Review Open Access
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 21, 2018; 24(23): 2441-2456
Published online Jun 21, 2018. doi: 10.3748/wjg.v24.i23.2441
Feasibility of using marginal liver grafts in living donor liver transplantation
Xiang Lan, Hua Zhang, Hong-Yu Li, Ke-Fei Chen, Fei Liu, Yong-Gang Wei, Bo Li
Xiang Lan, Hua Zhang, Ke-Fei Chen, Fei Liu, Yong-Gang Wei, Bo Li, Department of Liver Surgery and Liver Transplantation Center, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China
Hong-Yu Li, Department of Pancreatic Surgery, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China
ORCID number: Xiang Lan (0000-0002-5626-0106); Hua Zhang (0000-0002-5776-8286); Hong-Yu Li (0000-0002-9614-5700); Ke-Fei Chen (0000-0003-1657-0094); Fei Liu (0000-0002-9650-1576); Yong-Gang Wei (0000-0001-8776-289X); Bo Li (0000-0002-1411-3722).
Author contributions: Lan X and Zhang H contributed equally to this study and participated in the research design and manuscript preparation; Li HY, Chen KF, and Liu F generated the tables and figures; and Li B and Wei YG revised the article.
Conflict-of-interest statement: All authors declare that there are no conflicts of interest in this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Bo Li, MD, PhD, Professor, Department of Liver Surgery and Liver Transplantation Center, West China Hospital of Sichuan University, 37 Guoxue Road, Wuhou District, Chengdu 610041, Sichuan Province, China. hxcdlibo@126.com
Telephone: +86-18980601470
Received: March 25, 2018
Peer-review started: March 26, 2018
First decision: April 18, 2018
Revised: May 4, 2018
Accepted: May 18, 2018
Article in press: May 18, 2018
Published online: June 21, 2018

Abstract

Liver transplantation (LT) is one of the most effective treatments for end-stage liver disease caused by related risk factors when liver resection is contraindicated. Additionally, despite the decrease in the prevalence of hepatitis B virus (HBV) over the past two decades, the absolute number of HBsAg-positive people has increased, leading to an increase in HBV-related liver cirrhosis and hepatocellular carcinoma. Consequently, a large demand exists for LT. While the wait time for patients on the donor list is, to some degree, shorter due to the development of living donor liver transplantation (LDLT), there is still a shortage of liver grafts. Furthermore, recipients often suffer from emergent conditions, such as liver dysfunction or even hepatic encephalopathy, which can lead to a limited choice in grafts. To expand the pool of available liver grafts, one option is the use of organs that were previously considered “unusable” by many, which are often labeled “marginal” organs. Many previous studies have reported on the possibilities of using marginal grafts in orthotopic LT; however, there is still a lack of discussion on this topic, especially regarding the feasibility of using marginal grafts in LDLT. Therefore, the present review aimed to summarize the feasibility of using marginal liver grafts for LDLT and discuss the possibility of expanding the application of these grafts.

Key Words: Marginal liver grafts, Living donor liver transplantation, Liver transplant waiting lists, Small-for-size grafts, Older donors, ABO-incompatible, Steatosis, Chronic hepatitis

Core tip: There are few reviews concerning the feasibility of using marginal liver grafts in living donor liver transplantation (LDLT). We reviewed more than 300 articles, summarized new findings, and confirmed that marginal grafts are a feasible option for expanding options for patients on liver transplant waiting lists in emergency situations in LDLT (e.g., liver failure or hepatic encephalopathy). However, such grafts place the recipients at greater risk for adverse events. Although some indispensable treatments are needed to address the deficiencies of these grafts, recipients can receive a favorable prognosis, similar to that of patients who receive standard liver grafts, under these treatments.



INTRODUCTION

The high mortality of patients on waiting lists due to the shortage of cadaveric donors is a major challenge in liver transplantation (LT)[1]. This challenge has led to the emergence of living donor liver transplantation (LDLT) after the first successful procedure in 1989[2,3]. However, following a sharp increase in recipients who suffer from emergency situations, the wide gap between the demands of patients and suitable living donors is gradually increasing[4,5]. Therefore, the transplantation community has focused on the search for strategies to increase the pool of available liver grafts, including the use of organs that were previously considered “unusable” by many and often labeled “marginal” organs[6].

An accepted definition of marginal donors remains unclear in LDLT. These expanded-criteria grafts have the potential to increase the risk of poor graft function or primary nonfunction and are referred to as “marginal” organs[7]. In this review, we define marginal liver grafts for LDLT as small-for-size grafts, older donors, moderate or severe steatosis of liver grafts, chronic hepatitis, and grafts with tumors. The survival of recipients with marginal organs can be the same as that of patients with high-quality liver grafts under proper treatment[8].

Many previous studies have reported on the possibilities of using marginal grafts in orthotopic liver transplantation (OLT), but there is still a lack of discussion on this topic, especially regarding the feasibility of using marginal grafts in LDLT. Therefore, the present review aimed to summarize and discuss the possibility of expanding the application of marginal grafts in LDLT.

