2017 Resarch Forum

IM: C-4

Applicant: Shelly Gupta MD Principal Investigator: Rajinderpal S. Chahal MD

Severe aplastic anemia as a complication of autoimmune hyperthyroidism Rajinderpal S Chahal MD, Shelly Gupta MD, Arash Heidari, MD

INTRODUCTION There is growing evidence that aplastic anemia can develop secondary to insult or injury to the pluripotent stem cell in the setting of a T-cell mediated autoimmune pathology. We present a case in which autoimmune hyperthyroidism associated with severe aplastic anemia achieved clinical remission after treatment of patient’s hyperthyroidism with methimazole. PURPOSE Presenting a case of severe aplastic anemia as a complication of automimmune hypothyroidism. DISCUSSION A 29 year El Salvadoran male presented to the Emergency Department in September 2014 with complaint of palpitations, lightheadedness, night sweats, and 50 lb weight loss over several weeks. Complete blood count showed a white blood cell count of 2.9 x 10^3/μL, an absolute neutrophil count of 0.9 x10^3/μL, hemoglobin of 4.9 gram/deciliter, and platelet count of 13 x 10^3/μL. Patient’s thyroid stimulating hormone was noted to be less than 0.01 μIU/mL and free T4 of 2.2 ng/dL. Thyroid peroxidase antibodies were 187 IU/mL and thyroid stimulating immunoglobulins were noted to be 419. A radioactive thyroid scan was positive for multiple goiters consistent with hyperthyroidism. Bone marrow biopsy was performed and was consistent with less than 5% cellularity, flow cytometry for CD55/CD59 was negative. Patient was started on methimazole 2.5mg by mouth three times daily and was discharged with outpatient follow-up. During evaluations in December 2014 and January 2015 patient experienced improvement in all hematopoietic cell lineages and experienced a weight gain of 36.5 lbs along with complete resolution of his clinical symptoms without any treatment of his aplastic anemia. Patient was subsequently lost to follow-up and discontinued methimazole. Patient experienced a relapse of his clinical symptoms in July 2016 with a decrease in all cell lineages. CONCLUSION T-cell mediated autoimmune pathology has been hypothesized to play a central role in the pathogenesis of both hyperthyroidism and aplastic anemia. The presence of autoantibodies against stem cell antigens has been proposed as a mechanism to explain correlational relationships between aplastic anemia and autoimmune diseases including hyperthyroidism, hypothyroidism, celiac’s disease, and autoimmune hepatitis. It is our contention that treatment of the underlying autoimmune phenomenon may induce remission of aplastic anemia.