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Background/aims: New-onset diabetes after transplantation (NODAT) is a serious complication of liver transplantation (LT). The present study aimed to investigate the risk factors of NODAT by a national survey using the China Liver Transplant Registry database., Patients: A total of 10 204 non-pre-existing diabetic patients undergone primary LT between January 2000 and December 2013 were included. Risk factors were identified by logistic regression analysis., Results: NODAT occurred in 24.3% of liver recipients with a median follow-up time of 2.6 years, and was associated with a significantly lower patient survival. NODAT increased not only diabetes related complications (e.g., infection, kidney failure) but also biliary stricture and cholangitis. NODAT patients who received hypoglycaemic treatment had a worse prognosis and a higher hepatocellular carcinoma recurrence compared with those without treatment. New-onset hyperglycaemia (<30 days) was the major predictor of NODAT. Other risk factors included cold ischaemia time >9 h, recipient age >50 years, body mass index >25 kg/m(2) , other hepatitis (mainly hepatitis C), post-transplant intensive care unit stay >15 days, cytomegalovirus infection and corticosteroid at discharge., Conclusions: The incidence of NODAT in China is similar to that in Western countries. However, the NODAT-related complications are more common and severer in China compared with those in Western countries. The major risk factors are different., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Hepatitis B virus (HBV) recurrence is a major risk factor affecting the long-term survival of recipients for liver transplantation (LTx). Therefore, a model that can assess this risk before transplantation is highly desirable., Methods: One hundred and eighty-five consecutive liver transplant recipients because of HBV-related end-stage liver diseases were selected. Their perioperative laboratory examination results, treatment protocol and the status of HBV recurrence were the primary parameters used to assess their risk of post-transplant HBV recurrence. A model that may be generally used to evaluate the risk of post-transplant HBV recurrence was thus established. A cohort for further validation and a cross-validation were designed., Results: After a follow-up time of 26.0 ± 10.8 months, the overall HBV recurrence rate was 8.6%. The 1-, 2- and 3-year cumulative survival rates were 98.5, 89.2 and 83.4% respectively. By correlation with the pretransplant presence of hepatocelluar carcinoma (HCC), serum HBV DNA level and status of antiviral treatment (AVT), the risk assessment model can be summarized using the following equation: RISK=-4.378 + 1.493 × HCC + 1.286 × DNA - 2.426 × AVT. The HBV recurrence rate and survival were found to be significantly different between the recipients with risk scores ≤-2.8 and >-2.8. The model was well validated in this work., Conclusions: Pretransplant HBV DNA level, presence of HCC, AVT status and post-transplant viral mutation were identified as the major risk factors associated with HBV recurrence after LTx. A novel model incorporating these factors could effectively evaluate the risk of post-transplant HBV recurrence before transplantation., (© 2011 John Wiley & Sons A/S.)

Background: Single-nucleotide polymorphisms (SNP) of two-gene locus cytotoxic T lymphocyte antigen-4 (CTLA-4) +49 and CD86 +1057 were previously reported to influence the outcome of liver transplantation (LT) with respect to allograft acceptance. SNP at CTLA-4 +49 was also suggested to be associated with the individual difference in the clearance of hepatitis B virus (HBV). However, their influence on the incidence of post-LT HBV reinfection was not clear. With the increasing knowledge of costimulatory mechanisms on LT and host immune response, we designed this study to investigate the relationship between different alleles as well as genotypes at these two locations and HBV reinfection after LT., Methods: Genomic DNA from 167 LT recipients with HBV-related diseases was genotyped for CTLA-4 +49 and CD86 +1057 genomic polymorphisms using a sequence-specific primer-polymerase chain reaction (PCR-SSP). HBV recurrence was diagnosed based on the serological and pathological finding of HBV DNA and HBsAg., Results: The present study indicated that the recipients with CTLA-4 +49 GG genotype had a reduced risk (6.67%) of HBV recurrence compared with non-CTLA-4 +49 GG-carrying individuals (20.7%) (relative risk 3.098) (P=0.032). The allelic frequency of CTLA-4 +49 G was also significantly lower in patients with HBV recurrence, compared with that in patients without HBV recurrence (P=0.013, odds ratio 2.176, 95% confidence interval 1.170-4.046). However, no significant association was found between CD86 +1057 and HBV recurrence., Conclusion: Our result on CTLA-4 +49 A/G polymorphism indicated that the CTLA-4 +49 GG genotype was related to a reduced risk in the incidence of HBV recurrence.

