Delayed gastric emptying after pylorus-preserving pancreatoduodenectomy is strongly related to other postoperative complications.

Patients undergoing pylorus-preserving pancreatoduodenenectomy (PPPD) have a risk of up to 50% for developing delayed gastric emptying (DGE) in the early postoperative course. From 1994 to August 2002, a total of 204 patients underwent PPPD for pancreatic or periampullary cancer (50%), chronic pancreatitis (42%), and other indications (8%). Retrocolic end-to-side duodenojejunostomy was performed below the mesocolon. DGE was defined by the inability to tolerate a regular diet after day 10 (DGE10) or day 14 (DGE14) postoperatively, as well as the need for a nasogastric tube at or beyond day 10 (DGE10GT). Postoperative morbidity was 38%, 30-day mortality was 2.9%, and median postoperative length of stay was 15 days. DGE occurred in 14.7% (DGE10), 5.9% (DGE14), and 6.4% (DGE10GT), respectively. After further exclusion of 21 patients (10.3%) with major complications and no possible oral intake (because of death, reoperation, or mechanical ventilation), the frequencies of DGE10, DGE14, and DGE10GT in the remaining group of 183 patients were 9%, 2%, and 2%, respectively. Multivariate analysis revealed postoperative complications (P<0.001), the presence of portalvenous hypertension (P<0.01), and tumors as indications for surgery (P<0.01) as independent risk factors for DGE10. The overall incidence of DGE was low after PPPD. In those patients experiencing DGE, however, other postoperative complications were the most important factor associated with its occurrence.

Risk factors for complications after pancreatic head resection.

BACKGROUND: Postoperative morbidity is high after pancreatic head resections. Data about risk factors are controversial. The aim of this study was to evaluate risk factors for complications after pancreatic head resection and to assess whether the complication rate changed during the study period. METHODS: Data of 301 patients undergoing pancreatic head resection were recorded prospectively. Risk factors were assessed by multivariate analysis. The first and second part of the study period were compared. RESULTS: Mortality was 3%. Overall and surgery-related complications occurred in 42% and 28%, respectively. Independent risk factors for postoperative morbidity were impaired renal function (odds ratio [OR] 2.7), absence of preoperative biliary drainage (OR 1.9), and resection of other organs (OR 3.2). Complication rate, duration of surgery, amount of blood transfused, and length of hospital stay decreased during the study period. CONCLUSIONS: Increasing hospital experience decreased complication rates. Patients with risk factors should be considered for transferal to specialized centers.

Dendritic cell adhesion is enhanced on endothelial cells preexposed to calcineurin inhibitors.

Chronic rejection remains a major complication in solid organ transplantation. Host alloreactive T cells (TC) can be activated by donor dendritic cells (DCs; direct allorecognition) or by recipient DCs (indirect allorecognition). A fundamental aspect of DC function is vascular invasion to present donor antigens to recipient naive TC in secondary lymphoid organs. We investigated the impact of calcineurin inhibitors on DC binding and transmigration to allogeneic human microvascular endothelial cells (ECs) with and without blocking of specific adhesion molecules. Recipient immature DCs were generated by culturing CD14 human peripheral blood monocytes with GM-CSF and IL-4. DC adhesion and transmigration were investigated on allogeneic ECs preincubated with increasing concentrations of cyclosporine and tacrolimus. Experiments were repeated in the presence of blocking antibodies against LFA-1, PECAM-1, VCAM-1, and ICAM-1. Endothelial stimulation with cyclosporine A (100 and 300 ng/mL) and tacrolimus (15 ng/mL) significantly enhanced DC-EC adhesion and transmigration (P<0.01). LFA-1 blockade on DCs significantly reduced cyclosporine- and tacrolimus-induced DC adhesion (P<0.001). VCAM-1 blockade on ECs partially reversed cyclosporine-induced DC adhesion (P<0.001), whereas DC adhesion under tacrolimus exposure was significantly decreased by ICAM-1 (P<0.01) and PECAM-1 (P<0.001) blockade. DC binding and transmigration on allogeneic ECs exposed to calcineurin inhibitors is concentration-dependently increased. Different adhesion molecule patterns on ECs are responsible for enhanced DC invasion under cyclosporine and tacrolimus exposure. We speculate that long-term immunosuppression mediates enhanced invasion of recipient DCs to the donor organ and therefore may aggravate chronic rejection.

Immortalization of pancreatic stellate cells as an in vitro model of pancreatic fibrosis: deactivation is induced by matrigel and N-acetylcysteine.

Tissue fibrosis is one of the characteristics of chronic pancreatitis and pancreatic adenocarcinoma. Activated pancreatic stellate cells (PSC) play a central role in this process. However, analysis of the molecular mechanisms leading to PSC activation is hampered by the lack of an established human PSC line. To overcome this problem, we immortalized and characterized primary human PSC. The cells were isolated by the outgrowth method and were immortalized by transfection with SV40 large T antigen and human telomerase (hTERT). Primary human PSC served as controls. An immortalized line, RLT-PSC, was analyzed for the expression of stellate cell markers. Moreover, the effects of transforming growth factor beta 1(TGFbeta1) or platelet-derived growth factor stimulation and of cultivation on basement membrane components or N-acetylcysteine (NAC) treatment on gene and protein expression and proliferation were analyzed. Immortal RLT-PSC cells retained the phenotype of activated PSC proven by the expression of alpha-smooth muscle actin (alphaSMA), vimentin, desmin and glial fibrillary acidic protein (GFAP). TGFbeta1 treatment upregulated the expression of alphaSMA, collagen type I (Col I), fibronectin and TGFbeta1. Incubation of RLT-PSC cells and primary human activated PSC on Matrigel plus NAC treatment resulted in a deactivated phenotype as evidenced by a decrease of alphaSMA, connective tissue growth factor and Col I expression and by a decreased proliferation of the cells. Moreover, this treatment restored the ability of the cells to store vitamin A in cytoplasmic vesicles. In conclusion, we have established an immortal pancreatic stellate cell line, without changing the characteristic phenotype. Importantly, we were able to demonstrate that besides soluble factors, the matrix surrounding PSC plays a pivotal role in the maintenance of the activation process of PSC. Cultivation of activated PSC on a reconstituted basement membrane plus treatment with NAC was able to deactivate the cells, thus pointing to the possibility of an antifibrosis therapy in chronic pancreatitis.