Complete necrosis of hepatocellular carcinoma after preoperative portal vein embolization: a case report
Hepatocellular carcinoma has a poor prognosis; few patients can undergo surgical curative treatment according to Barcelona Clinic Liver Cancer guidelines. Progress in surgical techniques has led to operations for more patients outside these guidelines. Our case shows a patient with intermediate stage hepatocellular carcinoma presenting a good outcome after curative treatment.
We report the case of an 80-year-old Moroccan man, who was positive for hepatitis c virus, presenting an intermediate stage hepatocellular carcinoma (three lesions between 20 and 60 mm). He presented a complete tumor necrosis after portal vein embolization and achieved 24-month disease-free survival after surgery.
Perioperative care in liver surgery and multidisciplinary discussion can help to extend indications for liver resection for hepatocellular carcinoma outside European Association for the Study of the Liver/American Association for the Study of Liver Diseases recommendations and offer a curative approach to selected patients with intermediate and advanced stage hepatocellular carcinoma.
KeywordsHepatocellular carcinoma Portal vein embolization Liver resection Complete tumor necrosis
American Association for the Study of Liver Diseases
Barcelona Clinic Liver Cancer
European Association for the Study of the Liver
Future remnant liver volume
Hepatitis B virus
Hepatitis C virus
Hepatocyte growth factor
Portal vein embolization
Tumor necrosis factor
Less than one out of three patients diagnosed with hepatocellular carcinoma (HCC) may undergo a curative treatment: liver resection, liver transplantation, or percutaneous ablation . Refinement of surgical techniques and perioperative care helped to extend indications for liver resection for HCC outside European Association for the Study of the Liver (EASL)/American Association for the Study of Liver Diseases (AASLD) recommendations with encouraging short-term and long-term outcomes . When a liver resection of more than three segments is considered, preoperative portal vein embolization (PVE) is of critical importance because it induce a significant growth of the remnant liver, and prevent a potentially lethal postoperative liver failure . Because of a main arterial supply, HCC may respond to transarterial embolization or transarterial chemoembolization (TACE) but not PVE. We report a case of a complete histological necrosis of a HCC after preoperative right PVE.
The effect of PVE on HCC remains controversial and is not well established. Some authors have suggested an anti-tumor effect of PVE on HCC related to partial tumor necrosis after portal thrombosis  or total tumor necrosis after PVE . Others suggested a pro-tumor effect of PVE on primary tumors of the liver [6, 7] that may be explained by: (1) the compensatory augmentation of the arterial flow to the tumor after PVE , (2) expression of cytoprotective genes involved in remodeling and cell repair as a response to the stress, and (3) induction and modulation of cytokine secretion and growth factors such as tumor necrosis factor (TNF) and hepatocyte growth factor (HGF) .
Our report showed a complete histological necrosis of a well-differentiated HCC after preoperative right PVE. This result was unexpected because HCC have a predominant arterial vascularization . Hypothesis 1: some HCC may have predominant portal vascularization. In our patient, this may have been the case as initial imaging showed poor arterial enhancement. Hypothesis 2: a spontaneous regression may occur. Spontaneous regression is defined by a complete or partial clearance of malignant cells in the absence of all treatment or in the presence of therapy that is considered inadequate to exert a significant influence on the neoplastic disease. From a physiopathology point of view, this phenomenon may be caused by hypoxia due to rapid tumor growth, tumor infarction following hemorrhagic shock, circulatory failure by arterial thrombosis or venous thrombosis, or reactivation and recognition of tumor cells by the immune system. Spontaneous regression may occur in approximately 1/100,000 patients with malignant tumor including HCC. Only 12 pathologically proven cases of HCC regression (including our case) have been reported in the literature . Hypothesis 3: an arterial trauma may cause ischemia. In fact, an asymptomatic proximal intrahepatic arterial trauma may be caused during fine liver biopsy and/or percutaneous PVE procedure. This last hypothesis is validated by the facts that in our patient, PVE was performed with multiple right liver (ipsilateral) punctures and that complete necrosis was recorded in all of the three lesions. In our opinion, combined disruption of a predominant portal flow by PVE (hypothesis 1) and arterial flow by a puncture trauma may explain the result in our patient.
Complete necrosis should have been suspected while performing a second preoperative liver imaging to assess future liver remnant hypertrophy but it would not have changed our surgical strategy. In fact, relapse of spontaneously necrotized HCC has been reported  and viable persistence of tumoral cells has also been often observed despite a diagnosis of advanced tumor necrosis in imaging examinations .
Refinement of perioperative care in liver surgery, including preoperative portal embolization and multidisciplinary discussion, has helped to extend indications for liver resection for HCC outside EASL/AASLD recommendations and offers a curative approach to selected patients with intermediate (our patient) and advanced stage HCC.
There are no other contributors but the authors.
No funds were received in support of this study.
Availability of data and materials
Data and supporting materials are available freely to any scientist wishing to use them.
EBH was the patient's physician, in charge of the diagnosis and the follow up, he wrote the manuscript. SM was the professor in charge of the medical care and the following of the patient and did the first correction of the paper. KN is the chief of the medical department and took therapeutic decisions for the patient in the multidisciplinary meeting. BA is the surgeon of the patient who performed the portal vein embolization and the surgery; he corrected and rewrote the manuscript. All authors read and approved the final manuscript.
The authors declare that they have no competing interests.
Consent for publication
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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