Hepatobiliary Pancreat Dis Int

	2023 Vol. 22 No. 5
	Published: 2023-10-15


	Pages 441-550
	ORIGINAL ARTICLES/Liver ORIGINAL ARTICLES/Biliary ORIGINAL ARTICLES/Pancreas NEW TECHNIQUES Special issue on gut-liver axis

Special issue on gut-liver axis

	441	Jiang L, Fan JG
		The role of the gut microbiome in chronic liver diseases: Present insights and future outlook ^Hot!
		The human gastrointestinal tract harbors trillions of microbes including bacteria, viruses, and fungi that facilitate digestion and nutrient absorption, thereby affecting host metabolism and immunity. The liver communicates with the gut through portal vein, systemic circulation, and biliary tract to form the gut-liver axis [1]. The liver receives 70%-75% of its blood supply from the portal vein, positioning it as the first organ to encounter gut-derived microbes, microbial products, and toxins when microflora balance and gut barrier function are disrupted, which could contribute to the development of chronic liver diseases [2]. While alterations in gut microbial composition have been noted across various diseases, the causal connections remain elusive, and there are situations where the absence of microbiota does not impact the disease progression [3]. Therefore, it is imperative to review the role of gut microbiota and its products in pathogenesis of liver diseases such as nonalcoholic fatty liver disease (NAFLD), drug-induced liver injury (DILI), and cholestatic liver disease, etc.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 441-443 . [Abstract] ( 53 ) [HTML 1KB] [PDF 0KB] ( 32 )

	444	Wu MY, Fan JG
		Gut microbiome and nonalcoholic fatty liver disease ^Hot!
		Nonalcoholic fatty liver disease (NAFLD) has become the most prevalent chronic liver disease globally and imposed a heavy economic burden on society and individuals. To date, the pathological process of NAFLD is not yet fully elucidated. Compelling evidences have demonstrated the pivotal role of gut microbiota in the pathogenesis of NAFLD, and gut dysbiosis has been commonly observed in patients with NAFLD. Gut dysbiosis impairs gut permeability, allowing the translocation of bacterial products such as lipopolysac- charides (LPS), short-chain fatty acids (SCFAs), and ethanol to the liver via portal blood flow. This review aimed to shed light on the underlying mechanisms by which gut microbiota influences the development and progression of NAFLD. In addition, the potential application of gut microbiome as a non-invasive diagnostic tool and a novel therapeutical target was reviewed.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 444-451 . [Abstract] ( 39 ) [HTML 1KB] [PDF 0KB] ( 31 )

	452	Jiang L, Xu J, Cheng SY, Wang Y, Cai W
		The gut microbiome and intestinal failure-associated liver disease ^Hot!
		Intestinal failure-associated liver disease (IFALD) is a common hepatobiliary complication resulting from long-term parenteral nutrition (PN) in patients with intestinal failure. The spectrum of IFALD ranges from cholestasis, steatosis, portal fibrosis, to cirrhosis. Development of IFALD is a multifactorial process, in which gut dysbiosis plays a critical role in its initiation and progression in conjunction with increased intestinal permeability, activation of hepatic immune responses, and administration of lipid emulsion. Gut microbiota manipulation including pre/probiotics, fecal microbiota transplantation, and antibiotics has been studied in IFALD with varying success. In this review, we summarize current knowledge on the taxonomic and functional changes of gut microbiota in preclinical and clinical studies of IFALD. We also review the function of microbial metabolites and associated signalings in the context of IFALD. By providing microbiota-targeted interventions aiming to optimize PN-induced liver injury, our review provides perspectives for future basic and translational investigations in the field.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 452-457 . [Abstract] ( 49 ) [HTML 1KB] [PDF 0KB] ( 32 )

	458	Chu HK, Ai Y, Cheng ZL, Yang L, Hou XH
		Contribution of gut microbiota to drug-induced liver injury
		Drug-induced liver injury (DILI) is caused by various drugs with complex pathogenesis, and diverse clinical and pathological phenotypes. Drugs damage the liver directly through drug hepatotoxicity, or indirectly through drug-mediated oxidative stress, immune injury and inflammatory insult, which eventually lead to hepatocyte necrosis. Recent studies have found that the composition, relative content and distribution of gut microbiota in patients and animal models of DILI have changed significantly. It has been confirmed that gut microbial dysbiosis brings about intestinal barrier destruction and microorganisms translocation, and the alteration of microbial metabolites may cause or aggravate DILI. In addition, antibiotics, probiotics, and fecal microbiota transplantation are all emerging as prospective therapeutic methods for DILI by regulating the gut microbiota. In this review, we discussed how the altered gut microbiota participates in DILI.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 458-465 . [Abstract] ( 47 ) [HTML 1KB] [PDF 0KB] ( 32 )

