PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 8840442

Why laparoscopic cholecystectomy today?

J Sandor·A Sandor·A Zaborszky·S Megyaszai·G Benedek·Z Szeberin
View original source ↗Export metadata ↓

Abstract

Traditional open cholecystectomy became the "gold standard" of surgical treatment for symptomatic gallstone disease during the last century. In spite of its good results, clinicians have been trying to establish effective nonsurgical methods of eliminating gallstones. Although oral, percutaneous, or retrograde litholysis can be used effectively for cholesterol stones, these represent only 10% of all gallstones. Moreover, intracorporeal lithotripsy is an invasive method, and while extracorporeal shock wave lithotripsy is a promising procedure, even after careful selection, only 70%-80% of the patients become stone-free within 1 year. In fact, none of the methods which leave the gallbladder intact are free of complications, and they are followed by 50% stone recurrence within 5 years. Since 1987, laparoscopic cholecystectomy has become the procedure of choice as it is safe and only minimally invasive. We believe that the laparoscopic technique is a promising way to the surgery of the future.

Explore related subjects

Bile Acids and SaltsCholecystectomy, LaparoscopicHumansLithotripsyJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Sandor, A Sandor, A Zaborszky, S Megyaszai, G Benedek, Z Szeberin. 1996. Why laparoscopic cholecystectomy today?. https://doi.org/10.1007/bf00311567

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

KEEP EXPLORING

Related citations

PubMed2025

Clostridium scindens: history and current outlook for a keystone species in the mammalian gut involved in bile acid and steroid metabolism.

Clostridium scindens is a keystone bacterial species in the mammalian gut that, while low in abundance, has a significant impact on bile acid and steroid metabolism. Numerous studies indicate that the two most studied strains of C. scindens (i.e. ATCC 35704 and VPI 12708) are important for a myriad of physiological processes in the host. We focus on both historical and current microbiological and molecular biology work on the Hylemon-Björkhem pathway and the steroid-17,20-desmolase pathway that were first discovered in C. scindens. Our most recent analysis now calls into question whether strains currently defined as C. scindens represent two separate taxonomic groups. Future directions include developing genetic tools to further explore the physiological role of bile acid and steroid metabolism by strains of C. scindens and the causal role of these pathways in host physiology and disease.

Bile Acids and Salts↗
PubMed2006

Bile acid-mediated thrombospondin-1 induction in hepatocytes leads to transforming growth factor-beta-dependent hepatic stellate cell activation.

In cholestasis, bile acids induce hepatocyte apoptosis, while activation of hepatic stellate cells (HSCs) results in fibrosis. Since transforming growth factor-beta (TGF-beta) is a critical mediator in this process, we hypothesized that bile acids may participate in TGF-beta-mediated HSC activation in cholestasis. Bile acid treatment increased TGF-beta transcription in hepatocytes, while the total TGF-beta concentration in culture media rapidly decreased following bile acid treatment. Bile acid treatment promptly induced thrombospondin-1 expression in hepatocytes, which is a potent activator of latent TGF-beta, whereas this induction was not observed in bile acid-treated HSCs. HSCs co-cultured with hepatocytes showed a significantly higher level of Smad2 phosphorylation and collagen alpha1 synthesis following bile acid treatment than cells cultured without hepatocytes. Moreover, this enhanced collagen synthesis was significantly inhibited in the presence of TGF-beta receptor inhibitor. These observations imply that bile acids induce thrombospondin-1 expression in hepatocytes, which activates latent TGF-beta leading to HSC activation.

Bile Acids and Salts↗
PubMed2006

Matrix metalloproteinase-7-catalyzed release of HB-EGF mediates deoxycholyltaurine-induced proliferation of a human colon cancer cell line.

Prior evidence indicates that bile acids stimulate colon cancer cell proliferation by muscarinic receptor-induced transactivation of epidermal growth factor receptors (EGFR). To explore further the mechanism underlying this action, we tested the hypothesis that bile acids activate a matrix metalloproteinase (MMP) that catalyzes release of an EGFR ligand. Initial studies showed that non-selective MMP inhibitors blocked the actions of deoxycholyltaurine (DCT), thereby indicating a role for MMP-catalyzed release of an EGFR ligand. DCT-induced cell proliferation was reduced by increasing concentrations of EGFR kinase inhibitors, by antibodies to the ligand binding domain of EGFR, by neutralizing antibodies to heparin binding-EGF-like growth factor (HB-EGF) and by CRM197, an inhibitor of HB-EGF release. These findings and our observations with more selective MMP inhibitors suggested that MMP-7, an enzyme known to release HB-EGF, plays a key role in mediating bile acid-induced H508 colon cancer cell proliferation. We observed that recombinant HB-EGF and MMP-7 mimicked both the signaling and proliferative actions of bile acids. Strikingly, reducing MMP-7 expression with either neutralizing antibody or small interfering RNA attenuated the actions of DCT. MMP-7 expression in H508 cells was confirmed using quantitative reverse transcription PCR. DCT stimulated a greater than 10-fold increase in MMP-7 gene transcription. Co-localization of pro-MMP-7 and pro-HB-EGF at the cell surface (immunofluorescence microscopy) was demonstrated, indicating proximity of the enzyme to its substrate. These findings provide strong evidence that in H508 human colon cancer cells, DCT-induced transactivation of EGFR is mediated by MMP-7-catalyzed release of the EGFR ligand HB-EGF.

Bile Acids and Salts↗