Tumor recurrence is a life‐threatening complication after liver transplantation (LT) for hepatocellular carcinoma (HCC). Precise recurrence risk stratification before transplantation is essential for the management of recipients. Here, we aimed to establish an inflammation‐related prediction model for posttransplant HCC recurrence based on pretransplant peripheral cytokine profiling. Two hundred and ninety‐three patients who underwent LT in two independent medical centers were enrolled, and their pretransplant plasma samples were sent for cytokine profiling. We identified four independent risk factors, including alpha‐fetoprotein, systemic immune‐inflammation index, interleukin 6, and osteocalcin in the training cohort (n = 190) by COX regression analysis. A prediction model named inflammatory fingerprint (IFP) was established based on the above factors. The IFP effectively predicted posttransplant recurrence (area under the receiver operating characteristic curve [AUROC]: 0.792, C‐index: 0.736). The high IFP group recipients had significantly worse 3‐year recurrence‐free survival rates (37.9 vs. 86.9%, p < 0.001). Simultaneous T‐cell profiling revealed that recipients with high IFP were characterized by impaired T cell function. The IFP also performed well in the validation cohort (n = 103, AUROC: 0.807, C‐index: 0.681). In conclusion, the IFP efficiently predicted posttransplant HCC recurrence and helped to refine pretransplant risk stratification. Impaired T cell function might be the intrinsic mechanism for the high recurrence risk of recipients in the high IFP group. [ABSTRACT FROM AUTHOR]

Tertiary lymphoid structure (TLS) can predict the prognosis and sensitivity of tumors to immune checkpoint inhibitors (ICIs) therapy, whether it can be noninvasively predicted by radiomics in hepatocellular carcinoma with liver transplantation (HCC‐LT) has not been explored. In this study, it is found that intra‐tumoral TLS abundance is significantly correlated with recurrence‐free survival (RFS) and overall survival (OS). Tumor tissues with TLS are characterized by inflammatory signatures and high infiltration of antitumor immune cells, while those without TLS exhibit uncontrolled cell cycle progression and activated mTOR signaling by bulk and single‐cell RNA‐seq analyses. The regulators involved in mTOR signaling (RHEB and LAMTOR4) and S‐phase (RFC2, PSMC2, and ORC5) are highly expressed in HCC with low TLS. In addition, the largest cohort of HCC patients is studied with available radiomics data, and a classifier is built to detect the presence of TLS in a non‐invasive manner. The classifier demonstrates remarkable performance in predicting intra‐tumoral TLS abundance in both training and test sets, achieving areas under receiver operating characteristic curve (AUCs) of 92.9% and 90.2% respectively. In summary, the absence of intra‐tumoral TLS abundance is associated with mTOR signaling activation and uncontrolled cell cycle progression in tumor cells, indicating unfavorable prognosis in HCC‐LT. [ABSTRACT FROM AUTHOR]

To identify the mechanism underlying macrosteatosis (MaS)‐related graft failure (GF) in liver transplantation (LT) by multi‐omics network analysis. The transcriptome and metabolome were assayed in graft and recipient plasma in discovery (n = 68) and validation (n = 89) cohorts. Differentially expressed molecules were identified by MaS and GF status. Transcriptional regulatory networks were generated to explore the mechanism for MaS‐related inferior post‐transplant prognosis. The differentially expressed molecules associated with MaS and GF were enriched in ferroptosis and peroxisome‐related pathways. Core features of MaS‐related GF were presented on decreased transferrin and impaired anti‐oxidative capacity dependent upon dysregulation of transcription factors hepatocyte nuclear factor 4A (HNF4A) and hypoxia‐inducible factor 1A (HIF1A). Furthermore, miR‐362‐3p and miR‐299‐5p inhibited transferrin and HIF1A expression, respectively. Lower M2 macrophages but higher memory CD4 T cells were observed in MaS‐related GF cases. These results were validated in clinical specimens and cellular models. Systemic analysis of multi‐omics data depicted a panorama of biological pathways deregulated in MaS‐related GF. Transcriptional regulatory networks centered on transferrin and anti‐oxidant responses were associated with poor MaS graft quality, qualifying as potential targets to improve prognosis of patients after LT. [ABSTRACT FROM AUTHOR]

