Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 34 P298 | DOI: 10.1530/endoabs.34.P298

Imperial Centre of Endocrinology, Hammersmith Hospital, London, UK.


A 53-year-old retired military soldier had a 9 months history of recurrent blackouts predominately associated with blurred vision, feeling shaky, sweaty and they were mainly before meal. His past medical history included asthma, multiple shrapnel injuries, hearing impairment secondary to blast injury. He was on atorvastatin, ompeprazole and inhalers.

He was admitted acutely to his local hospital and blood glucose 0.6 mmol/l was found. Prolonged 72 h fast showed an elevated C-peptide and insulin in the context of hypoglycaemia and negative sulfonylurea (SU) screen consistent with a diagnosis of insulinoma. Subsequent CT abdomen revealed a 14 mm hypervascular lesion within the body of the pancreas. He was then referred to our outpatient endocrine clinic.

He experienced the above symptoms with normal capillary blood glucose (CBG) in clinic but was admitted for completion of investigations. He had a normal EEG and CT brain. Repeat prolonged fasting confirmed hypoglycaemia with blood glucose of 1.7 mmol/l at 52 h with inappropriately elevated C-peptide of 1396 pmol/l and insulin of 21.6 mU/l and negative SU screen. I addition, concomitant plasma GH of 1.93 μg/l (inappropriately low in context of hypoglycaemia) but normal cortisol of 651 nmol/l. LH, FSH, and testosterone were 3 IU/l (2–12), 3.3 IU/l (1.7–8), and 6.9 nmol/l (10–30) respectively which is suggestive of secondary hypogonadism. The reminder of a pituitary profile was normal.

Gallium 68 DOTOTATE PET–CT scan confirmed gallium avid lesion in the body of the pancreas and EUS also confirmed a lesion.He is currently waiting for formal ITT to confirm GH deficiency and has commenced testosterone replacement. He has been referred to surgeons for laparoscopic resection of the lesion.

In this case previous blast injury could be the cause of secondary hypogonadism and GH deficiency. It raises the possibility that elimination of GH counter-regulatory action in hypoglycaemia could have exacerbated insulinoma.

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