitating headaches with features of increased intracranial pressure. CT head excluded space occupying lesion. Symptoms resolved fully with normalisation of TFTs with carbimazole.
5. 67F with symptoms of parkinsonism. Started carbimazole and Sinemet with symptomatic improvement. Sinemet withdrawn after normalisation of TFTs, with symptoms returning slightly. Case suggests dual pathology (GD+PD), with symptom improvement through normalisation of TFTs. Thyroid hormones can increase dopamine catabolism or alter dopamine receptors sensitivity.
6. 50F with generalized pruritic urticaria refractory to antihistamines and topical steroids. Rash responded promptly to anti-thyroid treatment. Urticaria possibly due to raised IgE with GD, concurrent chronic idiopathic urticaria (CIU) and rash exacerbation by skin hyperperfusion in thyrotoxicosis.
7. 36F with leg oedema, breathlessness, splenomegaly and renomegaly. Organomegaly and symptoms resolved with control of TFTs.
8. 28F with acute manic psychotic episode requiring sectioning. Commenced risperidone and propylthiouracil with improvement in manic symptoms.
9. 39M with one month history of painful gynaecomastia, fully resolving within 2 months of normalisation of TFTs. Gynaecomastia could present with GD due to raised estradiol concentrations and increased aromatisation of testosterone to oestradiol.
10. 33F with increased abdominal swelling and pain from a large ovarian tumour. Histology revealed struma ovarii. Ovarian struma possibly grew due to TSH receptor stimulation with TRAb similarly to cervical goitre in GD.
Discussion: Variability of GD presentation highlights complex interactions between thyroid hormones, autoimmunity, genetics and biochemical processes, highlighting the need to consider TFTs in a wide range of presenting complaints.