	466	Bhattacharya A, Taylor RE, Guo GL
		In vivo mouse models to study bile acid synthesis and signaling
		The synthesis of bile acids (BAs) is carried out by complex pathways characterized by sequential chemical reactions in the liver through various cytochromes P450 (CYP) and other enzymes. Maintaining the integrity of these pathways is crucial for normal physiological function in mammals, encompassing hepatic and neurological processes. Studying on the deficiencies in BA synthesis genes offers valuable insights into the significance of BAs in modulating farnesoid X receptor (FXR) signaling and metabolic homeostasis. By creating mouse knockout (KO) models, researchers can manipulate deficiencies in genes involved in BA synthesis, which can be used to study human diseases with BA dysregulation. These KO mouse models allow for a more profound understanding of the functions and regulations of genes responsible for BA synthesis. Furthermore, KO mouse models shed light on the distinct characteristics of individual BA and their roles in nuclear receptor signaling. Notably, alterations of BA synthesis genes in mouse models have distinct differences when compared to human diseases caused by the same BA synthesis gene deficiencies. This review summarizes several mouse KO models used to study BA synthesis and related human diseases, including mice deficient in Cyp7a1, Cyp27a1, Cyp7a1/Cyp27a1, Cyp8b1, Cyp7b1, Cyp2c70, Cyp2a12, and Cyp2c70/Cyp2a12, as well as germ-free mice.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 466-473 . [Abstract] ( 33 ) [HTML 1KB] [PDF 0KB] ( 32 )

	474	Hartmann P, Lang S, Schierwagen R, Klein S, Praktiknjo M, Trebicka J, Schnabl B
		Fecal cytolysin does not predict disease severity in acutely decompensated cirrhosis and acute-on-chronic liver failure ^Hot!
		Background: Cirrhosis with acute decompensation (AD) and acute-on-chronic liver failure (ACLF) are characterized by high morbidity and mortality. Cytolysin, a toxin from Enterococcus faecalis ( E. faecalis ), is associated with mortality in alcohol-associated hepatitis (AH). It is unclear whether cytolysin also contributes to disease severity in AD and ACLF. Methods: We studied the role of fecal cytolysin in 78 cirrhotic patients with AD/ACLF. Bacterial DNA from fecal samples was extracted and real-time quantitative polymerase chain reaction (PCR) was performed. The association between fecal cytolysin and liver disease severity in cirrhosis with AD or ACLF was analyzed. Results: Fecal cytolysin and E. faecalis abundance did not predict chronic liver failure (CLIF-C) AD and ACLF scores. Presence of fecal cytolysin was not associated with other liver disease markers, including Fibrosis-4 (FIB-4) index, ‘Age, serum Bilirubin, INR, and serum Creatinine (ABIC)’ score, Child-Pugh score, model for end-stage liver disease (MELD) nor MELD-Na scores in AD or ACLF patients. Conclusions: Fecal cytolysin does not predict disease severity in AD and ACLF patients. The predictive value of fecal cytolysin positivity for mortality appears to be restricted to AH.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 474-481 . [Abstract] ( 71 ) [HTML 1KB] [PDF 0KB] ( 35 )

