SAT-605 Immune Thrombocytopenic Purpura in Graves' disease

Abstract

Background: Immune thrombocytopenic purpura (ITP) in association with autoimmune thyroid diseases is a well-known entity. We report a case of Graves’ disease patient with coexisting ITP, where the control of ITP is in close relationship to control with Graves’ disease. Case Presentation: A 17-year-old female presented in 10/2014 with hyperthyroid symptoms for 4-5 months. Thyroid function tests (TFT’s) showed TSH 0.011 (0.45-4.5 mcIU/ml) and Total T4 (TT4) - 34.3 (4.5-12 ug/dl). Thyroid ultrasound showed thyromegaly without any discrete nodules. Thyroid uptake scan showed a homogeneous increased radiotracer uptake of 65% at 24 hours consistent with Graves’ disease and she was started on Methimazole (MMI) 20 mg PO daily. Over time, her hyperthyroidism remained well controlled on MMI 5 mg q other day, hence it was discontinued in 5/2016. She presented with multiple skin bruises in 12/2016 and her platelet count was noted to be 19 (150-400x103/ml). TFT’s remained normal. Her presumptive diagnosis was ITP given another autoimmune condition - Graves’ disease and was started on Prednisone 80 mg daily. She followed with hematology and her platelet count was monitored regularly and prednisone dose was adjusted. In 7/2017 her platelet count dropped to 64 on prednisone 5 mg PO daily. Repeat TFT’s showed TSH 0.01 and free T4 3.31. MMI was resumed at 20 mg PO daily. Labs three months later show TSH 0.024, free T4 0.86, TT3 102 and platelets 186. Given the recurrence of Graves’ disease she underwent radioactive iodine (RAI) I131 therapy in 1/2018. Post RAI she required levothyroxine 50 mcg daily briefly. In 5/2018 her platelet count dropped again to 59 on prednisone. TFT’s showed TSH of 0.014, free T4 1.42 and TT3 117. Graves’ disease relapsed despite RAI therapy and MMI was started at 5 mg PO daily. Her thyroid function remains well controlled on MMI 5 mg PO daily. Her platelet count also returned to normal and remains stable on Prednisone 5 mg PO daily. Discussion: There are several case reports of Graves’ disease and ITP in the literature. Several mechanisms by which thrombocytopenia occurs have been postulated. Accelerated platelet turnover by an activated reticuloendothelial system, shortened platelet survival and consequently reduced platelet counts can occur in patients with hyperthyroidism. Platelet survival return to normal in patients maintained in euthyroid state for more than six months. Genetic predisposition to both Graves’ disease and ITP appears to be related to HLA B8 and DR3 haplotypes. In our patient, each time she had a low platelet count on prednisone therapy, thyroid function tests were suggestive of relapse of Graves’ disease. Treatment of Graves’ disease has resulted in improved response of ITP to glucocorticoid therapy and normalization of platelet count. In patients with ITP on glucocorticoid therapy, unexplained drop in platelet count should prompt checking for thyroid function abnormalities.