Early allograft dysfunction (EAD) is a life‐threatening and fast‐developing complication after liver transplantation. The underlying mechanism needs to be better understood, and there has yet to be an efficient therapeutic target. This study retrospectively reviewed 109 patients undergoing liver transplantation, with dynamic profiling of CD3/4/8/16/19/45/56 on the peripheral immune cells (before transplant and 2–4 days after). Altogether, 35 out of the 109 patients developed EAD after liver transplantation. We observed a significant decrease in the natural killer cell proportion (NK cell shift, p = 0.008). The NK cell shift was linearly correlated with cold ischemic time (p = 0.016) and was potentially related to the recipients' outcomes. In mouse models, ischemic/reperfusion (I/R) treatments induced the recruitment of NK cells from peripheral blood into liver tissues. NK cell depletion blocked a series of immune cascades (including CD8+ CD127+ T cells) and inhibited hepatocyte injury effectively in I/R and liver transplantation models. We further found that I/R treatment increased hepatic expression of the ligands for natural killer group 2 member D (NKG2D), a primary activating cell surface receptor in NK cells. Blockade of NKG2D showed a similar protective effect against I/R injury, indicating its role in NK cell activation and the subsequent immunological injury. Our findings built a bridge for the translation from innate immune response to EAD at the bedside. Peripheral NK cell shift is associated with the incidence of EAD after liver transplantation. NKG2D‐mediated NK cell activation is a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Hepatitis B surface antigen (HBsAg) persists after liver transplantation in almost all patients receiving HBsAg‐positive grafts. Chronic hepatitis B virus (HBV) infection is one of the main causes of hepatocellular carcinoma (HCC). We aimed to investigate possible interactions between HBsAg‐positive donors, HCC, HBV‐related transplant indication, and long‐term outcomes. This retrospective study enrolled 1176 patients from two centers between January 2015 and May 2019, of which 135 (11.5%) were HBsAg‐positive and 1041 (88.5%) were HBsAg‐negative donors. Cox regression models were fitted to study the association between variables and patient and graft survival. In univariate and multivariate analyses, the donor HBsAg status was not significantly associated with patient and graft survival in the entire cohort, but there was a significant interaction between HBsAg‐positive donors and HCC, independent of HBV‐related transplant indication. The cumulative incidence of patient and graft survival was significantly lower in the subgroup of HCC recipients receiving HBsAg‐positive grafts, but no significant difference was found in recipients with benign liver disease. In a subgroup analysis of HCC recipients, HBsAg‐positive donors were significantly associated with an increased risk of HCC recurrence (hazard ratio: 1.73; 95% confidence interval: 1.20–2.48; p = 0.003) and similar results were obtained after propensity score matching analysis. We showed excellent outcomes of using HBsAg‐positive grafts in patients with benign liver disease, regardless of HBV‐related transplant indications. However, positive grafts should be used with caution in recipients with HCC, which are associated with an increased risk of HCC recurrence. Highlights: •HBsAg‐positive grafts are safe for use in patients with benign liver disease.•HBsAg‐positive grafts increase mortality in patients with HCC.•HBsAg‐positive grafts are associated with an increased risk of HCC recurrence post‐LT. [ABSTRACT FROM AUTHOR]

