Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) is a great innovation in hepatic surgery, providing short-term curative resection opportunities for patients with previously unresectable liver tumors [1, 2]. Despite existing controversy, ALPPS has been increasingly applied in hepatic surgery in recent years, extending to hepatocellular carcinoma (HCC) with chronic liver disease [3–8]. In China, HCC is a major indication, and the experience of ALPPS in this patient population mainly comes from China’s contribution [4, 9–14]. In recent years, with reports from large Chinese liver cancer centers and evidence generated by clinical studies, including randomized controlled trials (RCT), the effectiveness of ALPPS for HCC has been elucidated [4, 10–14]. According to China’s practical experience, in highly selective patients, ALPPS enables optimal clinical outcomes. The overall safety profile has been significantly improved compared to early years, with satisfactory tumor resection and R0 resection rates. Mid/long-term survival benefits are reassuring, better than nonsurgical treatments such as transarterial chemoembolization (TACE), equivalent to the postoperative survival of those undergoing one-stage hepatectomy, and superior or non-inferior to traditional two-stage hepatectomy (TSH), including portal vein embolization (PVE)-TSH and TACE-PVE-TSH [4, 10–14]. For HCC patients with no or mild chronic liver disease, ALPPS can effectively induce future liver remnant (FLR) hypertrophy, and its effectiveness and safety are comparable to those of colorectal cancer liver metastasis (CRLM) and other tumors. However, the application of ALPPS for severe liver fibrosis or cirrhosis remains challenging. Studies have shown that FLR growth is negatively correlated with the severity of liver fibrosis/cirrhosis [3, 4, 10, 11]. The more severe the fibrosis/cirrhosis, the less potent the FLR induction. These patient populations often have limited FLR regeneration, predisposing them to ALPPS failure. Data reported by the International ALPPS Registry (35 HCC cases) showcased that the FLR kinetic growth ratios (KGR) in patients with cirrhosis and METAVIR grade 3 liver fibrosis were only (1.52 ± 0.40) mL/d and (2.98 ± 0.65) mL/d, respectively. In contrast, those in patients without fibrosis/cirrhosis and those with METAVIR grade 1 liver fibrosis were (30.94 ± 10.95) mL/d and (12.34 ± 4.38) mL/d, respectively [3]. Report from Zhongshan Hospital, Fudan University (45 HCC cases) also revealed that the median FLR KGR of patients with cirrhosis (METAVIR grade 4) and METAVIR grade 3 liver fibrosis were 9.6 mL/d and 19.8 mL/d, respectively. In comparison, patients with normal liver parenchyma (METAVIR grade 0) had a KGR of 50.1 mL/d [4]. Furthermore, it was found that the KGR of these patients in the second week after stage 1 ALPPS was usually significantly lower than that in the first week postoperatively. Due to limited FLR hypertrophy, the time required for liver regeneration in these patients was significantly longer than that in cases with normal livers (14 days vs. 7 days) [4]. A longer interstage interval is associated with tumor progression. Furthermore, the change of portal vein-arterial blood supply led by portal vein ligation (PVL) also exerts oncological effects. There is a compensatory increase in hepatic artery perfusion after PVL, and the tumor may grow with the increase in arterial blood supply [15–17]. This is more common when ALPPS is used to treat HCC (mostly large HCC). These factors often lead to a higher incidence of surgical failure or post-hepatectomy liver failure (PHLF) when ALPPS is used in this population. In the authors’ center, before the emergence of the new transarterial embolization salvaged ALPPS (TAE-salvaged ALPPS), two HCC patients failed to achieve sufficient FLR hypertrophy 3–4 weeks after stage 1 ALPPS and were unable to undergo the stage 2 surgery, thus being converted to other treatments; another HCC patient directly developed PHLF after stage 1 ALPPS [4]. In China, HCC patients are often complicated by chronic liver diseases such as liver fibrosis and cirrhosis. The implementation of ALPPS in patients with cirrhosis or severe fibrosis remains challenging, and appropriate solutions are urgently needed.