ORIGINAL ARTICLES/Liver

	482	Zeng JS, Zeng JX, Huang Y, Liu JF, Zeng JH
		The effect of adjuvant transarterial chemoembolization for hepatocellular carcinoma after liver resection based on risk stratification
		Background: There is currently no standard adjuvant treatment proven to prevent hepatocellular carcinoma (HCC) recurrence. Recent studies suggest that postoperative adjuvant transarterial chemoembolization (PA-TACE) is beneficial for patients at high risk of tumor recurrence. However, it is difficult to select the patients. The present study aimed to develop an easy-to-use score to identify these patients. Methods: A total of 4530 patients undergoing liver resection were recruited. Independent risk factors were identified by Cox regression model in the training cohort and the Primary liver cancer big data transarterial chemoembolization (PDTE) scoring system was established. Results: The scoring system was composed of ten risk factors including alpha-fetoprotein (AFP), albumin-bilirubin (ALBI) grade, operative bleeding loss, resection margin, tumor capsular, satellite nodules, tumor size and number, and microvascular and macrovascular invasion. Using 5 points as risk stratification, the patients with PA-TACE had higher recurrence-free survival (RFS) compared with non-TACE in > 5 points group ( P < 0.001), whereas PA-TACE patients had lower RFS compared with non-TACE in ≤5 points group ( P = 0.013). In the training and validation cohorts, the C-indexes of PDTE scoring system were 0.714 [standard errors (SE) = 0.010] and 0.716 (SE = 0.018), respectively. Conclusions: The model is a simple tool to identify PA-TACE for HCC patients after liver resection with a favorable performance. Patients with > 5 points may benefit from PA-TACE.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 482-489 . [Abstract] ( 42 ) [HTML 1KB] [PDF 0KB] ( 32 )

	490	Jia KF, Wang H, Yu CL, Yin WL, Zhang XD, Wang F, Sun C, Shen W
		ASARA, a prediction model based on Child-Pugh class in hepatocellular carcinoma patients undergoing transarterial chemoembolization
		Background: Due to the high heterogeneity among hepatocellular carcinoma (HCC) patients receiving transarterial chemoembolization (TACE), the prognosis of patients varies significantly. The decision-making on the initiation and/or repetition of TACE under different liver functions is a matter of concern in clinical practice. Thus, we aimed to develop a prediction model for TACE candidates using risk stratification based on varied liver function. Methods: A total of 222 unresectable HCC patients who underwent TACE as their only treatment were included in this study. Cox proportional hazards regression was performed to select the independent risk factors and establish a predictive model for the overall survival (OS). The model was validated in patients with different Child-Pugh class and compared to previous TACE scoring systems. Results: The five independent risk factors, including alpha-fetoprotein (AFP) level, maximal tumor size, the increase of albumin-bilirubin (ALBI) grade score, tumor response, and the increase of aspartate aminotransferase (AST), were used to build a prognostic model (ASARA). In the training and validation co- horts, the OS of patients with ASARA score ≤2 was significantly higher than that of patients with ASARA score > 2 (P < 0.001, P = 0.006, respectively). The ASARA model and its modified version “AS(ARA)”can effectively distinguish the OS (P < 0.0 01, P = 0.0 04) between patients with Child-Pugh class A and B, and the C-index was 0.687 and 0.706, respectively. For repeated TACE, the ASARA model was superior to As-sessment for Retreatment with TACE (ART) and ALBI grade, maximal tumor size, AFP, and tumor response (ASAR) among Child-Pugh class A patients. For the first TACE, the performance of AS(ARA) was better than that of modified hepatoma arterial-embolization prognostic (mHAP), mHAP3, and ASA(R) models among Child-Pugh class B patients. Conclusions: The ASARA scoring system is valuable in the decision-making of TACE repetition for HCC patients, especially Child-Pugh class A patients. The modified AS(ARA) can be used to screen the ideal candidate for TACE initiation in Child-Pugh class B patients with poor liver function.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 490-497 . [Abstract] ( 37 ) [HTML 1KB] [PDF 0KB] ( 29 )

	498	Li JH, Jia JJ, He N, Zhou XL, Qiao YB, Xie HY, Zhou L, Zheng SS
		Exosome is involved in liver graft protection after remote ischemia reperfusion conditioning
		Background: Remote ischemic perconditioning (RIPerC) has been demonstrated to protect grafts from hepatic ischemia-reperfusion injury (IRI). This study investigated the role of exosomes in RIPerC of liver grafts in rats. Methods: Twenty-five rats (including 10 donors) were randomly divided into five groups ( n = 5 each group): five rats were used as sham-operated controls (Sham), ten rats were for orthotopic liver transplantation (OLT, 5 donors and 5 recipients) and ten rats were for OLT + RIPerC (5 donors and 5 recipients). Liver architecture and function were evaluated. Results: Compared to the OLT group, the OLT + RIPerC group exhibited significantly improved liver graft histopathology and liver function ( P < 0.05). Furthermore, the number of exosomes and the level of P-Akt were increased in the OLT + RIPerC group. Conclusions: RIPerC effectively improves graft architecture and function, and this protective effect may be related to the increased number of exosomes. The upregulation of P-Akt may be involved in underlying mechanisms.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 498-503 . [Abstract] ( 36 ) [HTML 1KB] [PDF 0KB] ( 33 )

