Association between anomalous pancreaticobiliary ductal union and adenomyomatosis of the gall‐bladder

Tanno, Satoshi; Obara, Takao; Maguchi, Hiroyuki; Fujii, Tsuneshi; Mizukami, Yusuke; Shudo, Ryushi; Takahashi, Kuniyuki; Nishino, Noriyuki; Arisato, Satoshi; Ura, Hideki; Kohgo, Yutaka

doi:10.1111/j.1440-1746.1998.tb00634.x

Cited by 35 publications

(13 citation statements)

References 18 publications

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“…Although the high concentration of phospholipase A2 in bile is also thought to provide lithogenic circumstance, the frequency of gallstones in patients with AJPBD and gallbladder carcinoma is low. In contrast, incidence of adenomyomatosis, a fundic type, is considerably high in AJPBD patients without a cystic dilatation of common bile duct; adenomyomatosis is also proposed to be another premalignant lesion, although no direct information mechanistically supporting this has been established [42,43].…”

Section: Anomalous Junction Of the Pancreaticobiliary Ductmentioning

confidence: 79%

Carcinogenesis of malignant lesions of the gall bladder

Tazuma

Kajiyama

2001

Langenbeck's Arch Surg

111

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Gallbladder carcinoma is an uncommon but highly malignant tumor with a poor 5-year survival rate. The presence of gallstones is a well-established risk factor for gallbladder carcinoma, and the risk seems to correlate with stone size. Metaplastic changes of the gallbladder epithelium present in chronic cholecystitis may be a premalignant lesion. Solitary polyps with a size of greater than 1 cm are recognized as a predisposing factor for gallbladder carcinoma when their characteristics are echopenic, sessile, and high cell density. Endoscopic ultrasound is the most useful technique to detect the early changes of malignancy in polyps. Anomalous junction of pancreaticobiliary ducts (AJPBD) without a choledochal cyst and porcelain gallbladder is an additional risk factor for gallbladder malignancy. At the molecular level, it has been proposed that chronic inflammation of the gallbladder may lead to the loss of p53 gene heterozygosity and excessive expression of p53 protein. Furthermore, a proposed mechanism underlying the high risk of gallbladder carcinoma in patients with AJPBD is that chronic reflux of pancreatic juice causes intestinal metaplasia, hyperplasia, and dysplasia with the mutation of p53 and K-ras. In contrast, the causal relationship between porcelain gallbladder and malignancy is yet to be established. In this article, recognition of risk factors for gallbladder carcinoma was summarized with special attention to gallstones and chronic inflammation.

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Section: Anomalous Junction Of the Pancreaticobiliary Ductmentioning

confidence: 79%

Carcinogenesis of malignant lesions of the gall bladder

Tazuma

Kajiyama

2001

Langenbeck's Arch Surg

111

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“…However, in addition to primary neurogenic or hormonal deficit determining neurohormonal dysfunction, a possible explanation is the following: congenital anatomic factors, i.e., a long, narrow, and tortuous cystic duct or an alteration of the biliary^pancreatic confluence [29,30], could facilitate the periodic obstruction of GB outlet by intermittent formation of sludge, mucus, plugs, etc., because of chronic irritation of the GB mucosa. In the early phases of lithogenesis, i.e., those observed in young patients, so-called primary papillary hyperplasia occurs; it is associated with the formation of small R-A sinuses with mucus producing cells, which are detected at SEM examination.…”

Section: Discussionmentioning

confidence: 99%

Rokitansky-Aschoff Sinuses of the Gallbladder are Associated with Black Pigment Gallstone Formation: A Scanning Electron Microscopy Study

Cariati

Cetta

2003

Ultrastructural Pathology

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Rokitansky-Aschoff sinuses are the result of hyperplasia and herniation of epithelial cells through the fibromuscular layer of the gallbladder wall and are usually referred to as adenomyomatosis. The role of this study is to demonstrate that Rokitansky-Aschoff sinuses of the gallbladder are a risk factor for the formation of black pigment gallstones. A total of 179 removed gallbladders, were hystologically examined. Sixty-four of the 179 consecutive cholecystomized patients had typical adenomyomatosis. Thirty-eight of the 64 patients with adenomyomatosis had black pigment gallstones, alone (n=22) or in association with single (n=12) or multiple (n=4) cholesterol gallstones in the same gallbladder. Twelve of these patients did not have the typical risk factors for black stones (hemolysis, cirrhoses, gastrectomy, etc). Gallstones were examined by infrared spectroscopy and X-ray diffractometry. In addition, in a subset of 14 patients, the gallstones and the gallbladder wall were examined by scanning electron microscopy. At least in the initial phases of formation, Rokitansky-Aschoff sinuses were found close to small intraparietal vessels and sometimes they contained black pigment microstones. After the fourth to fifth decades of life, black gallstones can be found in the Rokitansky-Aschoff sinuses and in the main gallbladder lumen. Black pigment gallstones can form in Rokitansky-Aschoff sinuses of the gallbladder in absence of the typical risk factors for bilirubin suprasaturation of bile.

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“…A discrepancy exists in the results regarding the MSI status of gallbladder tumors. There is a marked variation in the reported MSI frequency between 3 and 35% [20,46,53,[56][57][58][59]. Increased prevalence of MSI up to 80% of the cases has been found in APBDJ patients [42].…”

Section: Msimentioning

confidence: 99%

K‐ras, p53 mutations, and microsatellite instability (MSI) in gallbladder cancer

Saetta

2006

Journal of Surgical Oncology

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Despite the considerable progress in understanding the molecular pathology of carcinogenesis, the genetic mechanisms underlying the development and progression of gallbladder cancer (GC) are poorly understood. The survival of GC patients is generally poor. Therefore, it is very useful to define valuable prognostic factors. The most extensively studied oncogenes in gallbladder carcinogenesis are ras, commonly mutated in neoplasms of the gastrointestinal tract. K-ras oncogene is altered in a subset of gallbladder patients and mainly in those having anomalous junction of the pancreaticobiliary tract. Most of the studies of genetic abnormalities in GC have focused on p53 gene. p53 mutation/overexpression and/or LOH is present in more than 50% of gallbladder carcinomas, suggesting an important role in their pathogenesis. However, these results have not any predictive value yet. Moreover, the involvement of an alternative molecular pathway, that of microsatellite instability (MSI), is found in a limited group of GC patients. Additional research is necessary to establish its possible relation to defects of the mismatch repair (MMR) system and its proposed prognostic significance. Further elucidation of the molecular events specific to GC will help to identify novel molecular targets for the diagnosis and clinical management of the patients.

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Association between anomalous pancreaticobiliary ductal union and adenomyomatosis of the gall‐bladder

Cited by 35 publications

References 18 publications

Carcinogenesis of malignant lesions of the gall bladder

Carcinogenesis of malignant lesions of the gall bladder

Rokitansky-Aschoff Sinuses of the Gallbladder are Associated with Black Pigment Gallstone Formation: A Scanning Electron Microscopy Study

K‐ras, p53 mutations, and microsatellite instability (MSI) in gallbladder cancer

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