Background and Aim: Donor shortage has become worldwide limitation in liver transplantation (LT). Use of hepatitis B virus surface antigen positive (HBsAg+) donors could be an alternative source of donor organs. This study aims to investigate the safety and efficacy of LT using HBsAg+ liver grafts and associated long‐term outcome. Methods: This was a retrospective study of adults LT registered in the database of the China Liver Transplant Registry between January 2015 and September 2018. By propensity score matching (1:1), 503 eligible patients who received HBsAg+ liver grafts were compared with 503 matched patients who received HBsAg− liver grafts. Results: The 1‐, 3‐, and 5‐year patient survival rates were 81.52%, 72.04%, and 66.65% in HBsAg+ donor group, which were comparable with 83.93%, 77.27%, and 65.73% in HBsAg− donor group (P = 0.222). The 1‐, 3‐, and 5‐year graft survival rates were also comparable between the two groups (81.49%, 71.45%, and 67.26% vs 83.62%, 77.11%, and 65.81%, respectively, P = 0.243). Most main complications were not increased in HBsAg+ donor group except for the retaining of HBsAg positivity after LT. Furthermore, transplanting HBsAg+ liver grafts did not result in inferior outcomes either in HBsAg+ or HBsAg− recipients. The risk of tumor recurrence after LT was not increased in hepatocellular carcinoma patients. Conclusions: The outcomes of using HBsAg+ liver grafts were comparable with those of HBsAg− liver grafts. Our study provided strong evidence for the safe use of HBsAg+ grafts in LT to expand the donor liver pool. [ABSTRACT FROM AUTHOR]

Objectives: The discrepancy between supply and demand of organ has led to an increased utilization of steatotic liver for liver transplantation (LT). Hepatic steatosis, however, is a major risk factor for graft failure due to increased susceptibility to ischaemia‐reperfusion (I/R) injury during transplantation. Materials and methods: To assess the plasticity and phenotype of immune cells within the microenvironment of steatotic liver graft at single‐cell level, single‐cell RNA‐sequencing (scRNA‐Seq) was carried out on 23 675 cells from transplanted rat livers. Bioinformatic analyses and multiplex immunohistochemistry were performed to assess the functional properties, transcriptional regulation, phenotypic switching and cell‐cell interactions of different cell subtypes. Results: We have identified 11 different cell types in transplanted livers and found that the highly complex ecosystem was shaped by myeloid‐derived cell subsets that transit between different states and interact mutually. Notably, a pro‐inflammatory phenotype of Kupffer cells (KCs) with high expression of colony‐stimulating factor 3 (CSF3) that was enriched in transplanted steatotic livers was potentially participated in fatty graft injury. We have also detected a subset of dendritic cells (DCs) with highly expressing XCR1 that was correlated with CD8+ T cells, mediating the severer steatotic liver damage by I/R injury. Conclusions: The findings of our study provide new insight into the mechanisms by which steatosis exacerbates liver damage from I/R injury. Interventions based on these observations create opportunities in attenuating fatty liver graft injury and expanding the donor pool. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the most aggressive tumours with marked fibrosis. Mycophenolate mofetil (MMF) was well‐established to have antitumour and anti‐fibrotic properties. To overcome the poor bioavailability of MMF, this study constructed two MMF nanosystems, MMF‐LA@DSPE‐PEG and MMF‐LA@PEG‐PLA, by covalently conjugating linoleic acid (LA) to MMF and then loading the conjugate into polymer materials, PEG5k‐PLA8k and DSPE‐ PEG2k, respectively. Hepatocellular carcinoma cell lines and C57BL/6 xenograft model were used to examine the anti‐HCC efficacy of nanoparticles (NPs), whereas NIH‐3T3 fibroblasts and highly‐fibrotic HCC models were used to explore the anti‐fibrotic efficacy. Administration of NPs dramatically inhibited the proliferation of HCC cells and fibroblasts in vitro. Animal experiments revealed that MMF‐LA@DSPE‐PEG achieved significantly higher anti‐HCC efficacy than free MMF and MMF‐LA@PEG‐PLA both in C57BL/6 HCC model and highly‐fibrotic HCC models. Immunohistochemistry further confirmed that MMF‐LA@DSPE‐PEG dramatically reduced cancer‐associated fibroblast (CAF) density in tumours, as the expression levels of alpha‐smooth muscle actin (α‐SMA), fibroblast activation protein (FAP) and collagen IV were significantly downregulated. In addition, we found the presence of CAF strongly correlated with increased HCC recurrence risk after liver transplantation. MMF‐LA@DSPE‐PEG might act as a rational therapeutic strategy in treating HCC and preventing post‐transplant HCC recurrence. [ABSTRACT FROM AUTHOR]

