Heterotopic gastric mucosa in the hilar bile duct mimicking hilar cholangiocarcinoma: report of a case

Surgery Today ◽  
2012 ◽  
Vol 43 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Saburo Fukuda ◽  
Syoichiro Mukai ◽  
Seiichi Shimizu ◽  
Masatoshi Kouchi ◽  
Seiji Fujisaki ◽  
...  
2018 ◽  
Vol 26 (8) ◽  
pp. 745-748 ◽  
Author(s):  
Yeseul Kim ◽  
Min Jung Jung ◽  
Su-Jin Shin

Gastric heterotopia within the biliary system is extremely rare. Moreover, the combination of gastric heterotopia in the bile duct with cholangiocarcinoma has not been reported. We describe a case of heterotopic gastric mucosa in the common bile duct with cholangiocarcinoma. An 80-year-old male was admitted with abdominal pain. Abdominal computed tomography revealed wall thickening from the hilar duct to the distal common bile duct. Biopsy from the distal bile duct showed only benign gastric foveolar-type epithelium and fundic glands. Although the diagnosis of the biopsy was benign, malignancy was strongly suspected from the radiologic findings, and excision of the bile ducts was performed. Microscopically, the resected specimen showed poorly formed malignant glands and gastric heterotopia also identified in the common bile duct. Three months later, the patient’s state worsened due to recurrence, and he died. To our knowledge, this is the first report of gastric heterotopia in the bile duct accompanying cholangiocarcinoma.


2020 ◽  
Author(s):  
Meng-yu Zhang ◽  
Jie-ping Wang ◽  
Kai he ◽  
Xian-ming Xia

Abstract Background: To develop a rat model of hilar cholangiocarcinoma and detect Farnesyl X receptor (FXR) expression in hilar cholangiocarcinoma tissues of this model, in order to provide a new method for the treatment of hilar cholangiocarcinoma.Methods: Forty male Wistar rats (body weight, 185 ± 5 g) were randomly divided into two groups (n = 20 each) as follows: The control group was fed a standard diet, and the experimental group was injected by cholangiocarcinoma QBC939 cell suspension along the hilar bile duct into the bile duct bifurcation with microsyringe. Every day note the rats’ mental state, diet, and fur condition. At 4 weeks, one rat of the experimental group was sacrificed, and we recorded changes in hilar bile duct size, texture, and form. This procedure was repeated at 6 weeks. After 6 weeks, hilar cholangiocarcinoma developed only in the experimental group, thereby establishing an experimental model for studying QBC939-induced hilar cholangiocarcinoma. Tumor formation was confirmed by pathological examination, and hilar bile duct tissues were harvested from both the groups. A real-time polymerase chain reaction assay and an immunohistochemical assay were used to analyze the expression of FXR in hilar cholangiocarcinoma and normal hilar bile duct tissues.Results: From the second week, the rats in experimental group began to eat less, and their body mass decreased compared with controls. After 6 weeks, we detected hilar cholangiocarcinoma in 17 rats (85%) in the experimental group. In the experimental group, we found that the levels of total cholesterol, total bilirubin, and direct bilirubin were higher compared with those of the control group. Simultaneously, muddy stones emerged from the bile ducts of rats in the experimental group. The FXR/Gapdh mRNA ratio in hilar cholangiocarcinoma and normal hilar bile duct tissues differed markedly. Light microscopy revealed a granular pattern of FXR expression which reacted with the anti-FXR antibody. Each section was randomly divided into six regions, with 80 cells were observed in every region. Sections with >10% positive cells were designated positive,Sections with <10% positive cells were designated negative. Each group included 4,800 cells. In the experimental group, 1,196 cells (24.9%) were positive and 3,538 cells (73.7%) were positive in the control group, and this difference was statistically significant.Conclusion: FXR expression significantly decreased in hilar cholangiocarcinoma of rats than in those of controls, suggesting that drugs targeting FXR may be a new strategy for hilar cholangiocarcinoma.


2020 ◽  
Vol 61 ◽  
pp. 101578
Author(s):  
Allison F. Linden ◽  
Manish T. Raiji ◽  
Ruba Azzam ◽  
Lindsay Alpert ◽  
Prashant Deshpande ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Meng-yu Zhang ◽  
Jie-ping Wang ◽  
Kai He ◽  
Xian-ming Xia