SMALL-FOR-SIZE GRAFTS IN LDLT

Choosing to use a liver graft can be a remarkably complex decision. There is an increasing trend of patients dying while on waiting lists due to the everyday risk of death or serious complications while waiting; this risk must be balanced against the use of a marginal graft, which may not be feasible. Size mismatching between the graft and the recipient is a critical predictor of the so-called “marginal liver grafts” in LDLT recipients. A small-for-size graft has become the main reason for unsuitability for liver donation in some transplantation centers[9]. The most common index with which to evaluate graft size matching is the graft-to-recipient weight ratio (GRWR) or graft volume (GV)/standard liver volume (SLV). The GRWR was first reported to require a safety range of above 1%; otherwise, the rate of graft survival could decrease[10]. With the increased demand for LDLT and the improvement of surgical techniques, however, many expanded-criteria grafts are used. Accordingly, the accepted arbitrary requirement for GRWR was reduced to 0.8%, and the GV/SLV value was 40%[11,12]. As many transplantation centers accumulated experience on small-for-size grafts for LDLT, grafts with a GRWR < 0.8% were used and reported to be as safe as those with a GRWR ≥ 0.8%[13-17]. After challenging the boundary of GRWR = 0.8%, the acceptable minimum GRWR has been continuously lowered. Lee SD et al[18] reported that a GRWR as low as 0.7% is safe and that there is no need to modulate portal pressure in adult-to-adult LDLT using the right-lobe in favorable conditions, such as a low Model for End-Stage Liver Disease (MELD) score. Furthermore, Alim A et al[19] even suggested that a GRWR as low as 0.6% may be safe if the MELD score is < 20, donor age is < 45, and there is no evidence of liver steatosis in the donor graft during portal inflow modulation performed according to the portal flow. To date, the reported lowest GRWR of grafts that have been successfully used is between 0.40% and 0.46% (Table 1)[20].

Table 1 Recommended minimum graft-to-recipient weight ratio in different studies.
Ref.Recommended minimum GRWRn (small vs large)One-year survival (small vs large)Five-year survival (small vs large)Study type
Kiuchi et al[10] (1999)1%276 (49 vs 215)61.2% vs 92.6%NSRS
Lee et al[11] (2003)0.8%141 (10 vs 131)Univariate and multiple analysisNSRS
Moon et al[13] (2010)Less than 0.8%427 (35 vs 392)87.8% vs 90.7%74.1% vs 79.4%RS
Lan et al[14] (2009)Less than 0.8%89 (15 vs 74)73.3% vs 71.6%NSRS
Selzner et al[15] (2009)Less than 0.8%271 (22 vs 249)91.0% vs 89.0%83.0% vs 87%RS
Chen et al[16] (2014)Less than 0.8%196 (45 vs 151)82.2% vs 81.4%71.1% vs 75.5%RS
She et al[17] (2017)Left lobe graft vs right lobe graft218 (19 vs 199)89.5% vs 95.9%89.5% vs 86.8%RS
Lee et al[18] (2014)Less than 0.7%317 (23 vs 294)100% vs 93.2%NSRS
Alim et al[19] (2016)0.6%649Seven patients had GRWR of 0.6%. If MELD score was below 20, donor age below 45, and no signs for any hepatosteatosis, GRWR of 0.6% was safeRS
Lee et al[20] (2015)0.40%NSLowest GRWR of 0.40% had been successfully usedRS

Small-for-size syndrome (SFSS), including small-for-size dysfunction (SFSD) and small-for-size nonfunction (SFSNF), is a concerning and life-threatening complication in patients receiving grafts with a GRWR < 0.8%[21,22]. The incidence of SFSS varies from 4.7% to 27.5% in different LT centers[23-30]. Specifically, the syndrome rate can be as high as 50%-75% in left-lobe LDLT or small-for-size grafts group and as low as 8.4% in right-lobe LDLT[31,32]. Graft size is the only independent predictor of SFSS[31]. However, other studies have described that SFSS can occur even in the presence of a normal GRWR[16]. Regardless of the definition used for SFSS, it seems clear that other key factors should be considered in addition to a mismatched graft size. The incidence of SFSS is listed in Table 2.

Table 2 Incidence of small-for-size syndrome when using small-for-size grafts n (%).
Ref.nSFSS (Incidence)Factors to SFSSStudy type
Goldaracena et al[21] (2017)NSNSA graft GRWR < 0.8% of predisposes the graft to SFSSRE
Graham et al[22] (2014)NSNSGRWR of 0.8 to 1.0 was established as a lower limit to prevent SFSSRE
Botha et al[23] (2010)211 (4.7)Hemi-portocaval shunt can decrease SFSS incidenceRS
Goralczyk et al[24] (2011)225 (22.7)Posterior cavoplasty can decrease SFSS incidenceRS
Soejima et al[25] (2003)368 (22.2)Cirrhosis predisposes the graft to SFSSRS
Ben-Haim et al[26] (2001)405 (8)Child’s class B or C with received grafts of GRWR < 0.85% predisposes the graft to SFSSRS
Sudhindran et al[27] (2012)NS10%-20%Left lobe grafts predisposes the graft to SFSSRE
Yi et al[28] (2008)298 (27.5)Left lobe grafts predisposes the graft to SFSSRS
Soejima et al[29] (2012)31243 (15.3)Left lobe grafts predisposes the graft to SFSSRS
Gruttadauria et al[30] (2015)8313 (15.7)Non-surgical modulation of the portal inflow can decrease SFSS incidenceRS
Shoreem et al[31] (2017)17420 (11.5)Left lobe grafts predisposes the graft to SFSSRS
Lauro et al[32] (2007)84 (50)Surgical modulation of the portal inflow can decrease SFSS incidenceRS

