PANCYTOPENIA SECONDARY TO AUTOIMMUNE VITAMIN B DEFICIENCY IN GRAVES DISEASE.

Objective: To describe a case of Graves disease (GD) and coexistent pancytopenia associated with autoimmune vitamin B deficiency. While thyrotoxicosis and antithyroid drugs can cause pancytopenia, other autoimmune conditions such as vitamin B deficiency can occur, leading to severe anemia and pancytopenia.

Methods: A 19-year-old female with GD treated with methimazole presented with thyrotoxicosis and evidence of pancytopenia. Diagnostic studies included a complete blood cell count, peripheral blood smears, thyroid function tests, and a bone marrow biopsy.

Results: White blood cells were 2.4 × 10 cells/L (reference range [RR] is 3.4 to 9.6 × 10 cells/L), hemoglobin was 7.9 g/dL (RR is 11.6 to 15.0 g/dL), neutrophil count was 1.2 × 10 cells/L, and platelets were 84 × 10 cells/L (RR is 157 to 371 × 10 cells/L). Thyroid-stimulating hormone was <0.01 mIU/L (RR is 0.50 to 4.30 mIU/L), free thyroxine was 3.7 ng/dL (RR is 1.0 to 1.6 ng/dL), and total triiodothyronine was 221 ng/dL (RR is 91 to 218 ng/dL). Due to suspicion for drug-induced pancytopenia, methimazole was discontinued. Three days later, she was hospitalized for a syncopal episode with a further decline in hemoglobin to 6.7 g/dL, neutrophils to 0.68 × 10 cells/L, and platelets to 69 × 10 cells/L. Bone marrow biopsy findings showing marrow hypercellularity and hypersegmented neutrophils suggested vitamin B deficiency. Vitamin B was <70 ng/L (RR is 180 to 914 ng/L). Intramuscular vitamin B injections were initiated, and pancytopenia resolved within 1 month.

Conclusion: Although rarely described in the literature, autoimmune vitamin B deficiency can be missed as an underlying etiology for pancytopenia in patients with GD. The clinical picture can be further confounded when these patients are treated with antithyroid drugs known to cause bone marrow suppression.