PANCYTOPENIA AND LYMPHOID ORGAN HYPERPLASIA IN A PATIENT WITH GRAVES DISEASE: RESPONSE TO ANTITHYROID DRUG THERAPY.

In rare instances, cytopenias manifest as a complication of thyrotoxicosis. Here, we report a case of Graves disease (GD) thyrotoxicosis presenting as pancytopenia that resolved with antithyroid therapy.A 35-year-old male presented with fever and chills following an outpatient colonoscopy. Initial blood work revealed pancytopenia. Workup included viral antigen titers, blood cultures, rheumatologic antibodies, inflammatory markers, immunocompetency, nutrient deficiency, metal toxicity, and malignancy. Bone marrow aspirate was analyzed by microscope, flow cytometry, fluorescence in situ hybridization, and genetic analysis. Computed tomography scan of the chest, abdomen, and pelvis was obtained. Thyroid labs included thyroid-stimulating hormone, total triiodothyronine, free thyroxine, thyroid-stimulating immunoglobulin, anti-thyroid peroxidase antibody, and radioiodine uptake scan.

All workup above was non-revelatory except as follows. Imaging revealed thymic hyperplasia and splenomegaly. Thyroid labs revealed thyroid-stimulating hormone <0.02 μIU/mL (reference range is 0.30 to 5.00 μIU/mL), free thyroxine of 4.7 ng/dL (reference range is 0.7 to 1.7 ng/dL), total triiodothyronine of 191 pg/mL (reference range is 90 to 180 pg/mL), thyroid-stimulating immunoglobulin of 522% (reference range is <140%). Bone marrow biopsy was consistent with a reactive process suggesting an infectious or autoimmune process. Radioiodine uptake scan confirmed GD. He was discharged on antithyroid medication. Two-month follow-up labs revealed improved cell counts; his absolute neutrophil count was 1.94 × 10⁹ cells/L (reference range is 1.50 to 8.00 × 10⁹ cells/L), hemoglobin was 12.9 g/dL (reference range is 14.0 to 17.0 g/dL), and platelets were 153 × 10⁹ cells/L (reference range is 140 to 400 × 10⁹ cells/L). Definitive treatment was obtained with 12 mCi of 131-iodine.

Pancytopenia and lymphoid organ hyperplasia (splenomegaly, thymic hyperplasia, and lymphadenopathy) have been previously reported to be associated with thyrotoxicosis secondary to GD, rarely simultaneously, and manifest from both thyrotoxic and immunologic mechanisms. After excluding alternative life-threatening pathologies, in such presentations, GD should be considered and treated if confirmed.