Endocrine Abstracts

Background: An 88 year old gentleman was referred to the endocrine team as an inpatient with recurrent episodes of spontaneous hypoglycaemia. These occurred in the early hours of the morning when he was found to be unrousable from sleep. There was no background history of diabetes. He was under the oncology team on this admission with pyrexia post-palliative chemotherapy with trabecitidine. Significant past medical history include metastatic solitary fibrous tumour of pelvis, bilateral hydronephrosis, stage 3B chronic kidney disease and congestive cardiac failure.

Investigations: Capillary blood glucose (CBG) was between 1.2 and 3.2 on 3 consecutive nights prior to endocrine review (daytime readings 4.1 – 8.2). Venous bloods were requested the following night during hypoglycaemia and the results were (normal range in parantheses): plasma glucose 2.2 mmol/l (3.5-11), insulin <10 pmol/l, C-peptide 380 pmol/l, sulphonylurea negative, IGF-I 7.1 nmol/l (4.6 – 23.4), IGF-II 137.2 nmol/l, IGF-II:IGF-1 ratio 19.3 (<10).

Management: Since the patient was for palliative care only, prednisolone 10 mg BD was started to avoid symptomatic hypoglycaemia, which was reduced to 5 mg BD before discharge. CBG remained from 6.5 – 10 following this, including nocturnally, and he was discharge home.

Discussion: Tumours of mesenchymal and epithelial origin (eg. fibroma, fibrosarcomas and hepatomas) can produce IGF-II which causes fasting hypoglycaemia similar to insulin-producing islet-cell tumours. Characteristically, insulin, C-peptide, IGF-I and growth hormone levels are normal or low in the presence of hypoglycaemia. Surgical resection of the tumour, where possible, can produce a cure. However in this instance we opted for symptomatic treatment with steroids to good effect.

Conclusion: In patients presenting with spontaneous hypoglycaemia with a background of fibrosarcoma tumours (particularly if they retroperitoneal or pelvic), it is important to consider IGF-II secretion as a paraneoplastic syndrome