A 70-year-old lady with known hypothyroidism and ischaemic heart disease (previous CABG) presented with tonic clonic seizures. Her BP was 245/110. She was admitted to the intensive care unit. MRI brain showed subcortical oedema with subarachnoid bleed in the left temporal parietal region. Investigation for malignant hypertension showed a solid mass measuring 17×17×11 cm completely replacing the left kidney on CT-scanning. She was discharged home on sodium valproate with a plan for a radical left nephrectomy.
One morning, 2 months later, her husband could not rouse her. No seizure activity was witnessed. The paramedic team found her to be hypoglycaemic (near patient blood glucose reading of 1.4 mmol/l). She was taken to the emergency department and discharged home on the same day. Two days later, her husband found her confused, sweating with incomprehensible speech. She also had haematuria on this occasion. Her blood glucose was 1.8 mmol/l. She was admitted for further investigations. She experienced spontaneous hypoglycaemia during the night and in the morning and blood samples were taken for insulin and C-peptide levels. She was provided with a glucometer and given dietary advice on how to avoid hypoglycaemia.
Her blood results came back showing low insulin (<2 mIU/l) and C-peptide (<33 pmol/l) levels. Further investigations showed an IGF2:IGF1 ratio of 16 (<10). This overproduction of IGF2 supports a diagnosis of non-islet cell tumour hypoglycaemia (NICTH).
NICTH is a rare but serious paraneoplastic complication of malignancy. Most commonly there is tumoural overproduction of incompletely processed IGF2, which results in stimulation of the insulin receptors and increased glucose utilisation. Other potential but less common causes include the production of autoantibodies against insulin or the insulin receptor and extensive hepatic or adrenal infiltration. Treating the underlying malignancy is the mainstay of treatment, but other options include glucocorticoids to prevent recurrent hypoglycaemia.