Percutaneous biliary procedures.

R Uflacker

Home/Archive/PubMed

PubMed · 8903570

Percutaneous biliary procedures.

R Uflacker

View original source ↗Export metadata ↓

Abstract

This article provides a review of percutaneous biliary procedures, including percutaneous treatment of malignant biliary obstruction using internal/external drainage and stents, percutaneous treatment of benign biliary obstruction with catheters and stents, stone treatment with percutaneous lithotripsy, and percutaneous cholecystostomy and stone treatment.

Explore related subjects

Bile Duct Neoplasms Bile Ducts, Intrahepatic Catheterization Cholangiocarcinoma Cholestasis Drainage Humans Treatment Outcome Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

R Uflacker. 1996. Percutaneous biliary procedures.. https://pubmed.ncbi.nlm.nih.gov/8903570/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Surgical management of proximal bile duct cancer: extended right lobe resection increases resectability and radicality.

BACKGROUND: Surgical resection provides the only chance of cure for patients suffering from hilar cholangiocarcinoma. Although appropriate procedures are not agreed upon, an increase in radicality has been observed during the past 20 years. METHODS: The literature as well as our own experience after 133 resections of hilar cholangiocarcinomas were reviewed. RESULTS: Tumor-free margins represent the most important prognostic parameter. Hilar resections as least radical resective procedure will generate rates of formally curative resections of less than 50%. Even after these formally curative resections, long-term survival cannot be achieved. Only additional liver resections will increase the number of long-term survivors to significant figures. In our series, the best 5-year survival rate of 72% was achieved after right trisegmentectomy with concomitant resection of the portal vein bifurcation. CONCLUSION: Right trisegmentectomy and combined portal vein resection represent the best way to comply with basic rules of surgical oncology for hilar cholangiocarcinoma. This procedure will provide the most pronounced benefit among various types of liver resection, whereas local resections of the extrahepatic bile duct must be considered as an oncologically inefficient procedure.

Bile Duct Neoplasms↗

PubMed2003

Simultaneous segmental obstruction of bile duct and portal vein markedly changes a population of biliary and hepatic cells in human liver.

BACKGROUND AND AIMS: No studies have investigated histologic changes caused by simultaneous segmental obstruction of the bile duct and portal vein in human liver. PATIENTS/METHODS: Liver tissues with simultaneous obstruction of the segmental bile duct and portal vein (O(+/+) liver), with segmental bile duct obstruction alone (O(+/-) liver), and without obstruction (O(-/-) liver) were obtained from patients who underwent hepatectomy, and studied morphologically and immunohistochemically. RESULTS: In O(+/+) liver, the proportional area consisting of hepatocytes was significantly less (31.0+/-25.8%) than in O(+/-) liver (78.4+/-18.9%) or O(-/-) liver (86.5+/-9.2%). In contrast, the proportional area consisting of biliary epithelial cells was significantly higher in O(+/+) liver (9.1+/-6.1%) than in O(+/-) liver (1.6+/-1.5%) or O(-/-) liver (0.7+/-0.6%). The proportional area consisting of fibrous tissue also was significantly higher in O(+/+) liver than in the other two groups. In O(+/+) liver, some cells located at the periphery of hepatocyte areas were immunoreactive for both hepatocyte and biliary epithelial cell markers. CONCLUSION: Simultaneous segmental obstruction of the bile duct and portal vein induces a marked ductular increase, periportal fibrosis, and a reduction in the number of hepatocytes in human liver tissue.

Bile Duct Neoplasms↗

PubMed2003

Transforming growth factor beta 1 stimulates vascular endothelial growth factor gene transcription in human cholangiocellular carcinoma cells.

The expression pattern and functional interaction of proangiogenic factors in human cholangiocellular carcinoma (CCC) have not been fully defined. We therefore investigated the expression of vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)-beta 1 as well as their respective receptors in human CCC tumor samples and further analyzed their functional interaction in vitro. Expression of VEGF, TGF-beta 1, and their receptors was examined by immunohistochemistry, in situ hybridization, quantitative competitive reverse transcription-PCR, and ELISA. VEGF promoter analysis and identification of transcription factors involved in promoter regulation were investigated using transient transfection and electrophoretic mobility shift assays. We observed strong expression of VEGF in CCC tumor cells and localization of VEGF receptors 1 and 2 in endothelial cells; in addition, coexpression of TGF-beta 1 and its receptors in tumor cells suggests a possible functional interaction between both cytokines. In vitro studies confirmed a paracrine/autocrine stimulation of VEGF by TGF-beta 1 at a transcriptional level. Additional molecular studies using 5' deletion and mutational analysis of the human VEGF promoter revealed that TGF-beta 1 stimulates VEGF through Sp1-dependent transcriptional activation. These data suggest that overexpression and functional interaction of TGF-beta 1 and VEGF might contribute to the "angiogenic switch" and the malignant phenotype in human CCC.

Bile Duct Neoplasms↗