Middle hepatic vein (MHV) or outflow reconstruction of the liver graft is associated with size mismatch. A small-for-size graft without MHV reconstruction can lead to various degrees of congestion of the anterior segment and a greater loss of hepatocellular function[33]. In our early observational studies with small sample sizes, we recommended a GRWR > 1.0%[34] or even 1.2%[35] as a security threshold for patients without MHV reconstruction. Asakuma M et al[36] established an algorithm known as the estimated congestion ratio (ECR, ECR = regional volume of v5 + v8 / right-lobe volume) to estimate whether MHV should be reconstructed for low-GRWR grafts. A liver with an ECR > 0.4 is an MHV-dominant liver, and higher GRWR grafts should be used. However, it is still unknown how far we can lower the GRWR following the improvement of postoperative management and surgical technique if there is no reconstruction of outflow. In addition to outflow reconstruction, the inflow of grafts, including portal hypertension following reperfusion and the hyperdynamic splanchnic state, is reported as a major factor that can trigger SFSS[37-39]; however, these views are controversial[40]. Enhanced cholestasis, hepatocyte ballooning, disruption of the sinusoidal line, and transformation of activated Ito cells into fibroblasts are observed under the conditions of portal hypertension, or overperfusion[41,42]. Recipients with a final portal vein pressure (PVP) ≤ 15 mmHg or a pressure gradient of PVP-central vein pressure (CVP) ≤ 5 mmHg have a better prognosis[43]. In another study, liver-graft-to-spleen-volume ratio was used to predict early graft function in children and young adults undergoing LDLT, in which < 0.88 predicted portal hyperperfusion[44]. Moreover, a MELD score > 20[45], a decline in the platelet (PLT) count at post operation day (POD) 3 > 56%[46] and donor age > 45 years are also risk factors for a poor prognosis in recipients of small-for-size grafts[19].

To increase the safety of the expanded use of small-for-size grafts, some treatments are recommended. Graft inflow or PVP modulation is at the forefront of these treatments. Portosystemic shunting techniques or preservation of collateral veins[19,47-50], as well as splenectomy or splenic artery ligation/embolization[51-53], are effective ways to address post-transplantation portal hyperperfusion. In cases where the GRWR of grafts is very low, dual grafts can be considered[54]. Moreover, autologous stem cell implantation[55] and auxiliary partial LDLT (a second transplant) are also reported to treat SSFS[56]. Remedies when using small-for-size grafts are listed in Table 3.

Table 3 Remedies when using small-for-size graft.
Ref.nRemedy for using small-for-size graftStudy type
Botha et al[23] (2010)21Hemi-portocaval shunt can decrease SFSS incidenceRS
Goralczyk et al[24] (2011)22Posterior cavoplasty can decrease SFSS incidenceRS
Kim et al[47] (2017)160Preserving collateral veins on small-for-size graftsRS + PSM
Hessheimer et al[48] (2011)NSPortocaval shuntAE
Xiao et al[49] (2012)1Transjugular intrahepatic portosystemic shuntCR
Sato et al[50] (2008)4Portocaval shunt using ligamentum teresCR
Nutu et al[51] (2018)2Complete splenic embolizationCR
Badawy et al[52] (2017)164SplenectomyRS
Troisi et al[53] (2016)NSSplenic artery ligation, splenectomy, meso-caval shunt, spleno-renal shunt, portocaval shunt, and splenic artery embolizationSR
Xu et al[54] (2015)NSDual graftsRE
Gao et al[55] (2017)NSAdipose-derived mesenchymal stem cells tranplantationAE
Kobayashi et al[56] (2009)5Auxiliary partial liver transplantationCR

Generally, a GRWR < 0.8% is no longer a critical predictor for recipients and can even be lowered to 0.5%-0.6% if there are accompanying factors of PVP ≤ 15 mmHg, MHV reconstruction, or young donor age.

OLDER DONORS IN LDLT

Because LDLT allows more choices in the use of a suitable liver graft compared with OLT, elderly donors were rarely considered in the early years of transplantation. However, following the increasing demands for LDLT and the urgent need to save the lives of patients suffering from hepatic encephalopathy, the use of elderly liver grafts has been reported more frequently in recent years as a means to increase the donor pool and address high waiting list mortality[57]. In Japan, the percentages of donors older than 50 and 60 years were 18.1% and 4%, respectively[58]. It is expected that the number of older donors will increase in the future because of the continuing donor shortage[59].

The definition of older donors is quite different in different transplantation centers. In the present review, we define older donors as donors older than 50 years. Controversy exists regarding the use of livers from older donors. The liver regeneration rate is impaired in older donors (donor age ≥ 50 years) compared with young donors (donor age < 30 years), according to computed tomography (CT) volumetric data after LDLT at POD 7[60], and donor age (≥50 years) was independently correlated with impaired remnant liver regeneration at 3[61] and 6 mo in right-lobe LDLT[58]. Kawano Y et al[62] analyzed telomeres in the hepatocytes of 12 paired donor-recipients and found that donor age was a crucial factor affecting the sustainability of telomere length in hepatocytes after pediatric LDLT. Based on the conclusion that older donors were significantly associated with impaired liver regeneration, some researchers found that the recipients of grafts from donors older than 45-50 years old, along with a GW/SLV ratio < 35%-40%, had worse outcomes[63,64]. Yoshizumi T et al[65] established the following formula, called a predictive score, to evaluate the impact of donor age, graft size, and MELD score on prognosis: predictive score = 0.011 × graft weight (%) - 0.016 × donor age - 0.008 × MELD score - 0.15 × shunt (if present) - 1.757. Patients with a predictive score ≥ 1.3 had a lower incidence of postoperative complications and a better prognosis.

