Brunner-gland hyperplasia
(A) Stenosis of the duodenum. The line without contrast across the stomach is created by peristalsis. (B) Resected tissue. (C) Section of the second part of the duodenum. Haematoxylin and eosin stain. Magnification ×10.
In April, 2006, a 33-year-old man was brought to our emergency department by ambulance, after collapsing on the pavement. On arrival, he described epigastric pain, and swelling of the upper abdomen. Recurrent epigastric pain, nausea, and episodic vomiting had troubled him for around 11 months. He had been diagnosed in another hospital with recurrent acute pancreatitis, and had been treated accordingly. Until 6 months before we saw him, the patient had drunk a bottle of whisky per day for 10 years—but he had since been abstinent. He had no other risk factors for pancreatitis.
The patient was afebrile but tachycardic, with low skin turgor. The serum concentrations of amylase and lipase were 314 U/L (normal range 25–125 U/L) and 146 U/L (normal range 7–58 U/L) respectively. Radiography of the chest and abdomen showed nothing of note. Oesophagogastroduodenoscopy revealed an oesophageal ulcer, marked retention of gastric juice, and a severely swollen, polypoid duodenal mucosa posteriorly and in the superior duodenal angle. We could not pass the scope into the second portion of the duodenum, because of severe luminal narrowing. Histological examination of a biopsy specimen of the polypoid duodenal mucosa showed only chronic inflammation. CT of the abdomen showed retained gastric fluid, and oedema of the head of the pancreas and the second part of the duodenum. We provisionally diagnosed pancreatitis, causing partial gastric outlet obstruction. The patient was managed conservatively, with nasogastric decompression and a proton-pump inhibitor, but his epigastric pain, distention, nausea, and vomiting persisted. After a week, radiography, with barium contrast, showed a long circumferential stenosis of the post-bulbar region of the duodenum . After 2 weeks, with the patient still unwell, we prescribed total parenteral nutrition and trace elements. A week later, we decided to operate—and found a firm mass in the pancreatic head. Provisionally diagnosing cancer, we did a pancreaticoduodenectomy. Histopathological examination showed focal chronic pancreatitis, and diffuse circumferential Brunner-gland hyperplasia (BGH) in the second part of the duodenum. When last seen, in May, 2007, the patient was well.
Chronic gastric retention is usually caused either by pyloric obstruction or by gastroparesis. Pancreatic cancer can block the pylorus, and appeared particularly likely in our patient, since chronic pancreatitis increases the risk of pancreatic ductal adenocarcinoma—and our patient's history of alcohol abuse, recurrent acute pancreatitis, and chronic epigastric pain had led us to suspect chronic pancreatitis.1 BGH is a rare—but far more benign—cause of pyloric obstruction.2 Because Brunner's glands are located in the submucosa, only a deep endoscopic or a surgical biopsy provides adequate tissue for diagnosis: a punch biopsy is often inadequate.
References
1 AB Lowenfels, P Maisonneuve and G Cavallini et al., Pancreatitis and the risk of pancreatic cancer, N Engl J Med 328 (1993), pp. 1433–1437
2 P Krishnamurthy, O Jumaid, J Moezzi, SA Ali and N Gopalswamy, Gastric outlet obstruction caused by Brunner's gland hyperplasia: case report and review of literature, Gastrointest Endosc 64 (2006), pp. 464–467
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