Small-for-size partial liver graft in an adult recipient; a new transplant technique

Boillot, Olivier; Delafosse, B.; Mechet, Isabelle; Boucaud, Catherine; Pouyet, M

doi:10.1016/s0140-6736(02)07593-1

Cited by 223 publications

(193 citation statements)

References 4 publications

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“…Also, PTX improved the survival from 0% to 60% in a non-heart-beating rat liver transplantation model with 60 min warm ischemia plus 9 h cold ischemia (29). It is tempting to correlate these findings with a number of clinical observations showing increased portal pressure and possibly flow in smallfor-size OLT, with a beneficial effects of a variety of strategies decreasing portal pressure such as porto-systemic shunt (30). We would postulate here that high portal pressure͞flow induces arterial vasoconstriction as shown in many studies looking at the respective role of portal and arterial flow to the liver (31)(32)(33).…”

Section: Discussionmentioning

confidence: 91%

Kupffer cell-dependent TNF-α signaling mediates injury in the arterialized small-for-size liver transplantation in the mouse

Tian¹,

Jochum

Georgiev³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Implantation of small liver grafts causes liver injury and defective regeneration leading to graft failure. We investigated whether Kupffer cell-dependent TNF-␣ signaling contributes to this poor outcome. Partial 30% liver transplantation was performed in C57BL͞6 wild-type mice (control group), and in three groups with down-regulation of the TNF-␣ pathway: (i) TNF receptor 1 knockout [TNFR-1(؊͞؊)] mice, and mice pretreated with (ii) gadolinium chloride or (iii) pentoxifylline (PTX). Fifty-percent partial liver transplantation, a model associated with full recovery, and transplantation in IL-6 knockout [IL-6(؊͞؊)] mice were performed in some experiments. Graft injury, regeneration, portal flow, liver microcirculation, leukocyte adhesion, and animal survival were assessed. Animal survival rates were 14% in the control group vs. 43% in the gadolinium chloride group, 57% for the TNFR-1(؊͞؊) group, and 86% in the PTX group (P < 0.001). Markers of liver injury were reduced in all treated groups when compared with controls. Each treated group disclosed better portal flow and sinusoid perfusion, decreased leukocyte adherence, particularly in the PTX group. Liver regeneration occurred only in the treated groups. IL-6 and IL-10 levels were dramatically up-regulated (50؋) in the PTX group, and at lower levels in other experimental groups. The protective effect of PTX was lost in IL-6(؊͞؊) mice and protection was restored by a single dose of r-IL-6. In conclusion, interruption of TNF-␣ signaling or depletion of Kupffer cells improves survival after 30% liver transplantation, reduces liver injury, and enhances regeneration. The superior effects of PTX are mediated by IL-6.

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Section: Discussionmentioning

confidence: 91%

Kupffer cell-dependent TNF-α signaling mediates injury in the arterialized small-for-size liver transplantation in the mouse

Tian¹,

Jochum

Georgiev³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…A trial of side-to-side mesocaval shunt construction with downstream ligation of the superior mesenteric vein has been reported to reduce portal overperfusion in the graft. 17 By the same token, construction of other collaterals, such as the creation of a distal splenorenal shunt, might be useful. Our preliminary results with regard to early posttransplant PVP measurements indicate that recipients with cirrhotic livers tend to have persistently elevated PVPs, even after graft implantation, despite the presence of abundant collaterals.…”

Section: Inflow Control Versus Collateral Constructionmentioning

confidence: 99%

Small-for-size graft in living donor liver transplantation: How far should we go?

Kiuchi

Tanaka

Ito

et al. 2003

Liver Transplantation

226

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With the extensive use of living donor liver grafts in adult patients, controversy over small-for-size syndrome has escalated in recent years. Although several symptoms have been suggested as manifestations of the syndrome, smallfor-size syndrome remains difficult to diagnose because these symptoms are neither specific nor inevitable. The occurrence of small-for-size syndrome also seems to depend on a number of recipient and graft factors. Potential pathogenic mechanisms include persistent portal hypertension and portal overperfusion. At present, several techniques are being explored in an attempt to ameliorate the impact of small-for-size syndrome. Recent experience suggests that the occurrence of small-for-size syndrome is multifactorial and that complications relating to smallfor-size grafts should be examined in relation to a variety of graft, recipient, and technical factors. (Liver Transpl 2003;9:S29-S35.)B efore split or living donor liver transplantation (LDLT) became commonplace, liver grafts were generally thought to adapt well to graft size mismatching. 1 Moreover, an early study documented adaptation in a series of LDLT patients in whom transplanted livers were observed to approach expected/standard liver volumes with time, regardless of whether the grafts were small or large for size. 2 Problems related to smallfor-size (SFS) grafts, however, have gradually come to light with expansion of LDLT to larger pediatric and adult patient populations. 3,4 Controversy regarding the pathogenesis, clinical manifestations, and management of SFS graft syndrome has escalated in recent years, which has been in parallel with the spread of larger right liver grafts. The incidence and clinical relevance of problems related to SFS grafts needs to be further evaluated. This article outlines a current concept on this syndrome in our program, in which living donor grafts have been almost exclusively used for the past 12 years. Definition of SFS GraftThe origin of the term SFS syndrome is not clear. However, indiscriminate use of this term should be avoided. Because partial liver grafts, unless the recipients are small children, are always SFS grafts, overuse of this term creates a risk of attributing all negative sequelae to the size of the graft without exploring other causes. In evaluating outcome, surgical error and inadequate posttransplantation management, regardless of whether they are related to anatomic problems of partial graft, should be strictly excluded. However, unfortunately, identification of the exact cause of negative events is often not possible. Nonetheless, only those negative events that can be exclusively attributed to a shortage of functional graft mass should be included in any evaluation of SFS syndrome.Graft-to-recipient weight ratio (GRWR) of less than 0.8% to 1.0%, or less than 30% to 50% of standard/ estimated liver volumes, have been used to define SFS grafts in previous reports. 3-7 However, recipient, donor, and graft variables, which might influence the success of SFS grafts, have not bee...

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“…The ongoing debate on the causes of the small-for-size syndrome mainly focuses on portal hyperperfusion with high intravascular shear stress [9][10][11]. To avoid liver failure by portal hyperperfusion, techniques for reduction of portal inflow, such as portal-caval and mesocaval shunts, splenic artery ligation, and splenectomy have been established [12][13][14]. As the splenic fraction accounts for up to 52% of the total portal venous inflow [15], its contribution to portal hypertension is evident.…”

Section: Introductionmentioning

confidence: 99%

Splenectomy improves survival by increasing arterial blood supply in a rat model of reduced-size liver

Eipel¹,

Abshagen²,

Ritter³

et al. 2010

Transplant International

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Small-for-size partial liver graft in an adult recipient; a new transplant technique

Cited by 223 publications

References 4 publications

Kupffer cell-dependent TNF-α signaling mediates injury in the arterialized small-for-size liver transplantation in the mouse

Kupffer cell-dependent TNF-α signaling mediates injury in the arterialized small-for-size liver transplantation in the mouse

Small-for-size graft in living donor liver transplantation: How far should we go?

Splenectomy improves survival by increasing arterial blood supply in a rat model of reduced-size liver

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