Endocrine Abstracts

Graves’ disease is the most common cause of hyperthyroidism. It is well established that hyperthyroidism promotes a hypermetabolic state characterized by increased resting energy expenditure, increased lipolysis and gluconeogenesis. 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 mmol/l 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 mg/l. A diagnosis of Graves’ disease was made based upon her positive thyroid stimulating hormone receptor antibody (TSH-R). The 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 on biphasic insulin and newly commenced on anti-thyroid medication. Our case emphasizes that inadequately treated thyroid disease can negatively impact diabetes control. 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.