Endocrine Abstracts

Graves’ disease is a common autoimmune disease causing hyperthyroidism. Thyroid has a catabolic effect on carbohydrate metabolism especially in the hyperthyroid state. We describe a rare complication of thyrotoxicosis in a patient with type II diabetes on insulin, with no previous thyroid history. An 83 year old woman with type 2 diabetes on biphasic insulin presented with symptoms of polyuria, polydipsia and fatigue. She was tachycardic and tachypneic but normotensive and apyrexial with no obvious focus of infection. Her clinical examination revealed no abnormalities and initial investigations showed blood glucose of 26 mmol/l, ketones 4.8 mmol/l, pH 7.19 and bicarbonate of 14 confirming diagnosis of Diabetic Keto-Acidosis (DKA). A thyroid function panel was ordered which showed her thyroid stimulating hormone was <0.003 with a free T4 level of 64.1 ug/l. She was also positive for thyroid stimulating hormone receptor antibody (TSH-R), confirming Graves’ disease. Our patient improved upon starting management for DKA with resultant closure of anion gap and resolution of DKA. Treatment for thyrotoxicosis was also initiated with propranolol and carbimazole to manage her thyroid state with good response. She was discharged once medically recovered back on biphasic insulin and newly commenced on anti-thyroid medication. Our case emphasizes the impact of thyroid state on diabetes control and the potential complications of uncontrolled hyperthyroidism in patients with diabetes. Increased glucose uptake and increased insulin clearance in hyperthyroidism creates a relative insulinopenic state that can manifest as DKA. Graves’ thyroid patients with diabetes can have suboptimal blood sugar control in hyperthyroid state and they should be warned about DKA as a potential complication.