Treatment of dysplastic Barrett's Oesophagus in lower volume centres after structured training

AIM: To investigate whether dysplastic Barrett's Oesophagus can be safely and effectively treated endoscopically in low volume centres after structured training. METHODS: After attending a structured training program in Amsterdam on the endoscopic treatment of dysplastic Barrett's Oesophagus, treatment of these patients was initiated at St Marys Hospital. This is a retrospective case series conducted at a United Kingdom teaching Hospital, of patients referred for endoscopic treatment of Barrett's oesophagus with high grade dysplasia or early cancer, who were diagnosed between January 2008 and February 2012. Data was collected on treatment provided(radiofrequency ablation and endoscopic resection), and success of treatment both at the end of treatment and at follow up. Rates of immediate and long term complications were assessed. RESULTS: Thirty-two patients were referred to St Marys with high grade dysplasia or intramucosal cancer within a segment of Barrett's Oesophagus. Twentyseven met the study inclusion criteria, 16 of these had a visible nodule at initial endoscopy. Treatment was given over a median of 5 mo, and patients received a median of 3 treatment sessions over this time. At the end of treatment dysplasia was successfully eradicated in 96% and intestinal metaplasia in 88%, on per protocol analysis. Patients were followed up for a median of 18 mo. At which time complete eradication of dysplasia was maintained in 86%. Complications were rare: 2 patients suffered from post-procedural bleeding, 4 cases were complicated by oesophageal stenosis. Recurrence of cancer was seen in 1 case. CONCLUSION: With structured training good outcomes can be achieved in low volume centres treating dysplastic Barrett's Oesophagus.

Glucagon receptor gene mutations with hyperglucagonemia but without the glucagonoma syndrome

Pancreatic neoplasms producing exclusively glucagon associated with glucagon cell hyperplasia of the islets and not related to hereditary endocrine syndromes have been recently described. They represent a novel entity within the panel of non-syndromic disorders associated with hyperglucagonemia. This case report describes a 36-year-old female with a 10 years history of nonspecific abdominal pain. No underlying cause was evident despite extensive diagnostic work-up. More recently she was diagnosed with gall bladder stones. Abdominal ultrasound, computerised tomography and magnetic resonance imaging revealed no pathologic findings apart from cholelithiasis. Endoscopic ultrasound revealed a 5.5 mm pancreatic lesion. Fine needle aspiration showed cells focally expressing chromogranin, suggestive but not diagnostic of a low grade neuroendocrine tumor. Octreo Scan was negative. Serum glucagon was elevated to 66 pmol/L(normal: 0-50 pmol/L). Other gut hormones, chromogranin A and chromogranin B were normal. Cholecystectomy and enucleation of the pancreatic lesion were undertaken. Postoperatively, abdominal symptoms resolved and serum glucagon dropped to 7 pmol/L. Although H and E staining confirmed normal pancreatic tissue, immunohistochemistry was initially thought to be suggestive of alpha cell hyperplasia. A count of glucagon positive cells from 5 islets, compared to 5 islets from 5 normal pancreata indicated that islet size and glucagon cell ratios were increased, however still within the wide range of normal physiological findings. Glucagon receptor gene(GCGR) sequencing revealed a heterozygous deletion,K349_G359del and 4 missense mutations. This case may potentially represent a progenitor stage of glucagon cell adenomatosis with hyperglucagonemia in the absence of glucagonoma syndrome. The identification of novel GCGR mutations suggests that these may represent the underlying cause of this condition.