Additionally, more studies have shown that LDLT using older donors could induce more serious postoperative complications and higher mortality rates than transplants using younger donors[66-70]; similarly, having a donor older than the recipient by > 20 years is problematic[68]. Moreover, it has been reported that fibrosis progression in patients with recurrent hepatitis C tended to be faster after LDLT with grafts from older donors[71]. Donor age is an independent, strong prognostic factor in LDLT. However, other researchers found that grafts from older donors can be used safely, even though the regenerative capacity of older grafts is impaired when the donor age is ≥ 50 years[72-75] or even ≥ 55 years[76]. The impact of older donors on the 1- and 5-year survival of recipients is shown in Table 4.

Table 4 Older donors for living donor liver transplantation.
Ref.Definition of older donorsn (older vs young)One-year survival (older vs young)Five-year survival (older vs young)Study type
Tanemura et al[58] (2012)50 yr old101 (24 vs 77)Older donor livers might have impaired regenerative abilityRS
Ono et al[60] (2011)50 yr old15 (6 vs 9)Liver regeneration is impaired with age after donor hepatectomyRS
Akamatsu et al[61] (2007)50 yr old299 (62 vs 237)85.0% vs 93.0%72.0% vs 87.0%RS
Kawano et al[62] (2014)NS12Donor age is a crucial factor affecting telomere length sustainability in hepatocytes after pediatric LDLTPS
Imamura et al[63] (2017)NS198A worse outcome might be associated with aging of the donorRS
Dayangac et al[64] (2011)50 yr old150 (28 vs 122)78.6% vs 83.4%NSRS
Yoshizumi et al[65] (2008)NS28Graft size, donor age, and patient status are the indicators of early graft functionRS
Han et al[66] (2014)55 yr old604 (26 vs 578)Median OS (M): 31.2 ± 31.3 vs 50.6 ± 40.6RS
Kamo et al[67] (2015)60 yr old1597 (69 vs 1528)69.5% vs 81.2%62.0% vs 79.3%RS
Shin et al[68] (2013)Donor-recipient age gradient > 20821Worse graft survival was observed if the donor is older than the recipient by > 20RS
Kubota et al[69] (2017)50 yr old315 (126vs 189)73.0% vs 80.9%39.7% vs 47.1%RS
Katsuragawa et al[70]NS24G/SLV and donor age were independent factors that affected graft survival ratesRS
Wang et al[72] (2015)50 yr old159 (10 vs 149)100% vs 93.0%90.0% vs 87.0%RS
Ikegami et al[73] (2008)50 yr old232 (32 vs 200)80.0% vs 81.7%73.8% vs 76.7%RS
Li et al[74] (2012)50 yr old129 (21 vs 108)90.0% vs 86.0%66.0% vs 75%RS
Goldaracena et al[75] (2016)50 yr old469 (91 vs 378)92.0% vs 96.0%83.0% vs 79.0%RS
Kim et al[76] (2017)55 yr old540 (42 vs 498)95.2% vs 94.6%NSRS

While donor age is a controversial topic, the impaired regenerative capacity of older grafts has been confirmed in some studies. According to these previous studies, older liver grafts can be prudent candidates but cannot be used in the presence of other marginal conditions (e.g., small-for-size grafts or moderate and severe steatosis). More high-quality and prospective studies are needed on this topic.

ABO-INCOMPATIBLE LDLT

Although more high-quality liver grafts are available for patients in LDLT than in OLT, donors are restricted to family members or domestic relationships in many transplantation centers because of ethical norms. ABO-incompatible LTs are performed only in emergencies, when ABO-compatible grafts are unavailable. Therefore, breaking ABO blood group barriers becomes inevitable. ABO-incompatible LT was first performed and reported by Starzl et al[77], and no acute rejections were observed after transplantation. Subsequently, ABO-incompatible LT gradually began to be performed in some LT centers, and hyperacute rejection was commonly reported[78,79].

In addition to antibody-mediated rejection, ABO-incompatible LDLT can involve other complications. Thrombotic microangiopathy (TMA) is a rare complication following LT, but it is reported to have a slightly higher incidence in ABO-incompatible LDLT[80-82]. ABO incompatibility, cyclophosphamide and recipient blood group (type O) are closely correlated with the occurrence of TMA[80,82]. The incidence of TMA is 37.9% following ABO-incompatible LDLT and 0.0%-2.8% following ABO-compatible LDLT (OR = 44.7)[80]. The elevation of fibrinolytic function markers, such as plasminogen activator inhibitor type 1, can be considered a predictor of TMA following LDLT. The incidence of biliary tract complications is more common than that of TMA. Biliary strictures are one of the most important complications associated with ABO incompatibility, with reported incidence rates between 15.8% and 20.7%[83,84]. An isoagglutinin attack on the graft vascular endothelium can result in ischemic cholangiopathy, and isoagglutinin can even directly attack the endothelium of the graft bile duct[85,86]. CT scans can provide a clear indication of biliary strictures in ABO-incompatible LDLT[87]. Yamada Y et al[88] reported a case of idiopathic hypereosinophilic syndrome following ABO-incompatible LDLT. The patient suffered from portal vein thrombosis on postoperative day 10, and the histopathological findings of the thrombus revealed dense eosinophilic deposition. Studies on the impact of ABO incompatibility on LDLT are listed in Table 5.

