Eosinophilic bodies in pyloric and Brunner's gland cells.
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A previously unreported cell phenotype occurred in the pyloric and Brunner glands in two gastrectomy specimens. The cells were characterised by homogeneous, eosinophilic material in the cytoplasm. The eosinophilic material had an abnormally strong reactivity for Cystatin C, a protein found recently in the normal secretion of pyloric and Brunner's gland cells. The reason for the apparent cytoplasmic accumulation of cystatin C in the two patients described remains unclear. (+info)
A case of Brunner's gland hamartoma presenting as obscure gastrointestinal hemorrhage.
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Brunner's gland hamartomas are rare tumors of duodenum, they are often discovered incidentally during esophagogastroduodenoscopy or upper gastrointestinal series. These tumors arise mainly in the duodenal bulb and can present with gastrointestinal hemorrhage and intestinal obstruction. Most of Brunner's gland hamartomas are located within the range of the standard esophagogastroduodenoscope. However, they are rarely located below the third portion of duodenum. As well known, the small intestine, including the 4th portion of duodenum, jejunum, and ileum, is relatively inaccessible with routine endoscopy. Thus, the diagnosis of Brunner's gland hamartoma in these area can be delayed up to several months after onset of symptoms. We report a case of Brunner's gland hamartoma which was located in the fourth portion of the duodenum and presented as obscure gastrointestinal hemorrhage. Radiologic, surgical, and pathologic appearances are presented. (+info)
Histochemical similarities of mucins produced by Brunner's glands and pyloric glands: A comparative study.
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Mucins of the gastroduodenal junction are secreted by the mucous surface and mucus-producing glandular cells in the stomach, and by goblet cells and Brunner's glands in the duodenum. Developmental studies have demonstrated that Brunner's glands can arise from undifferentiated gastric epithelium and/or intestinal epithelium in the proximal duodenum. The aim of this study was to investigate the carbohydrate composition of mucins from this region and compare it with that of mucins from Brunner's glands to evaluate the probable evolution of mucins from these glands. Toward that end, paraffin sections from 13 mammalian species were stained by classic carbohydrate histochemistry and treated with 13 lectins. In general, the mucous surface cells of the stomach, pyloric glands, duodenal goblet cells, and Brunner's glands secretory epithelium had different lectin-binding patterns. However, the lectin-binding profile of the secretory epithelium of Brunner's glands resembled that of pyloric glands more closely than that of duodenal goblet cells and mucous surface cells of the stomach. Mucins from Brunner's glands and pyloric glands showed a greater terminal carbohydrate residue diversity than those of gastric mucous surface cells or duodenal goblet cells. The lectin-binding profile argues for the evolution of similar mucins from the epithelia of Brunner's glands and pyloric glands. The greater diversity of carbohydrate residues in mucins secreted by Brunner's glands suggests that their mucus is more adaptable. This may explain why Brunner's glands metaplasia rather than goblet cell metaplasia is seen in the mucosa adjacent to chronic intestinal ulcers. (+info)
Brunner's gland adenoma of duodenum: a case report and literature review.
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AIM: To analyze the clinicopathological features of Brunner's gland adenoma of the duodenum. METHODS: A rare case of Brunner's gland adenoma of the duodenum was described and related literature was reviewed. RESULTS: Brunner's gland adenoma of the duodenum appeared to be nodular hyperplasia of the normal Brunner's gland with an unusual admixture of normal tissues, including ducts, adipose tissue and lymphoid tissue. We suggested that it might be designated as a duodenal hamartoma rather than a true neoplasm. CONCLUSION: The most common location of the lesion is the posterior wall of the duodenum near the junction of its first and second portions. It can result in gastrointestinal hemorrhage and duodenal obstruction. Endoscopic polypectomy is a worthy treatment for benign Brunner's gland adenomas, as malignant changes in these tumors have never been proven. (+info)
Subcellular redistribution of AQP5 by vasoactive intestinal polypeptide in the Brunner's gland of the rat duodenum.
