Hyperthyroidism and Immune Thrombocytopenia (ITP) Overlap Presenting as Hypoxic Ischemic Encephalopathy in a 38-Year-Old Filipino Female: A Case Report

Abstract

Background: The coexistence of these two conditions can mimic severe sepsis in critically ill patients which may leave severe thyrotoxicosis unrecognized. Its higher incidence in Asian population suggests a possible genetic propensity. Clinical Case: A 38-year-old Filipino female sought consult due to changes in behavior. Two months prior, patient had persistent heavy menstrual bleeding but refused work-up. There was progressive weakness and pallor in the interim but no consult was done until she had an aggressive behavior hitting everyone she sees. Patient has Graves disease, maintained on methimazole 15 mg/day and propranolol 30 mg/day. Patient was advised to undergo radioactive iodine therapy but was lost to follow-up for 2 years. Likewise, no medication adjustment nor monitoring of biochemical parameters was done during the same period. On admission, patient was disoriented, tachycardic and febrile. She was generally pale with petechiae on the extremities and blood clots on her lips. Internal examination of the introitus revealed fresh blood with clots. Pregnancy test was negative. Initial laboratory evaluation revealed severe anemia (3.3 g/dl) and thrombocytopenia (3000/uL). Peripheral smear showed mild anisocytosis of red blood cells with no blasts nor atypical lymphocytes and platelet clumps seen. Patient received 1 unit platelet apherese and 2 units packed red blood cells (PRBC) and was started on broad spectrum antibiotic. Neurologic evaluation was negative for craniopathies. Baseline cranial CT scan was not done due to absence of lateralizing signs and was managed as a case of hypoxic ischemic encephalopathy from severe blood loss. Patient was biochemically hyperthyroid with TSH 0.065 uIU/ml, FT4 2.67 ng/dl and 10-fold elevated anti-TPO. Methimazole was then resumed at 20 mg/day and propranolol at 30 mg/day. Neck ultrasound showed an enlarged thyroid with diffuse parenchymal disease. Furthermore, patient had negative Coombs test, normal fibrinogen and procalcitonin. Patient was weakly positive for ANA at 1:160 dilution but negative for other markers in the lupus panel. Consistent with ITP, patient was started on IV hydrocortisone. In the interim, patient had less vaginal bleeding but with persistent bicytopenia which required multiple platelet and PRBC transfusions. A bone marrow biopsy was contemplated. However, on the 7th hospital day, patient had sudden onset of right sided paresthesia with dysarthria and hematomas on extremities. MRI of the brain revealed a large intraparenchymal hemorrhage and patient eventually succumbed to it. Conclusion: Bone marrow dysfunction secondary to the hyperthyroid state may explain the lack of response to standard therapy of ITP. There is short platelet lifespan, which is rather metabolic in nature, from increased reticuloendothelial phagocytic activity by upregulation of Fc receptor activity in patients with hyperthyroidism.