Table 5 Impact of ABO-incompatible on living donor liver transplantation.
Ref.nComplicationsIncidence of related complication (%)Risk factorsStudy type
Miyata et al[80] (2007)57Thrombotic microangiopathy7.0ABO-incompatibility, CPA, and recipient blood group (type O)RS
Oya et al[81] (2008)1Thrombotic microangiopathyNSABO-incompatible LDLT (type B to O)CR
Kishida et al[82] (2016)129Thrombotic microangiopathy10.1ABO-incompatible, tacrolimusRS
Song et al[83] (2014)1102Biliary stricture15.8ABO-incompatible, acute cellular rejectionRS
Ikegami et al[84] (2016)408Biliary stricture20.4ABO-incompatibleRS
Yamada et al[88] (2010)1Idiopathic hypereosinophilicNSABO-incompatibleCR

Despite serious complications, ABO-incompatible LDLT can be a feasible option for patients if certain essential treatments are included[89,90]. Rituximab, an anti-CD20 immunoglobulin (IgG)1 terminating B-lymphocytes with an affinity for IgG Fc receptor (FcγR), is a critical strategy in the regimens for desensitization for ABO-incompatible LDLT and yields outcomes for ABO-incompatible LDLT that are similar to those for ABO-compatible LDLT[91,92]. Rituximab is given for 3 d[93], 3 wk, or even as soon as a suitable donor that is ABO-compatible is selected[94] at a dosage of 375 mg/m2. In the early stage of transplantation, rituximab was usually given along with one or more other protocols, such as a splenectomy[95,96], plasma exchanges[97-102], intravenous IgG[100,103], and intrahepatic arterial infusion of prostaglandin E1[92,104,105]. In some recent studies, pre-transplant rituximab and/or basiliximab monotherapy, without additional treatments, also yielded outcomes that are comparable to those of procedures with additional treatments[106]. The affinity between IgG Fcγ Receptor (FcγR) and rituximab, however, is influenced by the single-nucleotide polymorphisms (SNPs) of FcγR. SNPs of FCGR2A (131H/R) and FCGR3A (158F/V) are the alleles that encode FcγR. FCGR2A (131H/H) had a higher affinity for IgG1 than FCGR2A (131H/R or R/R). Accordingly, patients with FCGR2A (131H/H) have a better reaction to the effects of rituximab on B cells[91]. The treatment results of ABO-compatible LDLT are summarized in Table 6.

Table 6 Remedies when using ABO- incompatible on living donor liver transplantation.
Ref.nImmunosuppression strategyRemediesConclusionStudy type
Kawagishi et al[89] (2009)105TAC + MP + AZRituximabABO-incompatible LDLT can be feasible used if humoral rejection are overcomeRS
Yoon et al[90] (2018)918TAC + MP + steroidsRituximab and PEABO-incompatible LDLT is a feasible option under remediesRS
Sakai et al[91] (2017)20TAC+ MPRituximab and PEFCGR SNPs influence the effect of rituximab on B-cellsPS
Egawa et al[92] (2017)33TACRituximab, PE, local infusion, splenectomy and immunoglobulinsOnly rituximab dose is a significantly favorable factor for AMRRS
Ikegami et al[93] (2007)1TAC + MP + steroidsRituximab and PERituximab and plasma exchanges seemed ineffectiveCR
Ikegami et al[94] (2009)7TAC + MP + steroidsRituximab, IVIG, and PERituximab, IVIG, and PE seems to be a safe treatmentRS
Usui et al[95] (2007)73TAC + MP + steroidsRituximab, PE and splenectomyBone suppression is a big challenge when using rituximabRS
Chen et al[96] (2017)2TAC + MP + steroidsBasiliximab combine with splenectomyABO-i LDLT with splenectomy is undoubtedly life-savingCR
Uchiyama et al[97] (2011)15TAC + MP + steroidsRituximab and PEIsoagglutinin mediated-rejection should be more concernedRS
Soin et al[98] (2014)3TAC + MP + steroidsRituximab and PEABO-incompatible LDLT is a feasible option under remediesCR
Rummler et al[99] (2017)10TAC + MP + steroidsPEImmunosuppression only combining with PE is feasibleRS
Kim et al[100] (2016)182TAC + MP + steroidsRituximab, IVIG, and PEABO-incompatible LDLT can be safely performed under remediesRS
Kim et al[101] (2013)22TAC + MP + steroidsRituximab and PEABO-incompatible LDLT can be safely performed under remediesRS
Kawagishi et al[102] (2005)3TAC + MP + steroidsRituximab and PEABO-incompatible LDLT can be safely performed under remediesCR
Kim et al[103] (2017)43TAC + MP + steroidsRituximab and IVIGA simplified protocol using rituximab and IVIG for ABO-I LDLT is safeRS
Yoshizawa et al[104] (2005)8TAC + MP + cyclophosphamideRituximab and PGE1 infusionRituximab prophylaxis and HA infusion therapy is feasibleRS
Egawa et al[105] (2008)118TAC + steroidsMethylprednisolone and PGE1 infusionRecipients with preexisting high effector CD8 T- cells are unfavorable candidates for ABO-I LDLTRS
Yamamoto et al[106] (2018)40TAC + MP + steroidsRituximab monotherapyRituximab monotherapy is feasibleRS

These findings reveal that rituximab monotherapy in ABO-compatible LDLT is feasible, but it is better to test the SNPs of FcγR; otherwise, multiple treatments, such as plasma exchanges and intravenous IgG, must be performed in addition to rituximab if there is a lower affinity between IgG FcγR and rituximab. There is still a lack of more persuasive evidence to confirm the feasibility of splenectomy in conjunction with ABO-compatible LDLT treatments.

