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Abstract The liver and pancreas work together to recover homeostasis after hepatectomy. This study aimed to investigate the effect of liver resection volume on the pancreas. We collected clinical data from 336 living liver donors. They were categorized into left lateral sectionectomy (LLS), left lobectomy, and right lobectomy (RL) groups. Serum pancreatic enzymes were compared among the groups. Serum amylase values peaked on postoperative day (POD) 1. Though they quickly returned to preoperative levels on POD 3, 46% of cases showed abnormal values on POD 7 in the RL group. Serum lipase levels were highest at POD 7. Lipase values increased 5.7-fold on POD 7 in the RL group and 82% of cases showed abnormal values. The RL group’s lipase was twice that of the LLS group. A negative correlation existed between the remnant liver volume and amylase (r = − 0.326)/lipase (r = − 0.367) on POD 7. Furthermore, a significant correlation was observed between POD 7 serum bilirubin and amylase (r = 0.379)/lipase (r = 0.381) levels, indicating cooccurrence with liver and pancreatic strain. Pancreatic strain due to hepatectomy occurs in a resection/remnant liver volume-dependent manner. It would be beneficial to closely monitor pancreatic function in patients undergoing a major hepatectomy.

Abstract Background This study aimed to describe our experience with three-dimensional endoanal ultrasonography (3D-EAUS) in patients who underwent surgery for Hirschsprung disease and to summarize the relationship between postoperative anal function and the distance between the anastomosis and intersphincteric groove (DBAI) measured via 3D-EAUS. Results We retrospectively reviewed patients with a history of undergoing surgery for Hirschsprung disease who visited our outpatient clinic between December 2018 and December 2019. All patients underwent 3D-EAUS for DBAI measurement. We used the Krickenbeck classification to evaluate postoperative anorectal function. Eleven patients (all males aged 3–14 years) were evaluated. Four (36.4%), four (36.4%), and three (27.3%) patients had no soiling, grade 1 soiling, and grade 3 soiling, respectively. Four (36.4%) and seven (63.6%) patients had no constipation and grade 3 constipation, respectively. The median DBAI values were 7.0 mm, 8.4 mm, and 5.6 mm (p = 0.14) in the no soiling, grade 1, and grade 3 soiling groups, respectively. Conclusions 3D-EAUS enabled precise visualization of the anal anatomy and evaluation of the anastomosis. The DBAI was relatively short in patients with grade 3 soiling, although not significantly so. Further evaluation is warranted.

Abstract Background There have been no reports on the effectiveness of the administration of antithrombin III (AT III) for post-transplant portal vein thrombosis (PVT). We herein report a case of post-transplant PVT that was resolved by AT III treatment after living donor liver transplantation (LDLT). Case presentation The patient was a 57-year-old man who had been diagnosed with decompensate liver cirrhosis by hepatitis C virus infection. He presented with repeated hepatic coma and refractory ascites. Computed tomography (CT) revealed PVT of Yerdel classification grade II before LDLT. He underwent ABO-identical LDLT using a right lobe graft. A liver function test revealed elevated liver enzyme levels on post-operative day (POD) 14. The CT examination on POD 15 revealed PVT in the left side of the main portal vein at the side of left gastric vein ligation. AT III treatment from POD 15 to POD 24 was performed. Magnetic resonance imaging revealed that the PVT had decreased 10% on POD 27. Furthermore, AT III treatment from POD 28 to POD 32 was performed. The CT examination demonstrated the disappearance of PVT on POD 69 and thereafter, he had no recurrence of PVT on 10 post-operative month (POM). Conclusions The present case suggests that the administration of AT III is safe and suitable for the treatment of post-transplant PVT.

