Minimum invasive associating liver partition and portal vein ligation for staged hepatectomy

Kawka, Michal; Gall, Tamara; Jiao, Long R.

doi:10.1016/j.lers.2019.08.003

Cited by 6 publications

(4 citation statements)

References 52 publications

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“…To investigate the molecular mechanisms involved in the activation of HSCs, we isolated and purified primary mHSCs and then cultured them in a complete DMEM for five days. As previously reported, 4 most qHSCs store vitamin A–containing lipid droplets, which gives qHSCs a fading blue-green autofluorescence appearance. However, aHSC will lose their lipid droplets (Figure 3 A).…”

Section: Resultssupporting

confidence: 77%

“…Hepatic ischemia-reperfusion injury (IRI) is a pathophysiologic process characterized by reperfusion and hypoxia in ischemic tissue during liver trauma, hemorrhagic shock, hepatectomy, and liver transplantation, 1 2 leading to hepatic failure, hemorrhagic shock, and graft dysfunction. 3 4 The acute phase of IRI is caused by an imbalance in the innate immune responses involving several immune cells, including macrophages, natural killer cells, dendritic cells, CD4 + T cells, and CD8 + T cells, causing a complex inflammation. Despite significant advancements in perioperative management and surgical techniques, the occurrence of hepatic IRI is difficult to prevent during liver surgery, which calls for further investigation into the mechanisms of liver IRI and develop new treatment methods.…”

Section: Introductionmentioning

confidence: 99%

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BTLA deficiency promotes HSC activation and protects against hepatic ischemia-reperfusion injury

Shen,

Mai,

Han

et al. 2024

Hepatology Communications

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Background and Aims: Hepatic ischemia-reperfusion injury (IRI) is unavoidable even despite the development of more effective surgical approaches. During hepatic IRI, activated HSC (aHSC) are involved in liver injury and recovery. Approach and Result: A proportion of aHSC increased significantly both in the mouse liver tissues with IRI and in the primary mouse HSCs and LX-2 cells during hypoxia-reoxygenation. “Loss-of-function” experiments revealed that depleting aHSC with gliotoxin exacerbated liver damage in IRI mice. Subsequently, we found that the transcription of mRNA and the expression of B and T lymphocyte attenuator (BTLA) protein were lower in aHSC compared with quiescent HSCs. Interestingly, overexpression or knockdown of BTLA resulted in opposite changes in the activation of specific markers for HSCs such as collagen type I alpha 1, α-smooth muscle actin, and Vimentin. Moreover, the upregulation of these markers was also observed in the liver tissues of global BLTA-deficient (BTLA−/−) mice and was higher after hepatic IRI. Compared with wild-type mice, aHSC were higher, and liver injury was lower in BTLA−/− mice following IRI. However, the depletion of aHSC reversed these effects. In addition, the depletion of aHSC significantly exacerbated liver damage in BTLA−/− mice with hepatic IRI. Furthermore, the TGF-β1 signaling pathway was identified as a potential mechanism for BTLA to negatively regulate the activation of HSCs in vivo and in vitro. Conclusions: These novel findings revealed a critical role of BTLA. Particularly, the receptor inhibits HSC-activated signaling in acute IRI, implying that it is a potential immunotherapeutic target for decreasing the IRI risk.

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Section: Resultssupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

BTLA deficiency promotes HSC activation and protects against hepatic ischemia-reperfusion injury

Shen,

Mai,

Han

et al. 2024

Hepatology Communications

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“…Despite causing a certain prolongation of the surgical time compared to using dedicated ablation devices (such as the Habib ® 4× bipolar resection device), in our experience, this method represents a valid alternative. In fact, the time of surgery did not exceed 300 min, similarly to the timings reported in most series describing laparoscopic ALPPS [28] . This is also the "safe limit" above which the number of complications reported start to rise [29] .…”

Section: Discussionsupporting

confidence: 66%

Laparoscopic ICG-guided ralpps procedure for HCC on cirrhosis with 3D reconstruction implementation: a case report