LIVER GRAFT STEATOSIS

Steatosis is a common feature used to identify marginal liver function, and reports on the utility of steatotic liver grafts in clinical practice have yielded controversial results. The use of steatotic liver grafts has been confirmed to have a significant relationship with increased complications and poorer outcomes[107,108]. Traditionally, steatotic livers with > 60% fat must be discarded. Livers with < 30% fat are feasible and anticipated to have good function. Livers with 30%-60% fat have poor results, with decreased graft survival and decreased patient survival[109]. Moreover, hepatic steatosis is reported to be a leading cause of donor rejection in LDLT[110]. In some transplantation centers, approximately 40% of donor grafts are discarded because of severe liver steatosis[9]. Because of the release of inflammatory cytokines and inhibition of the capacity to differentiate steatosis hepatocytes, the early regenerative capacity of the remnant liver is injured, and, as a result of impaired hepatocyte replication, compensatory expansion of hepatic progenitor cells occurs during steatotic liver regeneration after LDLT[111]. Furthermore, Cho et al[112] confirmed that hepatic steatosis is associated with intrahepatic cholestasis and transient hyperbilirubinemia during regeneration after LDLT. In this study, 67 LDLT recipients examined on POD 10 were scored based on the numbers of portal tracts per area of liver tissue and intrahepatic cholestasis, and the preoperative degree of macrovesicular steatosis was found to be independently associated with cholestasis after LDLT. However, these researchers also found that the long-term capacity of hepatocyte regeneration was not impaired after LDLT with mild macrovesicular steatosis grafts[113]. Based on this finding, some recent studies have found that moderately steatotic liver grafts and donors with a BMI ≥ 30 kg/m2 are not contraindications for LDLT, and complications and survival are not significantly different compared with those associated with non-steatosis grafts[114,115]. Moreover, the risk of steatosis was determined by the presence of microsteatosis and macrosteatosis, rather than the total quantitative degree of steatosis. The grafts with high microsteatosis (30%) mixed with macrosteatosis showed no significant difference in postoperative biochemical liver function, 2-wk graft regeneration, postoperative complications, and 5-year survival[116]. The studies on the impact of graft steatosis on LDLT outcomes are listed in Table 7.

Table 7 Impact of graft steatosis on living donor liver transplantation.
Ref.nConclusionStudy type
Dirican et al[9] (2015)161Approximately 40% of donor grafts are discarded because of severe liver steatosisRS
Perkins et al[109] (2006)NSTypically steatotic livers with > 60% fat are not transplanted; with < 30% fat are usable and anticipated to have good function; with 30%-60% fat give poor resultsComments
Kotecha et al[110] (2013)340Hepatic steatosis is a leading cause of donor rejection in LDLTPS
Cho et a[111]l (2010)54Hepatocyte replication is impaired during steatotic liver regeneration after LDLTPS
Cho et al[112] (2006)67Hepatic steatosis is associated with intrahepatic cholestasis and transient hyperbilirubinemia during regenerationPS
Cho et al[113] (2005)55Mildly steatotic graft did not increase the risk of graft dysfunction or morbidity in LDLTPS
Gao et al[114] (2009)24Moderately steatotic (30%-60%) liver grafts provide adequate function in the first phase after transplantation and can be used for transplantationRS
Knaak et al[115] (2017)105Donors with BMI > 30, in the absence of graft steatosis, are not contraindicated for LDLTRS
Han et al[116] (2015)211The risk of steatosis may be determined by the relative composition of MiS and MaS, rather than the total quantitative degreeRS

To decrease the risk associated with fatty liver grafts, especially with severe steatosis, some treatments are suggested (Table 8). According to Oshita et al[117], donors who are diagnosed with hepatic steatosis pre-transplantation should undergo a diet treatment consisting of an 800-1400 kcal/d diet and a 100-400 kcal/d exercise regimen without drug treatment with a target body mass index of 22 kg/m². After these strategies, the average BMI was reduced from 23.3 ± 0.6 to 21.9 ± 0.4 kg/m². The liver biopsy results of most of these donors showed stage 0/1 fibrosis and minimal/mild steatosis after the diet therapy. In addition, surgical outcomes and overall survival did not significantly differ between the recipients of grafts from non-steatosis and diet-treated donors (with steatosis). In another study, bezafibrate (400 mg/d) was used along with a protein-rich (1000 kcal/d) diet and exercise (600 kcal/d) for 2-8 wk[118]. Even severely steatotic livers could be used for LDLT grafting subsequent to this short-term treatment regimen. Furthermore, a 1200 kcal/d diet and a minimum of 60 min/d of moderate cardio training are also recommended to rapidly reverse liver steatosis in donors[119]. In addition to lifestyle and dietary changes, dual-graft LDLT was reported when one donor had severe liver steatosis and another had a low GRWR[120].