Background: The outcomes of large‐sized graft mismatch in deceased donor liver transplantation (LT) have been rarely studied. The aim of this study was to determine whether a large‐sized graft for recipient influenced the post‐transplant outcomes. Methods: A total of 273 patients undergoing LT were enrolled and divided into a large and a normal‐sized graft group by graft weight to recipient weight (GWRW) >2.5% (n = 76) or GWRW ≤2.5% (n = 197). Post‐operative complications and outcomes were retrospectively analysed. Results: The two groups were comparable in demographic characteristics. The rate of complications was significantly higher in the large‐sized graft group including early allograft dysfunction (36.8% versus 17.8%, P = 0.001), hepatic necrosis (26.3% versus 13.7%, P = 0.01) and massive hydrothorax (25% versus 14.7%, P = 0.04). The large‐sized graft group suffered higher early mortality compared with the normal‐sized graft group (30 days: 14.5% versus 5.6%, P = 0.02, 90 days: 21.1% versus 9.6%, P = 0.01). The primary causes of early death were multiple organ failure (10.5% versus 2%, P = 0.002) and sepsis (2.6% versus 1.5%, P = 0.54). Four parameters including donor alanine transaminase, GWRW, estimated blood loss and model for end‐stage liver disease score were significant on multivariate analysis, and indicated significant risk factors for the early mortality of recipients. Conclusion: In deceased donor LT, GWRW >2.5% is associated with increased liver injury, risk of early mortality and other adverse outcomes. Thus, donor livers should be allocated to recipients with GWRW ≤2.5%. [ABSTRACT FROM AUTHOR]

Background The use of grafts from donors with hypertension ( HTN) in liver transplantation has grown rapidly recently, but whether HTN donors affect post- liver transplantation survival is unclear. Methods We used data from the Scientific Registry of Transplant Recipients database (2004-2008), and evaluated differences in baseline characteristics and outcomes between recipients of grafts from HTN and non- HTN donors. Kaplan-Meier and multivariate Cox regression models were used in assessing patient survival. Results We identified 8,411 recipients of HTN donor grafts (33.2%) and 16,891 (66.8%) recipients of non- HTN donor grafts. Graft and patient survival rates were significantly lower in recipients of HTN donor grafts versus non- HTN donor grafts (1-year, 3-year, and 5-year graft survival rates of 75%, 64%, 50% vs. 80%, 72%, 62% [ P < 0.001], respectively, and patient survival rates of 79%, 69%, 56% vs. 83%, 75%, 65% [ P < 0.001], respectively). A history of HTN >5 years was also associated with lower rates of graft and patient survival ( P < 0.001). A HTN donor was independently associated with a higher risk of graft loss (hazard ratio 1.10, 95% confidence interval 1.01-1.18). Conclusion The present study shows that graft and patient survivals were lower in recipients of hypertensive donor grafts, and highlights the importance of appropriately screening donors for HTN. [ABSTRACT FROM AUTHOR]

Background Whether the introduction of model for end-stage liver disease ( MELD) has an effect on transplant outcome for different age categories remain unclear. Methods We analyzed 49,762 adult hepatitis C virus ( HCV) candidates through 1 January 1995 to 31 December 2012 from the Scientific Registry of Transplant Recipients. Patients were divided into four age categories (18-34, 35-49, 60-64, ≥65 years) in the pre- MELD era and MELD era, respectively. Results Waiting list dropouts have decreased in the MELD era for all categories. A reduced trend in survival was observed for 18-34 years patients in the MELD era compared with the pre- MELD era, with 5-year intention-to-treat, overall and graft survival of 56.5%, 57.9%, 56.3% vs. 56.4%, 69.7%, 64.4% ( P = 0.604, 0.034, and 0.071, respectively). For other age categories, survival rates were all superior in the MELD era. Cox-regression analysis showed values of hazard ratio for age increased with advanced age (all >1) in the pre- MELD era compared with the reference group (18-34 years), while these hazard ratios were <1 for overall and graft survival in MELD era. Conclusions Our study provides useful evidence that the introduction of MELD for liver allocation may adversely affect survival of specific HCV patients. [ABSTRACT FROM AUTHOR]

