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Sökning: L773:2304 3881 OR L773:2304 389X

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  • Capobianco, Ivan, et al. (författare)
  • Development and internal validation of the Comprehensive ALPPS Preoperative Risk Assessment (CAPRA) score : is the patient suitable for Associating Liver Partition and Portal vein ligation for Staged hepatectomy (ALPPS)?
  • 2022
  • Ingår i: Hepatobiliary surgery and nutrition. - Hong Kong : AME Publishing Company. - 2304-3881 .- 2304-389X. ; 11:1, s. 52-66
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Preoperative patient selection in associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) is not always reliable with currently available scores, particularly in patients with primary liver tumor. This study aims to (I) to determine whether comorbidities and patients characteristics are a risk factor in ALPPS and (II) to create a score predicting 90-day mortality preoperatively. Methods: Thirteen high-volume centers participated in this retrospective multicentric study. A risk analysis based on patient characteristics, underlying disease and procedure type was performed to identify risk factors and model the CAPRA score. A nonparametric receiver operating characteristic analysis was performed to estimate the predictive ability of our score against the Charlson Comorbidity Index (CCI), the age-adjusted CCI (aCCI), the ALPPS risk score before Stage 1 (ALPPS-RS I) and Stage 2 (ALPPS-RS2). The model was internally validated applying bootstrapping. Results: A total of 451 patients were included. Mortality was 14.4%. The CAPRA score is calculated based on the following formula: (0.1*age) - (2*BSA) +1 (in the presence of primary liver tumor) +1 (in the presence of severe cardiovascular disease) +2 (in the presence of moderate or severe diabetes) +2 (in the presence of renal disease) +2 (if classic ALPPS is planned). The predictive ability was 0.837 for the CAPRA score, 0.443 for CCI, 0.519 for aCCI, 0.693 for ALPPS-RS I and 0.807 for ALPPS-RS2. After 1,000 cycles of bootstrapping the C statistic was 0.793. The accuracy plot revealed a cut-off for optimal prediction of postoperative mortality of 4.70. Conclusions: Comorbidities play an important role in ALPPS and should be carefully considered when planning the procedure. By assessing the patients preoperative condition in relation to ALPPS, the CAPRA score has a very good ability to predict postoperative mortality.
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  • Liu, Zhengtao, et al. (författare)
  • Clear mortality gap caused by graft macrosteatosis in Chinese patients after cadaveric liver transplantation
  • 2020
  • Ingår i: Hepatobiliary surgery and nutrition. - : AME Publishing Company. - 2304-3881 .- 2304-389X. ; 9:6, s. 739-758
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Liver transplantation (LT) is one of the most effective surgical treatment for patients with end-stage liver disease. Steatosis is a contributor for inferior graft quality. But its impact and safety on transplantation was less assessed in Chinese patients. Methods: Graft steatosis and related information involved in recipients, donors and surgical procedures were retrospectively collected from 239 patients. Results: Donor macrosteatosis (MaS) caused about 2.14 and 2.80 folds of increment on patient and graft mortality. Dose-response analysis revealed prominent risk of grafts on overall patient/organ mortality when MaS content exceeded 10% (P<0.05). Noteworthy, deaths were only observed in MaS group when concurrent with extremely higher post-transplant alanine aminotransferase (ALT, 64%). However, microsteatosis (MiS) grafts didn't affect outcomes after LT. In a cohort of Chinese patients, MaS had comprehensive effects on post-transplant outcomes with relatively lower safety threshold at 10%. Mortality gap caused by MaS grafts was observed in patients with severer ischemia reperfusion injury. Conclusions: Our study revealled the graft MaS affected the post-transplant outcomes in lower risk cutoff in Chinese patients. Further study is worthy to validate these results and investigate inner mechanism under the phenomenon.
