Primary autoimmune thrombocytopenia and co-existing Graves’ disease: Role of radioiodine-131

Sir,

A 24-year-old patient presented with a history of easy bruising, petechiae, gum bleeding, and menorrhagia in 2007. There was no history of any other medical illness or history of any medications. General physical and systemic examination was normal. Hemoglobin was 12 g/dl and complete blood count revealed an isolated thrombocytopenia of 10,000/mm³, total white cell count 7000/dl, erythrocyte sedimentation rate 12 mm/1^st h. Tests for antinuclear antibodies, HIV and hepatitis C virus were negative. Peripheral blood smear examination was normal. She was subsequently transfused three units of single donor platelets and the platelet counts increased to 60,000. Bone marrow biopsy revealed isolated megakaryocytic hyperplasia and a diagnosis of acute primary immune thrombocytopenia (ITP) was made. Platelets count fluctuated between 80,000 and 90,000 until November 2012. The patient then started having palpitations, fine tremors and heat intolerance. Neck examination revealed soft goiter (WHO Grade I) with diffuse enlargement of both the lobes of the thyroid gland. No bruits or palpable thrill was present. Thyroid function test (TFT) revealed elevated free T3 and T4 levels and thyroid-stimulating hormone (TSH) <0.002 in January 2013. Tests also revealed raised antithyrogobulin and anti-microsomal antibodies. A neck ultrasonography revealed diffuse enlargement of both the lobes of the thyroid gland, while ^99mTc thyroid scan revealed diffusely increased trapping function. Carbimazole 5 mg was then started in February 2013 following which there was improvement in the thyrotoxicosis symptoms. However, there was a dramatic decline of platelet counts from 68,000 before the initiation of carbimazole in January to 48,000 in May, 20,000 in August, 7000 in September 2013. An adverse reaction to carbimazole was considered and the drug was stopped and prednisolone at a dose of 50 mg/day was started in mid-September. Subsequently, there was a rise of platelet counts to 27,000 in the 1^st week of October. Dapsone at a dose of 100 mg/day was then started. However, the platelet count remained low, fluctuating between 20,000 and 25,000 until mid-November. The patient started having thyrotoxicosis symptoms once again and TFT revealed elevated free T3 and T4 and TSH of <0.02. Subsequently the patient underwent I-131 ablation with 8.2 mCi in end of November 2013. After I-131 ablation, dapsone was stopped and steroid was tapered to 10 mg/day. The patient is clinically euthyroid with normal TFTs currently and at a maintenance dose of prednisolone 5 mg has a platelet count of 2.4 lakhs. The graphical representation of thyroid status is given in Figure 1.

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Figure 1 The graphical representation of platelet counts in 1000's and thyroid function status during the period of treatment

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Thrombocytopenia as a finding in Graves’ disease is well-known.[12] Decrease in the platelet count is attributed either due to increased destruction of the platelets due to elevated thyroid hormone levels leading to activation and the reticuloendothelial system.[3] The autoimmune etiology of thrombocytopenia associated with Graves’ disease and overlap between thyroid and platelet autoimmunity has been well explained by Cordiano et al.[4] ITP and Graves’ disease can be simultaneously present or diagnosis of the two diseases can vary from months to years.[5] Correction of the hyperthyroid state by anti-thyroid drugs usually results in reversal of thrombocytopenia.[567] Here, in our case, correction of the thyrotoxicosis with carbimazole was counterproductive as it worsened thrombocytopenia, which is a documented side-effect of carbimazole itself.[8] Our case attempts to highlight two important aspects of treatment of ITP with co-existing Graves’ disease. First, how introduction of anti-thyroid drugs like carbimazole can sometimes be counterproductive and secondly how I-131 radio-ablation can be of immense benefit in such ITP patients.