Table 8 Treatments for fat donors.
Ref.nTreatmentsStudy type
Oshita et al[117] (2012)128Diet treatment consisting of an 800 to 1400 kcal/d diet and a 100 to 400 kcal/d exercise regimen without drug treatment, targeting body mass index of 22 kg/m²RS
Nakamuta et al[118] (2013)11Bezafibrate (400 mg/d) was used along with a protein-rich (1000 kcal/d) diet and exercise (600 kcal/d) for 2-8 wkRS
Choudhary et al[119] (2015)161200 kcal/d and a minimum of 60 min/d of moderate cardio training are also recommended to rapidly reverse liver steatosis in donorsPS
Moon et al[120] (2006)2Dual-graft living donor liver transplantation for severe graft steatosisCR

In conclusion, steatosis in the donor must be thoroughly evaluated before LDLT, either by biopsy or imaging diagnosis. The proportion of macrosteatosis is now considered a crucial predictor of the prognosis of recipients. If there are no further options, donors with hepatic steatosis can reach donation criteria through lifestyle and dietary changes in a short time.

CHRONIC HEPATITIS OF GRAFTS

The use of liver grafts that test positive for chronic hepatitis or other blood disseminated diseases found in epidemic areas is usually inevitable in cases of organ shortages associated with OLT. However, because LDLT recipients, to some degree, have more choices regarding his/her donors, there are a few studies reporting on HBsAg or HBcAb(+) liver grafts, while no studies refer to HCV-positive living liver grafts.

HBsAg(-) LDLT patients who have received HBsAg or HBcAb(+) grafts have a high risk of de novo HBV infection after transplantation (Table 9). However, these grafts are still considered to be safe and feasible with antiviral prophylaxis in both adult and pediatric LDLT[121-126]. Patients were given HBV vaccinations to achieve anti-HBs > 1000 IU/L pre-transplantation and > 100 IU/L post-transplantation, with a standard post-transplantation treatment regimen of high-dose hepatitis B IgG, lamivudine and/or adefovir (in cases of lamivudine resistance)[126]. Specifically, some studies have proposed a new strategy; specifically, patients with a pre-transplantation anti-HB titer > 1000 IU/L do not need post-transplantation prophylaxis; patients with a low pre-transplantation titer, < 1000 IU/L, should be given lamivudine post-transplantation (at a dose of 100 mg/d or 3 mg/kg/d for at least 2 years after transplantation) or adefovir prophylaxis (with lamivudine at a dose of 10 mg/d if a mutant strain for lamivudine is identified) and, hopefully, will respond appropriately to post-transplantation vaccinations by maintaining anti-HB titers > 100 IU/L; and low titer non-responders (anti-HB titer < 100 IU/L despite vaccination) should be given continuous lamivudine or adefovir indefinitely[121]. In some transplantation centers, nucleotide analogs (lamivudine) are routinely used first if HBsAg(-) LDLT patients receive HBsAg or HBcAb(+) grafts, regardless of the anti-HB titer, for at least 2 years. Moreover, patients who had a YMDD mutation were given adefovir combined with lamivudine[123]. Hara Y et al[127] reported one patient who experienced spontaneous eradication of de novo HBV after LDLT with an HBcAb(+) graft without any treatment. This 8-year-old female patient (HBsAg-negative) underwent LDLT, received an HBcAb(+) left-lobe graft, and was subsequently infected with HBV. Sixteen years after LDLT, her serological HBV status was as follows: HbsAg(-), HBsAb(+), HBeAb(-), HBeAb(+), HbcAb(+), and HBV DNA(-). In another study, recipients with HCV genotype 2 infections who had received an HBcAb(+) graft were given sofosbuvir and ribavirin, along with hepatitis B IgG to prevent recurrence of HCV and HBV[128].

Table 9 Impact of HBsAg or HBcAb(+) grafts on HBsAg(-) living donor liver transplantation patients.
Ref.DonorIncidence of de novo HBV infection (%)Prevention of de novo HBV infectionStudy type
Wang[121] (2017)HBcAb(+)4.2HBV vaccinations with the aim of achieving anti-HBs > 1000 IU/L pre-transplant and > 100 IU/L post-transplantRS
Xi et al[122] (2013)HBcAb(+)23.9No prophylaxis, adefovir, and lamivudine are given to de novo patientsRS
Dong et al[123] (2017)HBcAb(+)7.9HBIG 100 IU/kg during the operation and lamivudine 3 mg/kg per day after the surgery for at least 1 year until HBV vaccine reactionRS
Loggi et al[124] (2016)HBsAg(+)NSHBIG and lamivudine, adefovir or tenofovirSR
Lei et al[125] (2013)HBcAb(+)15.0No specific prophylaxisRS
Lin et al[126] (2007)HBcAb(+)3.3Lamivudine monoprophylaxis, HBV vaccinationsRS
Hara et al[127] (2016)HBcAb(+)NSLamivudine first and adefovir dipivoxil were combined with lamivudine 2 yr laterCR

In HbsAg(+) LDLT patients who receive HBsAg or HBcAb(+) grafts, the antiviral protocol must be performed as for HBsAg(-) LDLT patients to maintain the HBV DNA at a low or negative level, despite the persistence of the HBV marker (HBsAg). High-dose HBV IgG, lamivudine, famciclovir, and interferon were recommended (Table 10)[129-131].