TAE-Salvaged ALPPS (Zhou’s ALPPS)

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发表日期：

2025年

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Jian Zhou,
Yuanfei Peng

摘要

Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) is a great innovation in hepatic surgery, providing short-term curative resection opportunities for patients with previously unresectable liver tumors [1, 2]. Despite existing controversy, ALPPS has been increasingly applied in hepatic surgery in recent years, extending to hepatocellular carcinoma (HCC) with chronic liver disease [3–8]. In China, HCC is a major indication, and the experience of ALPPS in this patient population mainly comes from China’s contribution [4, 9–14]. In recent years, with reports from large Chinese liver cancer centers and evidence generated by clinical studies, including randomized controlled trials (RCT), the effectiveness of ALPPS for HCC has been elucidated [4, 10–14]. According to China’s practical experience, in highly selective patients, ALPPS enables optimal clinical outcomes. The overall safety profile has been significantly improved compared to early years, with satisfactory tumor resection and R0 resection rates. Mid/long-term survival benefits are reassuring, better than nonsurgical treatments such as transarterial chemoembolization (TACE), equivalent to the postoperative survival of those undergoing one-stage hepatectomy, and superior or non-inferior to traditional two-stage hepatectomy (TSH), including portal vein embolization (PVE)-TSH and TACE-PVE-TSH [4, 10–14]. For HCC patients with no or mild chronic liver disease, ALPPS can effectively induce future liver remnant (FLR) hypertrophy, and its effectiveness and safety are comparable to those of colorectal cancer liver metastasis (CRLM) and other tumors. However, the application of ALPPS for severe liver fibrosis or cirrhosis remains challenging. Studies have shown that FLR growth is negatively correlated with the severity of liver fibrosis/cirrhosis [3, 4, 10, 11]. The more severe the fibrosis/cirrhosis, the less potent the FLR induction. These patient populations often have limited FLR regeneration, predisposing them to ALPPS failure. Data reported by the International ALPPS Registry (35 HCC cases) showcased that the FLR kinetic growth ratios (KGR) in patients with cirrhosis and METAVIR grade 3 liver fibrosis were only (1.52 ± 0.40) mL/d and (2.98 ± 0.65) mL/d, respectively. In contrast, those in patients without fibrosis/cirrhosis and those with METAVIR grade 1 liver fibrosis were (30.94 ± 10.95) mL/d and (12.34 ± 4.38) mL/d, respectively [3]. Report from Zhongshan Hospital, Fudan University (45 HCC cases) also revealed that the median FLR KGR of patients with cirrhosis (METAVIR grade 4) and METAVIR grade 3 liver fibrosis were 9.6 mL/d and 19.8 mL/d, respectively. In comparison, patients with normal liver parenchyma (METAVIR grade 0) had a KGR of 50.1 mL/d [4]. Furthermore, it was found that the KGR of these patients in the second week after stage 1 ALPPS was usually significantly lower than that in the first week postoperatively. Due to limited FLR hypertrophy, the time required for liver regeneration in these patients was significantly longer than that in cases with normal livers (14 days vs. 7 days) [4]. A longer interstage interval is associated with tumor progression. Furthermore, the change of portal vein-arterial blood supply led by portal vein ligation (PVL) also exerts oncological effects. There is a compensatory increase in hepatic artery perfusion after PVL, and the tumor may grow with the increase in arterial blood supply [15–17]. This is more common when ALPPS is used to treat HCC (mostly large HCC). These factors often lead to a higher incidence of surgical failure or post-hepatectomy liver failure (PHLF) when ALPPS is used in this population. In the authors’ center, before the emergence of the new transarterial embolization salvaged ALPPS (TAE-salvaged ALPPS), two HCC patients failed to achieve sufficient FLR hypertrophy 3–4 weeks after stage 1 ALPPS and were unable to undergo the stage 2 surgery, thus being converted to other treatments; another HCC patient directly developed PHLF after stage 1 ALPPS [4]. In China, HCC patients are often complicated by chronic liver diseases such as liver fibrosis and cirrhosis. The implementation of ALPPS in patients with cirrhosis or severe fibrosis remains challenging, and appropriate solutions are urgently needed.