Pegoraro¹,

Montalti²,

Rompianesi³

et al. 2021

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We present a fully laparoscopic partial RALPPS (radiofrequency-assisted liver partition with portal vein ligation for staged hepatectomy) on a cirrhotic 71-year-old man with a bifocal hepatocellular carcinoma. The patient's liver was preoperatively studied through a CT-guided 3D-reconstruction. During stage-1, the right portal vein was ligated and injected with alcohol distally; the vascular limit between the right and left anterior sectors was defined through the systemic infusion of indocyanine green for a negative staining. Hence, laparoscopic ablations, guided by luminescence and checked with intraoperative ultrasounds, were performed. After 55 days, the future liver remnant increased from 28.6% to 46.3%, allowing a laparoscopic RALPPS stage-2. Fully laparoscopic RALPPS technique shows several advantages compared to the original procedure, especially in patients with cirrhosis. The avoidance of liver transection during stage-1 reduced blood loss and intraabdominal adhesions, and it eliminated the risk of biliary fistulae and allowed an easier liver transection during stage-2.

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“…Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) has attracted interest due to accelerated hypertrophy of future liver remnants (FLRs) by ligating the branch of the portal vein combined with transecting the parenchyma to improve surgical resection rates (1,2). Despite the significant improvements in morbidity and mortality, the feasibility and safety of ALPPS in patients with fibrosis remain controversial (3,4). Many ALPPS recipients suffer from chronic hepatitis virus infections, alcoholism, or nonalcoholic liver diseases, which may progress to liver fibrosis and cirrhosis, post-hepatectomy liver failure caused by an insufficient proliferation of FLRs can give rise to life-threatening complications associated with the ALPPS procedure.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunction attenuates rapid regeneration in livers with toxin-induced fibrosis

Li¹,

Liang²,

Ying³

et al. 2021

Ann Transl Med

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Background: The mechanism of associating liver partition and portal vein ligation for staged hepatectomy (ALPPS)-induced rapid liver regeneration remains poorly documented, especially in patients with fibrosis.Therefore, this study aims to investigate the underlying mechanism of ALPPS-induced accelerated regeneration in toxin-induced fibrosis models. Methods:The ALPPS-induced regeneration model was established in livers with thioacetamide (TAA)induced fibrosis to determine the regenerative pathways involved in rapid regeneration. Confirmatory experiments were performed in transforming growth factor beta 1 (TGFβ1)-treated AML12 cells and mice with carbon tetrachloride (CCl 4 )-induced fibrosis. Finally, mitochondrial dysfunction was validated in fibrotic/non-fibrotic patients.Results: In TAA-induced fibrotic mice, ALPPS-induced regeneration was significantly inferior to that of the control group (P=0.027 at day 2 and P<0.001 at day 7). Furthermore, mitochondria-associated genes were significantly downregulated in TAA-challenged mice. Accordingly, the reduced production of ATP and elevated levels of malondialdehyde indicated disturbances in intracellular energy metabolism during the ALPPS-induced regenerative process after TAA treatment. Further investigations were performed in TGF-β1-treated AML12 cells and CCl 4 -treated mice, which indicated that mitochondrial dysfunction attenuated the capacity for rapid regeneration after ALPPS.Conclusions: In summary, this study revealed that mitochondrial dysfunction led to inferior regeneration in livers with toxin-induced fibrosis and identified new therapeutic targets to improve the feasibility and safety of the ALPPS procedure. Further studies in human patients are required in the future.

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Minimum invasive associating liver partition and portal vein ligation for staged hepatectomy

Cited by 6 publications

References 52 publications

BTLA deficiency promotes HSC activation and protects against hepatic ischemia-reperfusion injury

BTLA deficiency promotes HSC activation and protects against hepatic ischemia-reperfusion injury

Laparoscopic ICG-guided ralpps procedure for HCC on cirrhosis with 3D reconstruction implementation: a case report

Mitochondrial dysfunction attenuates rapid regeneration in livers with toxin-induced fibrosis

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