Hypoxia-inducible factor-1alpha (HIF-1alpha), a transcription factor, plays a critical role in adaption to hypoxia, which is a major feature of diseases, including cancer. Protein disulfide isomerase (PDI) is up-regulated in numerous cancers and leads to cancer progression. PDI, a member of the TRX superfamily, regulates the transcriptional activities of several transcription factors. To investigate the mechanisms by which PDI affects the function of HIF-1alpha, the overexpression or knockdown of PDI was performed. The overexpression of PDI decreased HIF-1alpha expression in the human hepatocarcinoma cell line, Hep3B, whereas the knockdown of endogenous PDI increased its expression. NH4Cl inhibited the decrease in HIF-1alpha expression by PDI overexpression, suggesting that HIF-1alpha was degraded by the lysosomal pathway. HIF-1alpha is transferred to lysosomal membranes by heat shock cognate 70 kDa protein (HSC70). The knockdown of HSC70 abolished the decrease, and PDI facilitated the interaction between HIF-1alpha and HSC70. HIF-1alpha directly interacted with PDI. PDI exists not only in the endoplasmic reticulum (ER), but also in the cytosol. Hypoxia increased cytosolic PDI. We also investigated changes in the redox state of HIF-1alpha using PEG-maleimide, which binds to thiols synthesized from disulfide bonds by reduction. An up-shift in the HIF-1alpha band by the overexpression of PDI was detected, suggesting that PDI formed disulfide bond in HIF-1alpha. HIF-1alpha oxidized by PDI was not degraded in HSC70-knockdown cells, indicating that the formation of disulfide bond in HIF-1alpha was important for decreases in HIF-1alpha expression. To the best of our knowledge, this is the first study to show the regulation of the expression and redox state of HIF-1alpha by PDI. We also demonstrated that PDI formed disulfide bonds in HIF-1alpha 1-245 aa and decreased its expression. In conclusion, the present results showed that PDI is a novel factor regulating HIF-1alpha through lysosome-dependent degradation by changes in its redox state.

There is little information about the outcomes of pediatric patients with hepatolithiasis after living donor liver transplantation (LDLT). We retrospectively reviewed hepatolithiasis after pediatric LDLT. Between May 2001 and December 2020, 310 pediatric patients underwent LDLT with hepaticojejunostomy. Treatment for 57 patients (18%) with post-transplant biliary strictures included interventions through double-balloon enteroscopy (DBE) in 100 times, percutaneous transhepatic biliary drainage (PTBD) in 43, surgical re-anastomosis in 4, and repeat liver transplantation in 3. The median age and interval at treatment were 12.3 years old and 2.4 years after LDLT, respectively. At the time of treatments, 23 patients (7%) had developed hepatolithiasis of whom 12 (52%) were diagnosed by computed tomography before treatment. Treatment for hepatolithiasis included intervention through DBE performed 34 times and PTBD 6, including lithotripsy by catheter 23 times, removal of plastic stent in 8, natural exclusion after balloon dilatation in 7, and impossibility of removal in 2. The incidence of recurrent hepatolithiasis was 30%. The 15-years graft survival rates in patients with and without hepatolithiasis were 91% and 89%, respectively (p = 0.860). Although hepatolithiasis after pediatric LDLT can be treated using interventions through DBE or PTBD and its long-term prognosis is good, the recurrence rate is somewhat high. [ABSTRACT FROM AUTHOR]

Background Sinusoidal obstruction syndrome (SOS) after liver transplantation (LT) is a rare and potentially lethal complication. We retrospectively reviewed the outcomes of patients with post-transplant SOS. Methods Between May 2001 and December 2019, of 332 patients who underwent LT, 5 (1.5%) developed SOS. The median age at LT was 1.7 years (range 0.1–66.5). SOS was histopathologically diagnosed and classified as early-onset (<1 month) or late-onset. Results The median time to diagnosis of SOS was one month after LT. All patients developed acute cellular rejection before SOS, and the cause of SOS was acute cellular rejection in four patients and unknown in one. The treatment of SOS included conversion to tacrolimus from cyclosporine, intrahepatic hepatic vein stent placement, strengthening of immunosuppression, and plasma exchange. The 5-year graft survival rates in patients with and without SOS were 53.0% and 92.5%, respectively (p < 0.001). Of three patients with early-onset SOS, two patients improved and are doing well, and one patient died of graft failure four months after LT. Conclusions The cause and treatment of post-transplant SOS are not yet defined. The poor outcomes in patients with early-onset SOS may be improved by strengthening of immunosuppression. Patients with late-onset SOS are ultimately treated by repeat LT. [ABSTRACT FROM AUTHOR]