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Aquaporin (AQP)5, an exocrine-type water channel, was detected in the rat duodenum by Western blot analysis, and was localized by immunohistochemistry in the secretory granule membranes as well as in the apical and lateral aspects of the plasma membrane of Brunner's gland cells. Incubation of duodenal slices with vasoactive intestinal polypeptide (VIP) in vitro significantly increased the amount of AQP5 in the apical membrane fraction in a dose- and time-dependent manner with the amount reaching a plateau at 100 nM VIP and becoming near maximal after a 30-s incubation. Protein kinase inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7, 50 muM), and N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89; PKA-specific, 1 muM) blocked this increase, but PKC-specific inhibitor calphostin C did not, implying the involvement of PKA but not PKC in this cellular event. Intravenous injection with VIP (40 mug/kg body wt) provoked dilation of the lumen of the Brunner's gland at 2 and 7 min and increased the staining intensity of AQP5 in the apical and lateral membranes. AQP1 (both nonglycosylated and glycosylated forms) was also found to localize in the apical and basolateral membranes of cells of Brunner's gland. VIP, however, did not provoke any significant change in the AQP1 level in the apical membrane, as judged from the results of the above in vitro and in vivo experiments. These results suggest that VIP induced the exocytosis of granule contents and simultaneously caused translocation of AQP5 but not of AQP1 to the apical membrane in Brunner's gland cells. (+info)
Ageing and duodenal morphometry.
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Small bowel morphometry was studied in 25 subjects under the age of 70 years and 22 over the age of 70. There was no evidence of malabsorption or malnutrition in either group. Two distal duodenal endoscopic biopsy specimens were examined morphometrically. There were no significant correlations between age and areas of duodenal surface epithelium, crypts and lamina propria, heights of villi and surface epithelium, depth of crypts, crypt to villus ratio, number of intraepithelial lymphocytes, duodenal architecture, enterocytes, brush border and Brunner glands. Contrary to previous reports there was no evidence for a significant effect of age on proximal small bowel morphometry. (+info)
Brunner's gland hamartoma: 'over-treatment' of a voluminous mass simulating a malignancy of the pancreatic-duodenal area.
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CONTEXT: Brunner's gland hyperplasia is rarely associated with clinical symptoms. Most of the lesions are less than 1 cm in diameter and accounts for about 6.8% of all endoscopically removed duodenal polyps. When symptoms occur, this hyperplasia can be effectively treated with endoscopy. However, when the lesion is too large to pass through the endoscopic snare, endoscopic treatment is not possible and surgical treatment is necessary. This treatment may vary from local excision to more complex operations. When Brunner's gland hyperplasia does not have common dimensions, it may also mimic a malignancy of the duodenal-pancreatic area. In this case, a biopsy is indicated even though its result may be not informative. CASE REPORT: We report the case of a 60-year-old man with a large Brunner's gland hyperplasia mimicking a malignancy and in which the impossibility of a correct diagnosis by pre-operative and intra-operative biopsy led to 'over-treatment' involving a duodenocephalopancreatectomy. CONCLUSION: This 'over-treatment' may be justified since nowadays the consequences of leaving an undiagnosed pancreatic cancer are much worse than the risk of undergoing a major pancreatic operation. (+info)
Brunner's gland hyperplasia at the ampulla of Vater.
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Brunner's gland hyperplasia (BGH) is a diagnostic challenge where in the pathophysiology and natural history remain poorly understood. This Case Report describes BGH arising at the ampulla of Vater, causing abdominal pain and vomiting in a 46-year-old man. Owing to the inconclusive nature of imaging studies and suspicious intraoperative findings, a Whipple resection was performed without any complications. Histological analysis showed that the obstructing lesion was BGH, with no evidence of malignancy. This is only the second such case of its kind at the ampulla of Vater to be reported. In addition, we present the previously unreported endoscopic ultrasound findings. The subsequent literature review focuses on the pathophysiology, clinical presentation, diagnosis and management of BGH. (+info)