Aim Neutrophil to lymphocyte ratio (NLR) is an inflammatory biomarker that has a close relationship with tumor progression and metastasis. In this study, we aimed to investigate the role of NLR in the prognosis of male candidates with hepatocellular carcinoma (HCC) undergoing liver transplantation (LT). Methods We analyzed the clinical data of 248 male HCC candidates who underwent LT in our Liver Transplantation Center between 2002 and 2012. All risk factors were analyzed by univariate and multivariate Cox analysis and survival rates were calculated by Kaplan-Meier log-rank test. Results NLR was proved to be an independent risk factor affecting overall survival (OS) ( P < 0.001) and tumor-free survival (TFS) ( P = 0.003) of male candidates with HCC following LT. Additionally, our study showed that elevated NLR (>4) was associated with early tumor recurrence by Kaplan-Meier analysis. Furthermore, we established Model_OS and Model_TFS to predict prognosis based on multivariate Cox analysis. Our study showed that male candidates with HCC who exceeded the Milan criteria but within Model_OS could achieve similar OS as those within the Milan criteria ( P = 0.220). Similarly, male patients who exceeded the Milan criteria but within Model_TFS could achieve similar TFS as those within the Milan criteria ( P = 0.197). Conclusion Proper inflammatory response may effectively reduce tumor recurrence after LT. Elevated NLR (>4) within a certain range is associated with early tumor recurrence. NLR-based models are efficient and safe for prognostic prediction among male candidates with HCC for LT. [ABSTRACT FROM AUTHOR]

Recurrence of hepatocellular carcinoma (HCC) is one of the leading causes of death after liver transplantation (LT). We aim to evaluate the association of donor and recipient single nucleotide polymorphisms (SNPs) with the risk of HCC recurrence after LT. A total of 155 adult patients who underwent primary LT for HCC were enrolled. Ten SNPs associated with HCC susceptibility were genotyped. Patients who received donor livers with the rs11614913 homozygous CC variant presented significantly higher recurrence rates of HCC (41.7 vs. 15.3%, p50.009) and lower cumulative tumor-free survival (p50.005) than those who received TT wild-type donor livers. The donor rs11614913 genetic variant was an independent risk factor for HCC recurrence (odds ratio52 per each C allele, p < 0.05) and could significantly improve the predictive abilities of clinical models (Milan, UCSF and Hangzhou criteria). Donor livers homozygous for rs11614913 CC were associated with a higher miR-196a expression than TT (p50.002). In a lentiviral infection of mouse liver and orthotopic mouse model of HCC, the liver miR-196a overexpression group showed a significantly larger tumor size than the control group (p50.001). There is a close association between the tumor size and expression of miR-196a in the liver (r50.693, p50.001). In conclusion, the donor miR-196a-2 rs11614913 polymorphism is associated with HCC recurrence after LT and improves the predictive value of clinical models. The overexpression of miR-196a in the liver might provide a tumor-favorable environment for the development of HCC. [ABSTRACT FROM AUTHOR]

Aim The aim of the present study was to evaluate the risk factors and outcomes of gastrointestinal perforation post-liver transplantation. Patients and Methods Eleven patients were found to have complications as a result of gastrointestinal perforation post-liver transplantation at our centre from May 2008 to February 2014. Seven of these patients were selected for statistical analysis. Each patient was randomly matched with six recipients in age (± 10 years), primary disease and sex. Factors, including cold ischaemic time, blood loss volume, previous hepatobiliary surgery history and 1-year survival rate, were compared between the two groups. Results The sites of perforation were the stomach ( n = 2), duodenum ( n = 2), jejunum ( n = 1), ileum ( n = 3) and colon ( n = 3). Univariate analysis showed a significant difference in previous hepatobiliary surgery history ( P < 0.01). No difference was found in portal venous cross-clamp time, cold ischaemic time, model for end-stage liver disease score, body mass index, steroid therapy or blood type incompatibility. Previous hepatobiliary surgery history was found to be an independent risk factor in the multivariate analysis ( P < 0.05). The 1-year survival rate was lower in the perforation group ( P < 0.01). Conclusion Gastrointestinal perforation leads to a high rate of morbidity and mortality, and significantly decreases graft and recipient survival. A history of hepatobiliary surgery is a risk factor of this complication. Careful dissection and avoiding iatrogenic injury during operation are important. [ABSTRACT FROM AUTHOR]