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  • Sparrelid, Ernesto, et al. (författare)
  • How should liver hypertrophy be stimulated? A comparison of upfront associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) and portal vein embolization (PVE) with rescue possibility
  • 2021
  • Ingår i: Hepatobiliary surgery and nutrition. - : AME Publishing Company. - 2304-3881 .- 2304-389X. ; 10:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The role of associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) in comparison to portal vein embolization (PVE) is debated. The aim of this study was to compare successful resection rates (RR) with upfront ALPPS vs. PVE with rescue ALPPS on demand and to compare the hypertrophy of the liver between ALPPS and PVE plus subsequent rescue ALPPS. Methods: A retrospective analysis of all patients treated with PVE for colorectal liver metastasis (CRLM) or ALPPS (any diagnosis, rescue ALPPS included) at five Scandinavian university hospitals during the years 2013-2016 was conducted. A Chi-square test and a Mann-Whitney U test were used to assess the difference between the groups. A successful RR was defined as liver resection without a 90-day mortality. Results: A total of 189 patients were included. Successful RR was in 84.5% of the patients with ALPPS upfront and in 73.3% of the patients with PVE and rescue ALPPS on demand (P=0.080). The hypertrophy of the future liver remnants (FLRs) with ALPPS upfront was 71% (48-97%) compared to 96% (82-113%) after PVE and rescue ALPPS (P=0.010). Conclusions: Upfront ALPPS offers a somewhat higher successful RR than PVE with rescue ALPPS on demand. The sequential combination of PVE and ALPPS leads to a higher overall degree of hypertrophy than upfront ALPPS.
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  • Ansari, David, et al. (författare)
  • Pancreatic cancer and thromboembolic disease, 150 years after Trousseau.
  • 2015
  • Ingår i: HepatoBiliary surgery and nutrition. - 2304-3881. ; 4:5, s. 325-335
  • Forskningsöversikt (refereegranskat)abstract
    • The connection between pancreatic cancer and venous thrombosis has been discussed for almost 150 years. The exact pathophysiological mechanisms are still partly understood, but it is known that pancreatic cancer induces a prothrombotic and hypercoagulable state and genetic events involved in neoplastic transformation (e.g., KRAS, c-MET, p53), procoagulant factors [e.g., tissue factor (TF), platelet factor 4 (PF4), plasminogen activator inhibitor type 1 (PAI-1)], mucin production (e.g., through activation of P- and L-selectin) and pro-inflammatory factors [e.g., cytokines, cyclooxygenase-2 (COX-2)] may be implicated. Also pancreatitis, both acute and chronic, is associated with increased risk of venous thrombosis, but in this circumstance a direct inflammatory process may be more important. This article discusses the incidence, treatment and outcome of venous thromboembolism (VTE) complicating pancreatic disease, with special emphasis on new knowledge obtained during the last fifteen years.
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  • Stickel, Felix, et al. (författare)
  • PNPLA3 genetic variation in alcoholic steatosis and liver disease progression.
  • 2015
  • Ingår i: Hepatobiliary surgery and nutrition. - 2304-3881. ; 4:3, s. 152-60
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Alcoholic liver disease (ALD) accounts for the majority of chronic liver diseases in Western countries, and alcoholic cirrhosis is among the premier causes of liver failure, hepatocellular carcinoma (HCC) and liver-related mortality causes. Studies in different genders and ethnic groups, as well as in twins provide strong evidence for a significant contribution of host genetic factors to liver disease development in drinkers. The intense quest for genetic modifiers of alcohol-induced fibrosis progression have identified and repeatedly confirmed a genetic polymorphism in the gene coding for patatin-like phospholipase domain-containing 3 (PNPLA3; adiponutrin; rs738409 C/G, M148I) as a risk factor for alcoholic cirrhosis and its related complication, HCC, in different populations. Although carriership of one or both mutated PNPLA3 alleles does not explain the entire liver phenotypic variability in drinkers, it clearly represents one of the strongest single genetic modulators in a complex trait such as ALD. As more genetic data supporting its important role aggregates, novel insight as to PNPLA3's function and that of its genetic variation in liver injury is unveiled pointing to an important novel pathway in alcohol-mediated hepatic lipid turnover with strong implications on inflammation, extra cellular matrix remodelling, and hepatocarcinogenesis. Future study shall decipher whether the gathered knowledge can be translated into therapeutic benefits of patients.
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