Endocrine Abstracts

We present the case of assumed ectopic GHRH from residual bronchial carcinoid on the basis of an elevated serum GH, an elevated IGF-1 impaired glucose tolerance and an acromegalic appearance. The patient was diagnosed with a left bronchial carcinoid in 1985, aged38 years. Treated with a left pneumonectomy. She remained well until she presented in 1994 with an oesophageal variceal bleed. She had no evidence of portal hypertension or liver disease. CT chest revealed a mediastinal mass and urinary 5-HIAA was elevated consistent with residual/recurrent carcinoid tumour. She was commenced on octreotide 50 mcg subcutaneously BD, when she had a variceal rebleed. She continued on this for several years. No significant change was seen on follow-up CT scans and an octreoscan in 2004 was positive in the mediastinal area but no uptake elsewhere. She was referred to the Diabetes team following an impaired glucose tolerance test. Clinically she had evidence of prognathism and frontal bossing. Biochemically, serum GH of 23 mU/l, IGF-1 of 61 nmol/l (12–44), urinary 5-HIAA 155 (normal <40), pancreastatin 299 ng/l (0–50), pancreatic polypeptide 260 ng/l (0–200) and total chromogranin A 480 U/l (0–30). MRI of pituitary showed no pituitary tumour just diffuse enlargement. An octreotide challenge test showed a good response to 50 mcg of subcutaneous octreotide, baseline growth hormone of 36.2 mU/l and a nadir of growth hormone of 1.7 at 3 h. She was changed to somatostatin LAR and subsequent growth hormone profiles have improved significantly. She remains well and asymptomatic. GHRH assay is awaited. GH hyperproduction due to ectopic secretion of GHRH is a rare cause of acromegaly. Since 1959, only around 50 cases have been described. In this case ectopic GHRH is the most likely cause of her acromegaly. Also cases of oesophageal varices secondary to mediastinal tumours have been described but never secondary to a bronchial carcinoid.