This is the first report of living donor liver transplantation (LDLT) for congenital hepatic fibrosis (CHF) using a mother's graft with von Meyenburg complex. A 6-year-old girl with CHF, who suffered from recurrent gastrointestinal bleeding, was referred to our hospital for liver transplantation. Her 38-year-old mother was investigated as a living donor and multiple biliary hamartoma were seen on her computed tomography and magnetic resonance imaging scan. The mother's liver function tests were normal and she did not have any organ abnormality, including polycystic kidney disease. LDLT using the left lateral segment (LLS) graft from the donor was performed. The donor LLS graft weighed 250 g; the graft recipient weight ratio was 1.19%. The operation and post-operative course of the donor were uneventful and she was discharged on post-operative day (POD) 8. The graft liver function was good, and the recipient was discharged on POD 31. LDLT using a graft with von Meyenburg complex is safe and useful. Long-term follow-up is needed with respect to graft liver function and screening malignant tumors., Competing Interests: Conflict-of-interest statement: The authors have no competing to disclose.

Utilizing the opened round ligament as venous grafts during liver transplantation is useful but controversial, and there are no pathological analyses of this procedure. Herein, we describe the first reported case of a pathological analysis of an opened round ligament used as a venous patch graft in a living donor liver transplantation (LDLT). A 13-year-old female patient with biliary atresia underwent LDLT using a posterior segment graft from her mother. The graft had two hepatic veins (HVs), which included the right HV (RHV; 15 mm) and the inferior RHV (IRHV; 20 mm). The graft RHV and IRHV were formed into a single orifice using the donor's opened round ligament (60 mm × 20 mm) as a patch graft during bench surgery; it was then anastomosed end-to-side with the recipient inferior vena cava. The recipient had no post-transplant complications involving the HVs, but she died of septic shock with persistent cholangitis and jaundice 86 d after LDLT. The HV anastomotic site had no stenosis or thrombus on autopsy. On pathology, there was adequate patency and continuity between the recipient's HV and the donor's opened round ligament. In addition, the stains for CD31 and CD34 on the inner membrane of the opened round ligament were positive. Hepatic venous reconstruction using the opened round ligament as a venous patch graft is effective in LDLT, as observed on pathology., Competing Interests: Conflict-of-interest statement: We declare that we have no conflict-of-interest.

Aim: To assessed the clinical significance of protocol liver biopsy (PLB) in pediatric liver transplantation (LT)., Methods: Between July 2008 and August 2012, 89 and 55 PLBs were performed in pediatric patients at two and five years after LT, respectively. We assessed the histopathological findings using the Metavir scoring system, including activity (A) and fibrosis (F), and we identified factors associated with scores of ≥ A1 and ≥ F1. Our results clarified the timing and effectiveness of PLB., Results: The incidences of scores of ≥ A1 and ≥ F1 were 24.7% and 24.7%, respectively, at two years after LT and 42.3% and 34.5%, respectively, at five years. Independent risk factors in a multivariate analysis of a score of ≥ A1 at two years included ≥ 2 h of cold ischemic time, no acute cellular rejection and an alanine amino transaminase (ALT) level of ≥ 20 IU/L (P = 0.028, P = 0.033 and P = 0.012, respectively); however, no risk factors were identified for a score of ≥ F1. Furthermore, no independent risk factors associated with scores of ≥ A1 and ≥ F1 at five years were identified using multivariate analysis. A ROC curve analysis of ALT at two years for a score of ≥ A1 demonstrated the recommended cutoff value for diagnosing ≥ A1 histology to be 20 IU/L. The incidence of scores of ≥ A2 or ≥ F2 at two years after LT was 3.4% (three cases), and all patients had an absolute score of ≥ A2. In contrast to that observed for PLBs at five years after LT, the incidence of scores of ≥ A2 or ≥ F2 was 20.0% (11 cases), and all patients had an absolute score of ≥ F2. In all cases, the dose of immunosuppressants was increased after the PLB, and all ten patients who underwent a follow-up liver biopsy improved to scores of ≤ A1 or F1., Conclusion: PLB at two years after LT is an unnecessary examination, because the serum ALT level reflects portal inflammation. In addition, immunosuppressive therapy should be modulated to maintain the ALT concentration at a level less than 20 IU/L. PLB at five years is an excellent examination for the detection of early reversible graft fibrosis because no serum markers reflect this finding.