	504	Lin TY, Zhang YF,Wang Y, Liu Y, Xu J, Liu YL
		Nonalcoholic fatty liver disease aggravates acute pancreatitis through bacterial translocation and cholesterol metabolic dysregulation in the liver and pancreas in mice
		Background: Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for severe acute pancreatitis (AP). The underlying mechanism remains unclear. We sought to determine how bacterial translocation and cholesterol metabolism in the liver and pancreas affect the severity of AP in NAFLD mice. Methods: C57BL/6N mice were fed on a high-fat diet (HFD) to generate the NAFLD model, and mice in the control group were provided with a normal diet (ND). After being anesthetized with ketamine/xylazine, mice got a retrograde infusion of taurocholic acid sodium into the pancreatic duct to induce AP, and sham operation (SO) was used as control. Serum amylase and Schmidt’s pathological score system were used to evaluate AP severity. Bacterial loads, total cholesterol level, and cholesterol metabolic-associated molecules [low-density lipoprotein receptor (LDLR) and ATP-binding cassette transporter A1 (ABCA1)] were analyzed in the liver and pancreas. Results: Compared with the ND-AP group, mice in the HFD-AP group had severer pancreatitis, mani- fested with higher serum amylase levels and higher AP pathologic scores, especially the inflammation and hemorrhage scores. Compared with the HFD-SO group and ND-AP group, bacterial loads in the liver and pancreas were significantly higher in the HFD-AP group. Mice in the HFD-AP group showed a decreased LDLR expression and an increased ABCA1 expression in the pancreas, although there was no significant difference in pancreas total cholesterol between the HFD-AP group and the ND-AP group. Conclusions: NAFLD aggravates AP via increasing bacterial translocation in the liver and pancreas and affecting pancreas cholesterol metabolism in mice.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 504-511 . [Abstract] ( 42 ) [HTML 1KB] [PDF 0KB] ( 30 )

ORIGINAL ARTICLES/Biliary

	512	Dondorf F, Graf M, Ali Deeb A, Rohland O, Felgendreff P, Ardelt M, Settmacher U, Rauchfuss F
		Pathogen detection in patients with perihilar cholangiocarcinoma: Implications for targeted perioperative antibiotic therapy
		Background: Cholestasis should be relieved by biliary drainage prior to major liver resection. This condition is often associated with bacterial colonization of the otherwise sterile biliary system. Cholangitis reduces the regenerative capacity of the remaining liver. Therefore, targeted antibiotic therapy is a key feature in perioperative treatment in patients with perihilar cholangiocarcinoma (pCCC). Methods: Between December 1999 and December 2017, 251 pCCC patients were treated in our center. In total, 115 patients underwent a microbiological analysis. In addition to the characterization of the specific microorganisms and antibiotic resistance, we analyzed subgroups according to preoperative intervention. Results: Enterococci (87/254, 34%) and Enterobacteria (65/254, 26%) were the most frequently detected genera. In 43% (50/115) of patients, Enterococcus faecalis was found in the bile duct sample. Enterococcus faecium (29/115) and Escherichia coli (29/115) were detected in 25% of patients. In patients with percutaneous transhepatic biliary drainage (3/8, 38%) or stents (24/79, 30%), Enterococcus faecium was diagnosed most frequently ( P < 0.05). Enterococcus faecium and Klebsiella oxytoca were significantly more frequently noted in the time period after 2012 ( P < 0.05). With regard to fungal colonization, the focus was on various Candida strains, but these strains generally lacked resistance. Conclusions: pCCC patients exhibit specific bacterial colonization features depending on the type of pre- operative biliary intervention. Specifically, targeted antibiosis should be applied in this patient cohort to minimize the risk of biliary complications after major liver resection. In our cohort, the combination of meropenem and vancomycin represents an effective perioperative medical approach.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 512-518 . [Abstract] ( 35 ) [HTML 1KB] [PDF 0KB] ( 34 )

