[Pathophysiology and strategy for small-for-size graft syndrome after living-donor liver transplantation]

Abstract

Small-for-size (SFS) graft syndrome is an important problem after living-donor liver transplantation in adults. Hemodynamic change is thought to be the main cause of graft injury. Excessive portal flow is associated with hepatic sinusoidal injury, and reduction of portal flow improves postoperative liver function. Increased venous outflow due to hepatic venoplasty or reconstruction of the middle hepatic vein decrease the risk of graft congestion. However, the intragraft acute-phase response remains unclear. Recent studies have revealed that downregulation of heat shock protein (HSP) may account for SFS graft injury, and induction of HSP may prevent SFS syndrome. On the other hand, derangement in the regulation of liver regeneration is recognized as another important factor. Further investigation of the regulatory mechanisms of liver regeneration in SFS grafts may suggest a strategy for the prevention and treatment of SFS syndrome. Successful transplantation of marginal-size liver grafts would improve outcome for recipients and increase the margin of safety for living donors.