AbstractDevelop a rat model of hilar cholangiocarcinoma for detecting bile salt export pump (Bsep) expression in hilar cholangiocarcinoma tissues, in order to provide a new therapeutic target for the gene therapy of hilar cholangiocarcinoma. Sixty male Wistar rats (body weight, 190 ± 8 g) were randomly divided into three groups (the experimental group, the control group and the sham operation group, n = 20 each) as follows: The three groups were fed a standard diet, the experimental group was injected by cholangiocarcinoma QBC939 cell suspension along the hilar bile duct into the bile duct bifurcation with microsyringe, the control group was injected by normal saline, the sham operation group did not inject anything. Every day assess the rats’ mental state, diet, and motion by using Basso–Beattie–Bresnahan and combined behavioral score. At 4 weeks, one rat of the experimental group was sacrificed after it was administered anesthesia, and we recorded changes in hilar bile duct size, texture, and form. This procedure was repeated at 6 weeks. After 6 weeks, hilar cholangiocarcinoma developed only in the experimental group, thereby establishing an experimental model for studying QBC939-induced hilar cholangiocarcinoma. Tumor formation was confirmed by pathological examination, and hilar bile duct tissues were harvested from both the groups. A real-time polymerase chain reaction assay and an immunohistochemical assay were used to analyze the expression of Bsep in hilar bile duct tissues of each group. From the second week, the rats in experimental group began to eat less, and their body mass decreased compared with control group and sham operation group. After 6 weeks, we detected hilar cholangiocarcinoma in the hilar bile duct tissues of 18 rats (90%) in the experimental group. In the experimental group with hilar cholangiocarcinoma, we found that the levels of total cholesterol, total bilirubin, and direct bilirubin were higher compared with those in the control group and sham operation group. Simultaneously, muddy stones emerged from the bile ducts of rats in the experimental group. The Bsep/Gapdh mRNA ratio in hilar cholangiocarcinoma, control group and sham operation group differed markedly. Light microscopy revealed a granular pattern of Bsep protein expression which reacted with the anti-Bsep antibody. Each section was randomly divided into six regions, with 80 cells were observed in every region. Sections with > 10% positive cells were designated positive, Sections with < 10% positive cells were designated negative. Each group included 4800 cells. In the experimental group, 1200 cells (25%) were positive, in the control group, 3648 cells (76%) were positive and in the sham operation group 3598 cells (75%) were positive, and this difference was statistically significant. Bsep expression significantly decreased in hilar cholangiocarcinoma of rats than those in control group and sham operation group, suggesting that drugs targeting Bsep are a new strategy for hilar cholangiocarcinoma.


2020 ◽  
Author(s):  
Meng-yu Zhang ◽  
Jie-ping Wang ◽  
Kai he ◽  
Xian-ming Xia

Abstract AIM: To develop a rat model of hilar cholangiocarcinoma and detect Farnesyl X receptor (FXR) expression in hilar cholangiocarcinoma tissues of this model, in order to provide a new method for the treatment of hilar cholangiocarcinoma. METHODS: Forty male Wistar rats (body weight, 185 ± 5 g) were randomly divided into two groups (n = 20 each) as follows: The control group was fed a standard diet, and the experimental group was injected by cholangiocarcinoma QBC939 cell suspension along the hilar bile duct into the bile duct bifurcation with microsyringe. Every day note the rats’ mental state, diet, and fur condition. At 4 weeks, one rat of the experimental group was sacrificed after it was administered anesthesia, and we recorded changes in hilar bile duct size, texture, and form. This procedure was repeated at 6 weeks. After 6 weeks, , hilar cholangiocarcinoma developed only in the experimental group, thereby establishing an experimental model for studying QBC939-induced hilar cholangiocarcinoma. Tumor formation was confirmed by pathological examination, and hilar bile duct tissues were harvested from both the groups. A real-time polymerase chain reaction assay and an immunohistochemical assay were used to analyze the expression of FXR in hilar cholangiocarcinoma and normal hilar bile duct tissues. RESULTS: From the second week, the rats in experimental group began to eat less, and their body mass decreased compared with controls. After 6 weeks, we detected hilar cholangiocarcinoma in 17 rats (85%) in the experimental group. In the experimental group with hilar cholangiocarcinoma, we found that the levels of total cholesterol, total bilirubin, and direct bilirubin were higher compared with those of the control group. Simultaneously, muddy stones emerged from the bile ducts of rats in the experimental group. The FXR /Gapdh mRNA ratio in hilar cholangiocarcinoma and normal hilar bile duct tissues differed markedly (16 and 35, respectively). Light microscopy revealed a granular pattern of FXR expression which reacted with the anti- FXR antibody. Each section was randomly divided into six regions, with 80 cells were observed in every region. Sections with >10% positive cells were designated positive, Sections with <10% positive cells were designated negative. Each group included 4,800 cells. In the experimental group, 1,196 cells (24.9%) were positive and 3,538 cells (73.7%) were positive in the control group, and this difference was statistically significant (χ2 = 10.35, P < 0.05). CONCLUSION: FXR expression significantly decreased in hilar cholangiocarcinoma of rats than in those of controls, suggesting that drugs targeting FXR may be a new strategy for hilar cholangiocarcinoma.


Author(s):  
Masatoshi NUNOME ◽  
Toshiaki NONAMI ◽  
Yoshihiro OOWA ◽  
Takashi ARIKAWA ◽  
Nobuhiro ITOH ◽  
...  

HPB ◽  
2016 ◽  
Vol 18 ◽  
pp. e504
Author(s):  
F. Watanabe ◽  
H. Noda ◽  
Y. Kaneda ◽  
T. Rikiyama

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