ORIGINAL ARTICLES/Pancreas

	519	Wang W, Jiang CF, Yin HS, Gao S, Yu BP
		Targeting mitochondrial transcription factor A sensitizes pancreatic cancer cell to gemcitabine
		Background: The survival of pancreatic cancer cells, particularly cancer stem cells which are responsible for tumor relapse, depends on mitochondrial function. Mitochondrial transcription factor A (TFAM) is critical for the regulation of mitochondrial DNA and thus mitochondrial function. However, the possible involvement of TFAM in pancreatic cancer is unknown. Methods: Human samples were obtained from pancreatic cancers and their adjacent tissues; human pancreatic cell lines were cultured in RPMI1640 medium. TFAM expressions in pancreatic tissues and cultured cells were determined using immunohistochemistry, ELISA, and reverse transcription polymerase chain reaction (RT-PCR). The effect of TFAM on cell growth, migration, colony formation and apoptosis were evaluated. Mitochondrial biogenesis in pancreatic cancer and normal cells were examined. Results: The majority of pancreatic cancer tissues exhibited higher TFAM expression compared to the adjacent counterparts. Consistently, TFAM mRNA and protein levels were higher in pancreatic cancer cell lines than in immortalized normal pancreatic epithelial cells. There was no difference on TFAM level between gemcitabine-sensitive and resistant pancreatic cancer cells. Functional analysis demonstrated that TFAM overexpression activated pancreatic normal and tumor cells whereas TFAM inhibition effectively inhibited the growth of pancreatic cancer cells. TFAM inhibition enhanced gemcitabine’s cytotoxicity and suppressed growth, anchorage-independent colony formation and survival of gemcitabine-resistant pancreatic cancer cells. Mechanistic studies showed that TFAM inhibition resulted in remarkable mitochondrial dysfunction and energy crisis followed by oxidative stress. The basal mitochondrial biogenesis level correlated well with TFAM level in pancreatic cancer cells. Conclusions: TFAM played essential roles in pancreatic cancer via regulating mitochondrial functions which highlighted the therapeutic value of inhibiting TFAM to overcome gemcitabine resistance.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 519-527 . [Abstract] ( 36 ) [HTML 1KB] [PDF 0KB] ( 34 )

NEW TECHNIQUES

	528	Chen JY, Han J, Liu ZW, Xin XL,Wang PF, Cai SW
		Combined hepatic segment color rendering technique improves the outcome of anatomical hepatectomy in patients with hepatocellular carcinoma
		Hepatocellular carcinoma (HCC) is the third most common cause for cancer-related death worldwide, especially in China [1]. Hepatectomy is considered one of the most potentially curative therapies for HCC [2]. As HCC is capable of vascular invasion and metastasis via the portal venous system, anatomical resection is often performed to reduce tumor recurrence. This process involves resecting the tumor-bearing portal branches and the corresponding hepatic parenchyma [3]. Certain comparative studies have demonstrated better overall survival and disease-free survival with the use of anatomical resection when compared with nonanatomical resection [4–6].
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 528-531 . [Abstract] ( 37 ) [HTML 1KB] [PDF 0KB] ( 34 )

	532	Zhou J, Song YH, Qi YC, Li O, Xia GY, Mo MJ, Peng C, Liu SL
		Full laparoscopic anatomical liver segment VII resection with preferred Glissonean pedicle and dorsal hepatic approach
		Anatomical liver resection was an option for liver cancer proposed by the Japanese scholar Masatoshi Makuuchi in 1985 [1]. Reich et al. performed the first laparoscopic liver resection in 1991 [2]. The safety and effectiveness of laparoscopic anatomical liver resection had been verified in recent years [2–4] . However, laparoscopic anatomical segment VII liver resection (LAS7) was the most difficult procedure because of complex adjacent structures, difficult exposure, and limited laparoscopic view [3,5]. Therefore, the LAS7 had only been explored in some large national and international medical centers. Ishizawa et al. [3] reported a surgical protocol to resect segment VII of the liver that included parenchymal separation from the foot to the head side, which was identical to open anatomical liver resection. However, the liver pedicle of segment VII is difficult to locate and ligate precisely; and it is difficult to show the ischemic demarcation line completely. Herein we implemented a new, convenient approach for precise liver resection that can be used during LAS7.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 532-536 . [Abstract] ( 38 ) [HTML 1KB] [PDF 0KB] ( 32 )

