Endocrine Abstracts

Graves’ disease (GD) is a common cause of hyperthyroidism. Associated hematological complications rarely occur. Most review articles describe it as a rare manifestation and often reported as isolated cases or series. These disorders in hyperthyroidism may stem from the primary thyroid pathology or its treatment. In untreated primary hyperthyroidism, effects on hematological parameters range from mild single lineage involvement to pancytopenia. The most feared treatment related hematological disorder is drug induced agranulocytosis. We present a middle-aged gentleman with 10 year’s history of GD. Over the last 2 years, he had repeated admissions for severe thyrotoxicosis, sepsis and recurrent pancytopenia. In end 2014, he was admitted for an episode of neck cellulitis. He was floridly hyperthyroidism and had developed new onset bicytopenia – leucopenia (neutropenia) and thrombocytopenia. He had stopped taking his regular dose of Carbimazole 30 mg OM for the last 2 weeks. The bicytopenia was unlikely drug-induced agranulocytosis due to his non compilance. A multidisciplinary team was involved including endocrinology, hematology and nuclear medicine. An attenuated dose of Carbimazole 20 mg daily was restarted with close monitoring of his cell counts. Cholestyramine was added as an adjunct. Granulocyte-colony-stimulating-factor (GCSF) injections were initiated to boost the neutrophil counts. The patient also underwent a bone marrow examination (BME). The BME showed quantitatively adequate granulopoiesis with normal neutrophil count and increased megakaryopoiesis. The mildly hypercellular marrow with adequate hematopoiesis in all 3 cell lines suggested that the ongoing neutropenia and thrombocytopenia is secondary to peripheral consumption and destruction. Carbimazole induced agranulocytosis would result in a hypocellular marrow. Thus, the most evident cause of the bicytopenia was an autoimmune cause from hyperthyroidism. The patient’s neutrophil and platelet counts improved as he achieved an improved thyroid state. This improvement of cell counts together with his thyroid status further reinforced the hypothesis of hyperthyroidism induced bicytopenia. The patient discharged well with an outpatient appointment for definitive therapy with radio-iodine ablation. However, he remained poorly compliant. This resulted in three further admissions for similar presentations of sepsis, florid hyperthyroidism and bi- or pancytopenia. His recovery of his cell counts would always mirror the improvement of thyroid status. He eventually received two doses of RAI 6 months apart. Mr N responded adequately to the 2^nd dose of RAI therapy. At 8 weeks’ mark, he was euthyroid status. The hematological abnormalities had fully resolved along with this.