SUN-322 - Graves' Disease-Induced Pancytopenia: An Uncommon Complication with Challenging Management

Graves’ disease (GD) is the most common cause of hyperthyroidism. Although it presents with a wide range of clinical manifestations, pancytopenia is a rare and infrequently reported complication that has poorly understood mechanisms and major implications for disease management.

Clinical

Case: A 72-year-old woman was diagnosed with GD outpatient with symptoms of fatigue and diarrhea. Labs showed thyrotoxicosis and positive TSH receptor antibodies (TRAb) with hemoglobin (Hb) 11.1 g/dL, platelets 122 109/L, white blood cell count (WBC) 2.7 109/L, and absolute neutrophil count (ANC) of 1.3 109/L. She was started on a beta blocker, while anti-thyroid drugs (ATD) were deferred due to pancytopenia. Symptoms of fatigue, diarrhea, and dyspnea persisted. She underwent scheduled bone marrow biopsy to further evaluate cause of cytopenias. Labs showed TSH < 0.005 mIU/L, free T4 >7.77 ng/dL, total T3 >651 ng/dL, and an ANC of 0.9 109/L. Shortly after her biopsy she developed bradycardic arrest requiring resuscitation, prompting discontinuation of propranolol and cardiac catheterization. Cardiac evaluation and bone marrow biopsy were both benign. She was transferred to our hospital for consideration of plasmapheresis and thyroidectomy.

Labs on arrival showed decreasing thyroid hormone levels. Plasmapheresis was deferred, and she was managed with cholestyramine and SSKI. ANC improved and methimazole was initiated. Outpatient, thyroid hormone levels continued to decrease. Methimazole was stopped and she required replacement levothyroxine 50 mcg daily. TRAb levels remained >40 IU/L while TPO antibodies were negative. She continued to experience recurrence of episodic cytopenias despite biochemical euthyroidism.

Conclusion: Pancytopenia from GD is a rarely reported complication in case reports. It is not specific to GD hyperthyroidism and has been reported in cases of toxic multinodular goiter and iatrogenic thyrotoxicosis, suggesting a direct suppressive effect of thyroid hormone on bone marrow production. The majority of reported cases had resolution of pancytopenia following achievement of euthyroidism, and ATD use did not appear to worsen cytopenias. While resolution typically occurs within weeks to months, persistence of pancytopenia up to one year has been described which underlies the involvement of immune mediated mechanisms as well. As with our patient, resolution of thyrotoxicosis alone has not lead to resolution of cytopenias.

No existing literature reviews have investigated any correlation between the severity of thyrotoxicosis or antibody status and the extent of pancytopenia. Our own analysis of prior case reports ultimately found no correlation between thyroid hormone levels or antibody titers and the severity of pancytopenia. This case and literature review underscores the need for further investigation into the risk factors for this rare complication of GD.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*