Table 10 Impact of HBsAg or HBcAb(+) grafts on HBsAg(+) living donor liver transplantation patients.
Ref.DonorIncidence of de novo HBV infectionPrevention of De Novo HBV infectionStudy type
Hwang et al[129] (2006)HBsAg(+)NSHigh-dose HBIG and lamivudine, famciclovir and interferon; a final regimen of lamivudine and adefovirCR
Soejima et al[130] (2007)HBsAg(+)NSlamivudine and adefovir dipivoxilCR
Jeng et al[131] (2015)HBsAg(+)NSEntecavir 0.5 mg once dailyRS

Populations with HBsAg-negative/HBcAb-positive and undetectable serum HBV DNA have been gradually increasing over the past several decades. Most patients are now considered to have a covert HBV infection and have a high risk of HBV reactivation when treated with a robust immunosuppressive agent[132]. Therefore, the use of HBsAg-negative/HBcAb-positive liver grafts has a high risk of de novo HBV for HBsAg(-) recipients. However, with active immunization and an antiviral protocol, the HBsAg-negative/HBcAb-positive liver grafts can be transplanted safely.

GRAFTS WITH A BENIGN HEPATIC TUMOR

Usually, there are rare recipients of LDLT or doctors who are willing to make an active choice to use a graft with an undetermined tumor. This is not only an ethical issue but also indicates a high risk for recipients to face rapid dysfunction of their liver grafts. However, if recipients are in an emergency situation and have no other proper donors, grafts with benign tumors may be a last choice. Li G et al[133] recently reported on 15 consecutive recipients using an otherwise discarded, partial liver resection graft with a benign hepatic tumor. These benign tumors are as follows: Cavernous hemangioma, perivascular epithelioid cell tumor, inflammatory pseudotumor, and focal nodular hyperplasia. One patient died from a pulmonary embolism, and the other 14 patients had a good prognosis. Additionally, a vanishing tumor in a liver graft from an HBV(+) donor was observed. Contrast-enhanced magnetic resonance imaging (MRI) showed hypervascularity in the arterial phase and in the hepatobiliary phase, the tumor showed a low intensity, findings similar to those in HCC. Regardless, the graft with suspected HCC was accepted by the recipient, and the tumor disappeared completely within several months after LDLT[134].

For LDLT patients using grafts with a benign hepatic tumor, only two observational studies with a small sample size are present in the literature (Table 11). It seems that grafts with benign tumors are feasible in some conditions, but more studies with long-term follow-ups are needed to evaluate the safety of these marginal grafts.

Table 11 Graft with hepatic benign tumor.
Ref.nType of tumors in graftsPrognosisStudy type
Li et al[133] (2017)15Cavernous hemangioma, perivascular epithelioid cell tumor, inflammatory pseudotumor, and focal nodular hyperplasiaOne patient died from pulmonary embolismOS
Fuchino et al[134] (2017)1HBsAg(+) and inflammatory pseudotumorTumor vanished after 3 yrCR
CONCLUSION

To our knowledge, this is the first review on marginal donors specifically for LDLT. This review, which includes cohort studies, case-control studies, and case reports on marginal liver grafts in LDLT, demonstrated that marginal grafts are a feasible way to expand the options for patients on LT waiting lists in emergency situations (e.g., liver failure or hepatic encephalopathy); however, these grafts place the recipients at a greater risk of liver dysfunction. Some indispensable treatments are needed to address the deficiencies of these grafts.

There are some new findings in this review: (1) It is permissible for the GRWR to be as low as 0.5%-0.6% (not 0.8%, as currently specified) if PVP is controlled under 15 mmHg; otherwise, outflow reconstruction is needed. (2) There is controversy surrounding older liver grafts. These grafts can be used prudently, but other marginal conditions must be absent (e.g., small-for-size grafts or moderate and severe steatosis). (3) Splenectomy is no longer necessary when an ABO-incompatible LDLT is performed. Rituximab monotherapy is even confirmed to be an effective treatment if there is a high affinity between IgG FcγR and rituximab. (4) Total steatosis of liver grafts is not a proper predictor of prognosis. Instead, the presence of microsteatosis and macrosteatosis is a crucial factor. Donors with steatosis of the liver can meet the donation criteria through lifestyle and dietary changes before surgery. (5) HbsAg or HbcAb(+) grafts increase the risk of de novo HBV infection after transplantation in HBsAg(-) LDLT patients but can also be used safely with active immunotherapy. And (6) Grafts with benign tumors that have been discarded from other patients are feasible, but the long-term prognosis cannot be determined.

According to the new findings of this review listed above, we summarized a selection of strategies for different types of marginal liver grafts in LDLT and their related treatments (Figure 1). With this review, based on more than 100 references, we expect that the transplantation pool can be effectively and safely expanded in the situation of organ shortage.

Figure 1
Figure 1 Selective strategies and remedies of using marginal donors in living donor liver transplantation.
ACKNOWLEDGMENTS

We thank Dr. Lunan Yan (Department of Liver Surgery and Liver Transplantation Center, West China Hospital of Sichuan University) for the assistance with data collection.

Footnotes

Manuscript source: Invited manuscript

Specialty type: Gastroenterology and hepatology

Country of origin: China

Peer-review report classification

Grade A (Excellent): 0

Grade B (Very good): B, B

Grade C (Good): C

Grade D (Fair): 0

Grade E (Poor): 0

P- Reviewer: Chiu KW, Kanda T, Qi XS S- Editor: Wang XJ L- Editor: Filipodia E- Editor: Huang Y

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