	537	Kim SH, Moon DB, Kang WH, Jung DH, Lee SG
		A surgical technique using the gastroepiploic vein for portal inflow restoration in living donor liver transplantation in a patient with diffuse portomesenteric thrombosis
		Portal vein thrombosis (PVT) is no longer a definitive contraindication in liver transplants (LTs) [1]. Complex vascular reconstructions such as cavoportal hemitransposition (CPHT) [2–5], renoportal anastomosis (RPA) [6,7], and use of sizable collaterals (pericholedochal varix [8,9], coronary vein, peripancreatic or perigastroesophageal varices [10], right superior colic vein [11], ileocolic vein [12], and left gastric vein [13]), or combined liverpancreas-small bowel transplant [14] are required for portal inflow in patients with total portosplenomesenteric thrombosis. A deceased donor liver transplantation (DDLT) case of successful portal inflow restoration directly from the gastroepiploic vein (GEV) without the use of an interposition graft was introduced [15,16]. Here, we report a successful living donor liver transplantation (LDLT) case using GEV for portal inflow restoration in a patient with totally obliterated splanchnic vein.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 537-540 . [Abstract] ( 37 ) [HTML 1KB] [PDF 0KB] ( 32 )

	541	Liu YS, Qi DF, Zhang J, Li HS, Jiang XC, Cui L
		Total three-dimensional laparoscopic radical resection for Bismuth type IV hilar cholangiocarcinoma
		Hilar cholangiocarcinoma (HCCA) (also known as Klatskin tumor) has a poor prognosis worldwide, and accounts for more than half of cholangiocarcinoma cases. HCCA originates from epithelium and often arises from the confluence of the bile ducts or the right or left hepatic ducts [ 1 , 2 ]. Because of its aggressiveness and refractory biological characteristics, the median survival time of patients with unresectable HCCA is less than 1 year. Radical resection is the most effective treatment for HCCA. Surgery for Bismuth type IV HCCA requires radical lymphadenectomy, corresponding hemihepatectomy combined with caudate lobectomy, resection of extrahepatic bile duct, and hepaticojejunostomy for biliary reconstruction to achieve long-term patient survival [ 3 , 4 ]. Due to the difficult surgical procedure and specific malignant biological behaviors of HCCA, laparoscopic radical resection of HCCA has been implemented only in specific and highly selective cases [5–8] . However, surgeons work in a three-dimensional (3D) space under the guidance of traditional two-dimensional (2D) laparoscopy, which lacks true depth perception and spatial orientation, potentially increasing the risk of surgical complications and the duration of surgery. The development of 3D high-definition laparoscopy for surgical application offers surgeons a better and clearer depth of surgical field and improves hand-eye coordination. Some studies have reported that 3D laparoscopy can effectively reduce performance errors, operative time, and intraoperative and postoperative complications and shorten the time required for surgical novices to learn new surgical procedures compared with 2D laparoscopy [9–11] . We recently first implemented 3D laparoscopy radical resection for Bismuth type IV HCCA for selected patients into our daily routine, and the results were encouraging. In this report, we documented the use of 3D high-definition laparoscopy in radical Bismuth type IV HCCA surgery in a patient and assessed the patient’s recovery over a 3-month follow-up period.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 541-546 . [Abstract] ( 37 ) [HTML 1KB] [PDF 0KB] ( 35 )

	547	Subasinghe D, Sivaganesh S
		Right hepatectomy with a cholangiojejunostomy and hepaticojejunostomy for unilobar Caroli’s syndrome
		Choledochal cysts are benign cystic dilatations of the extra- and intrahepatic bile ducts [ 1 , 2 ]. If untreated, their sequelae include recurrent cholangitis, secondary biliary cirrhosis, acute pancreatitis, and cholangiocarcinoma [ 3 , 4 ]. Todani et al. [5] classified choledochal cysts into 5 subtypes, of which type V is Caroli’s disease. The disease is either localized, where unilobar biliary dilatation, commonly in the left, is present, or diffuse, where the entire liver is involved. The surgical treatment of Caroli’s disease depends on the pattern of duct involvement and involves hemi-hepatectomy and liver transplantation. A partial hepatectomy is the best curative option in unilobar disease, providing long-term survival, free of symptoms and complications [4] . Caroli’s syndrome is defined as Caroli’s disease with congenital hepatic fibrosis [6] . Herein, we describe a patient with unilobar Caroli’s syndrome treated for septic complications, who subsequently had a right hepatectomy and complex bilioenteric anastomosis.
		Hepatobiliary Pancreat Dis Int. 2023; 22(5): 547-550 . [Abstract] ( 42 ) [HTML 1KB] [PDF 0KB] ( 29 )

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