ECE2019 Poster Presentations Thyroid 3 (74 abstracts)
North Middlesex University Hospital NHS Trust, London, United Kingdom.
Case History: 38 year old male presented with thyrotoxic symptoms and exophthalmos with an initial Free T4 of > 100 pmol/l; TSH < 0.01 mIU/l and thyroid receptor antibody positivity. He had a platelet count of 72* 109 /L at presentation and was started on carbimazole. A month later he had platelet count of 9* 109 /L with normal white cell count and haemoglobin levels. He was switched to propylthiouracil, but was readmitted with platelet count of 10* 109 /L. Propylthiouracil was stopped and he was investigated with bone marrow aspiration and diagnosed with immune thrombocytopenic purpura (ITP). He was started on glucocorticoids with no improvement. However, the thyroid tests returned to normal without anti-thyroid drugs. He was later started on rituximab as the platelet count did not respond to high dose glucocorticoids and he later suffered spontaneous intracranial haemorrhage.
Discussion: It was initially assumed that the thrombocytopenia was either related to Graves itself or due to either carbimazole or propylthiouracil. Mild immune thrombocytopenia is known to be associated with Graves and improves with treatment. Platelet lifespan is reduced in thyrotoxicois due to increased destruction of the platelets from elevated thyroid hormone levels leading to activation and the reticuloendothelial system. There is an overlap of auto-immune aetiology between Graves and ITP with platelet associated antibodies found in Graves. Usually the platelet count imporves with treatment. Here however the thrombocytopenia worsened with treatment. High dose glucocorticoids used to combat ITP however improved thyroid function. Glucocorticoids are known to block the peripheral T4 conversion to T3 as well as restoring euthyroid status in thyroiditis. The evidence for high dose glucocorticoids in Graves disease is unclear. This case demonstrates the intriguing effects of glucocorticoids in Graves disease as well as the association of ITP with Graves and failure to improve with anti-thyroid treatment or glucocorticoids.