Endocrine Abstracts

Introduction: haemangiopericytoma is a rare soft tissue tumour originating from pericytes and manifest rarely as hypoglycaemia that can be difficult to treat. We report a case of haemangiopericytoma induced hypoglycaemia treated successfully with radiotherapy.

Case report: A 72-year-old lady presented with an episode of confusion. She had had similar episodes usually in the early morning hours. She had had a large bladder haemangiopericytoma removed surgically 7 years ago. On examination she was confused and disoriented. Abdominal palpation revealed a large mass arising from the pelvis. The rest of the examination was unremarkable. Her blood glucose was low 1.8 mmol/l. She was given dextrose infusion and responded dramatically. CT scan of abdomen showed a large mass arising from the broad ligament. A core biopsy was performed, Histology confirmed recurrence of the haemangiopericytoma. Hormonal studies showed low insulin, C-peptide and growth hormone. IGF-II/IGF-I ratio was 20.8 (normal range <10) suggesting non-islet tumour induced hypoglycaemia (NICTH).

Over the next 14 days she had recurrent sever hypoglycaemic episodes despite frequent meals. Daily subcutaneous GH injection (0.8 mg) was successful in reducing the frequency and severity of the hypoglycaemic episodes. 3 months latter she undergone local radiotherapy and GH was stopped 2 weeks after radiotherapy. Over the next 18 months she was free from hypoglycaemic episodes.

Discussion: NICTH is caused by the production of excessive quantities of a high molecular weight form of pro-IGF II by the tumour, called big-IGF II with subsequent increase of it is bioavailability in the peripheral tissue to bind insulin receptors causing hypoglycaemia. As demonstrated in this case, radiotherapy is an effective treatment if surgical removal of the tumour is not possible. In fact, Clinically radiotherapy was more effective than GH. It is tempting to conclude that radiotherapy may have been successful in eradicating IGF-II producing cells in the tumour.