Background and Aims Absolute lymphocyte count ( ALC) and the recovery of ALC after treatment have been identified as a prognostic biomarker for several malignancies. In this study, we aimed to investigate the prognostic role of peritransplant ALC and ALC recovery after liver transplantation ( LT) in hepatocellular carcinoma ( HCC) patients. Methods A total of 269 HCC patients undergoing LT were enrolled in our study. Clinicopathological data were retrospectively collected and reviewed. Peritransplant ALC and the change of ALC (2 weeks, 1 month, 3 months post- LT) were carefully monitored. All potential risk factors were analyzed by univariate and multivariate cox regression analysis. Results Over a mean follow-up of 35.9 months, 120 recurrences and 89 deaths were recorded. In the multivariate analysis, HCC with ALC no recovery at 1 month after LT ( P < 0.001), high pretransplant alpha fetoprotein ( P = 0.010), total tumor size > 8 cm ( P = 0.003), and beyond Milan criteria ( P < 0.001) were four independent risk factors for HCC recurrence. For overall survival ( OS) after LT, ALC no recovery at 1 month after LT ( P = 0.003), total tumor size > 8 cm ( P = 0.011), pretransplant albumin < 2.8 g/dL ( P = 0.049), model of end-stage liver disease score > 15 ( P = 0.017), and beyond Milan criteria ( P = 0.001) were significantly related to poor OS. When subgroup analyses were performed according to the Milan criteria, the results showed that the recovery of ALC at 1 month after LT still indicated longer recurrence-free survival ( RFS) ( P < 0.001) and OS ( P = 0.005) beyond Milan criteria as well as RFS ( P < 0.001) within Milan criteria, but not OS ( P = 0.157) within Milan criteria. Conclusions ALC recovery at 1 month after LT indicated favorable outcomes of HCC patients. [ABSTRACT FROM AUTHOR]

Hepatic vein reconstruction is one of the crucial issues in living donor liver transplantation ( LDLT). In the present study, we report on a right liver LDLT excluding middle hepatic vein ( MHV) using an MHV-dominant graft. Two large-sized inferior right hepatic veins were anastomosed to the recipient's inferior vena cava, respectively, in an end-to-side fashion. MHV tributaries were reconstructed using Y-shaped cryopreserved iliac artery, but resulted in segment VIII congestion. A Fogarty catheter was then used to take out the thrombus and control the bleeding when anastomosis was being performed. The patient recovered uneventfully. Postoperative computed tomography showed patent interposition grafts and normal perfusion of the liver. The patient was doing well 13 months after transplantation. [ABSTRACT FROM AUTHOR]

Background: Liver transplantation is an effective therapy for end‐stage liver diseases and acute liver failure. After the operation, however, recipients may suffer grafts loss induced by alloimmune reaction, which is termed as acute allograft rejection. The interaction between costimulatory molecules, CD276, and its ligand, TREML2, promotes T cell‐mediated immune response, as well as acute or chronic allograft rejection. Our research aimed at correlating genetic polymorphisms of CD276/TREML2 with acute rejection, and evaluating its prognostic value of acute rejection after liver transplantation. Methods: The study enrolled a total of 388 recipients. Among them, acute allograft rejection was observed in 54 cases. We performed single nucleotide polymorphism genotyping of CD276, including rs11072431, rs11574495, rs12593558, rs12594627, rs2127015, rs3816661 and rs7176654, and TREML2, including rs4714431, rs6915083, rs7754593, and rs9394767 from preoperative peripheral blood genome DNA. Results: We found rs2127015 of CD276, rs6915083 and rs7754593 of TREML2, and HBV infection as well were associated with acute rejection. And, rs2127015 influences CD276 expression. Moreover, we established a risk assessment model, composited by statistically proved risk factors. Conclusion: By integrating both clinical and genetic variables, liver transplant recipients can be categorized into different risk groups, and might benefit from individualized therapies. [ABSTRACT FROM AUTHOR]