PubMed · 13512586
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L FRIEDRICH. 1957. [Intubation with minute interval method].. https://pubmed.ncbi.nlm.nih.gov/13512586/
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BACKGROUND: Gallstone disease remains the most common disease of the digestive system in Western societies and laparoscopic cholecystectomy one of the most common surgical procedures performed. Bile leaks remain a significant cause of morbidity for patients undergoing this procedure. These occur in 0.2-2% of cases. The bile ducts of Luschka, or subvesical ducts, are small ducts which originate from the right hepatic lobe, course along the gallbladder fossa, and usually drain in the extrahepatic bile ducts. Injuries to these ducts are the second most frequent cause of postcholecystectomy bile leaks. METHODS: A literature search using MEDLINE's Medical Subject Heading terms was used to identify recent articles. Cross-references from these articles were also used. RESULTS: Subvesical bile duct leaks can be detected by drip-infusion cholangiography using computed tomography preoperatively, direct visualization or cholangiography intraoperatively, and fistulography, endoscopic retrograde cholangiopancreatography (ERCP), and magnetic resonance cholangiopancreatography with intravenous contrast postoperatively. ERCP is the most common diagnostic method used. Most patients with subvesical duct leaks are symptomatic, and most leaks will be detected postoperatively during the first postoperative week. Drainage of extravasated bile is mandatory in all cases. Reduction of intrabiliary pressure with endoscopic sphincterotomy and stent placement will lead to preferential flow of bile through the papilla, thus permitting subvesical duct injuries to heal. This is the most common treatment modality used. In a minority of patients, relaparoscopy is performed. In such cases, the leaking subvesical duct is visualized directly, and ligation usually is sufficient treatment. Simple drainage is adequate treatment for a small number of asymptomatic patients with low-volume leaks. CONCLUSIONS: Subvesical duct leaks occur after cholecystectomy regardless of gallbladder pathology or urgency of operation. They have been encountered more frequently in the era of laparoscopic cholecystectomy. Intraoperative cholangiography does not detect all such leaks. Staying close to the gallbladder wall during its removal from the fossa is the only known prophylactic measure. ERCP and stent placement are the most common effective diagnostic and therapeutic methods used. Intraoperative and perioperative adjunctive measures, such as fibrin glue instillation and pharmacologic relaxation of the sphincter of Oddi, can potentially be used in lowering the incidence of subvesical bile leaks.
Mucosal tissues require constant immune surveillance to clear harmful pathogens while maintaining tolerance to self Ags. Regulatory T cells (Tregs) play a central role in this process and expression of alpha(E)beta(7) has been reported to define a subset of Tregs with tropism for inflamed tissues. However, the signals responsible for recruiting Tregs to epithelial surfaces are poorly understood. We have isolated a subset of CCR10-expressing CD25+CD4+Foxp3+ Tregs with potent anti-inflammatory properties from chronically inflamed human liver. The CCR10+ Tregs were detected around bile ducts that expressed increased levels of the CCR10 ligand CCL28. CCL28 was secreted by primary human cholangiocytes in vitro in response to LPS, IL-1beta, or bile acids. Exposure of CCR10+ Tregs to CCL28 in vitro stimulated migration and adhesion to mucosal addressin cell adhesion molecule-1 and VCAM-1. Liver-derived CCR10+ Tregs expressed low levels of CCR7 but high levels of CXCR3, a chemokine receptor associated with infiltration into inflamed tissue and contained a subset of alpha(E)beta7(+) cells. We propose that CXCR3 promotes the recruitment of Tregs to inflamed tissues and CCR10 allows them to respond to CCL28 secreted by epithelial cells resulting in the accumulation of CCR10+ Tregs at mucosal surfaces.
BACKGROUND/AIMS: Results of our previous studies supported the concept that in the human liver, the smallest ramification of the biliary tree, the bile ductules, might contain hepatic progenitor cells. An insufficient proliferative response and loss of bile ductules preceded bile duct loss whereas preservation of bile ductules mitigated bile duct loss. METHODS: Presently we investigated the vascular profile of the bile ductules in diseased human livers and livers showing normal histological features as controls, using CD34, CK7 and alphaSMA antibodies in a double immunolabeling technique. VEGF-A expression was also studied. In control livers bile ductules traversed the boundaries of the portal tract into the lobule as ductular-vascular units, in a pattern outlining the classic hexagonal lobule, following the vascular septa. The latter are thought to be extensions of portal veins. In diseased states the two structures reacted in unison. Increased or decreased numbers of ductules were consistently accompanied by similar changes of accompanying microvessels. Increased numbers of ductules and microvessels were paralleled by increased ductular expression of VEGF-A. RESULTS: Our data support the concept that the smallest branches of the biliary tree might have their own vascular supply and that the ductules might in turn maintain their vasculature during regenerative processes.