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BACKGROUND Biliary complications (BCs) after liver transplantation (LT) remain a considerable cause of morbidity, mortality, increased cost, and graft loss. AIM To investigate the impact of BCs on chronic graft rejection, graft failure and mortality. METHODS From 2011 to 2016, 215 adult recipients underwent right-lobe living-donor liver transplantation (RT-LDLT) at our centre. We excluded 46 recipients who met the exclusion criteria, and 169 recipients were included in the final analysis. Donors’ and recipients’ demographic data, clinical data, operative details and postoperative course information were collected. We also reviewed the management and outcomes of BCs. Recipients were followed for at least 12 mo post-LT until December 2017 or graft or patient loss. RESULTS The overall incidence rate of BCs including biliary leakage, biliary infection and biliary stricture was 57.4%. Twenty-seven (16%) patients experienced chronic graft rejection. Graft failure developed in 20 (11.8%) patients. A total of 28 (16.6%) deaths occurred during follow-up. BCs were a risk factor for the occurrence of chronic graft rejection and failure; however, mortality was determined by recurrent hepatitis C virus infection. CONCLUSION Biliary complications after RT-LDLT represent an independent risk factor for chronic graft rejection and graft failure; nonetheless, effective management of these complications can improve patient and graft survival.

BACKGROUND Stem cell autophagy disruption is responsible for the development of hepatocellular carcinoma (HCC). Many non-coding RNAs are linked to the activation and inhibition of certain genes. The SQSTM1 gene controls stem cell autophagy as shown in previous studies. The upregulation of SQSTM1 is associated with the inhibition of autophagy in cancerous stem cells in patients with HCC. AIM To determine whether serum microRNA, hsa-miR-519d, is linked to SQSTM1 gene and whether they could be used as diagnostic biomarkers for early-stage HCC. METHODS In silico analysis was performed to determine the most correlated genes of autophagy with microRNAs. SQSTM1 and hsa-miR-519d were validated through this pilot clinical study. This study included 50 Egyptian participants, who were classified into three subgroups: Group 1 included 34 patients with early-stage HCC, Group 2 included 11 patients with chronic liver disease, and Group 3 (control) included 5 healthy subjects. All patients were subjected to full laboratory investigations, including viral markers and alpha-fetoprotein (AFP), abdominal ultrasound, and clinical assessment with the Child–Pugh score calculation. Besides, the patients with HCC underwent triphasic computed tomography with contrast to diagnose and determine the tumor site, size, and number. Quantitative real-time polymerase chain reaction was used to assess hsa-miR-519d-3p and SQSTM1 in the serum of all the study participants. RESULTS Hsa-miR-519d-3p was significantly upregulated in patients with HCC compared with those with chronic liver disease and healthy subjects with an area under the curve (AUC) of 0.939, with cutoff value 8.34, sensitivity of 91.2%, and specificity of 81.8%. SQSTM1 was upregulated with an AUC of 0.995, with cutoff value 7.89, sensitivity of 97.1%, and specificity of 100%. AFP significantly increased in patients with HCC with an AUC of 0.794, with cutoff value 7.30 ng/mL, sensitivity of 76.5%, and specificity of 72.7%. CONCLUSION This study is the first to show a direct relation between SQSTM1 and hsa-miR-519d-3p; they are both upregulated in HCC. Thus, they could be used as surrogate diagnostic markers for stem cell autophagy disturbance in early-stage HCC.