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• W2039235091 abstract "Surgical resection was the sole therapeutic option for patients with hepatocellular carcinoma until very few years ago. As a consequence, indication of resection was based on technical feasibility. Estimation of operative risk and stratification of long-term survival prediction according to patients' clinical profile was not a major issue as it was assumed that effective resection would always provide better outcome than no treatment. The development of therapeutic options that provide survival benefit, such as transplantation 1, ablation 2, chemoembolization 3 and sorafenib 4, has prompted the need to estimate what would be the outcome for each option 5. According to tumour burden, liver function and physical condition, it is feasible to estimate the survival to be offered by each option and then select the one that would provide the best long-term outcome or at least a similar one with more or less cost and quality of life impairment 6. Several prospective studies with each option and a varied patients' clinical profile allow to do such evaluation, but at this point, it is worth stressing the need to take into account only those studies that have based their outcome description on the tumour burden of the patients at radiology, and not at the time of analysis of a resected specimen. This is frequently the case for liver resection and transplantation and obviously, such information is not available at the time of treatment decision. At the same time, it is of paramount importance to use contemporary cohort studies to inform about the expected outcome, as improvements in patients care and imaging techniques for staging have allowed to increase the accuracy of tumour burden assessment and hence, proper selection of patients for each option. This is exemplified in the field of transarterial chemoembolization: whereas the survival figures in the trials that established it as an effective approach did not reach 50% survival at 2 years 3, the current outcomes applying state of the art methodology exceed 50% survival at almost 4 years 7. In potential candidates for resection, the evaluation of outcome takes into account the number of tumour nodules, the existence of vascular invasion or extra-hepatic spread and the degree of liver function impairment. At the same time, general health status, comorbidities, and extent of resection and residual hepatic volume are entered into the evaluation. Major hepatectomies are not recommended in cirrhotic patients and subcapsular tumours in the anterior surface of the liver are easier to resect than those in deeper locations. It is well known that single nodules have a better life expectancy of multifocal disease 8, and recognition of vascular invasion at radiology (this means macroscopic vascular invasion and cannot be equalled to microscopic invasion detected at pathology) and extra-hepatic spread reflect advanced cancer stage. Thus, these are usually considered contraindications for surgery even if this would be technically feasible. How is liver function impairment assessed? The Child–Pugh classification was developed to estimate the risk of surgical porto-systemic shunt in patients with bleeding varices, but its simplicity and clinical appeal has consolidated it as a conventional descriptor for liver function. However, Child–Pugh A class includes patients with fully compensated cirrhosis and no portal hypertension and patients with a significantly impaired liver function even presenting ascites. Thus, the mere adscription to Child–Pugh A does not serve to predict perioperative risk and survival. The transition from cirrhosis without portal hypertension to cirrhosis with increased portal pressure, development of oesophageal varices and ultimately, ascites is paralleled by a reduction in the safety of surgical resection and even without it, the life expectancy of the patient is progressively reduced 9. Years ago, we described that clinically significant portal hypertension (defined by a hepatic venous pressure gradient >10 mmHg) was associated with an increased risk of post-operative decompensation 10 and later on, we also established that such cut-off was able to predict a better or worse survival after resection 11. As a consequence, assessment of portal pressure became key to predict survival after surgery and to allow a sound comparison with that to be obtained with transplantation or ablation. Some authors misunderstood the message of the data and took portal hypertension as a contraindication of surgery within the BCLC model. This is not the case but clearly, if other options offer the same (ablation) or even better (transplantation) survival, resection should no longer be seen as the first-line option 6. It could be technically feasible and not responsible for major perioperative mortality, but sure long-term outcome would be worse than in patients without portal hypertension. The impact of portal hypertension in long-term survival was validated by the group of Makuuchi in Japan 8 and now, assessment of portal hypertension is used by several major groups to evaluate surgical candidacy in patients with liver cancer. Interestingly, some groups have challenged the validity of portal pressure measurement to predict outcome after surgery. When reviewing such investigations, it frequently emerges that they are retrospective 8, 12-16 and as such, they are at risk of major bias as indication of surgery may have already taken into account parameters that are either surrogates of portal hypertension or have included patients with portal hypertension but with small sub-capsular HCC in whom the surgical stress is highly minimized. Furthermore, in some instances, the quality of the surgical procedure may be controversial as the transfusion rate, the perioperative mortality and the median survival exceed by far the current standards in expert setting. If not performing high-risk operations in suboptimal candidates, transfusion rate should optimally be less than 10%, mortality should be less than 1% and 5-year survival should be higher than 60%. Another important flaw of some investigations is how portal hypertension has been estimated. Measurement of portal pressure should be done by hepatic vein catheterization and surrogate markers may not have optimal accuracy. The presence of dilated portal vein, splenomegaly and platelet count <100.000 is highly suggestive, but if portal vein dilatation is excluded, there is a significant overestimation of the presence of portal hypertension and this is especially true in patients with HCV infection. The simple assessment of platelet count is even less accurate in patients with compensated cirrhosis as even if it mildly correlates with portal pressure, a threshold for diagnosing clinically significant portal hypertension cannot be found 17. In addition, platelet count may fluctuate and cross the 100.000 value in any direction without any correlation with variations in portal pressure values 18. Liver stiffness (LS) estimation by transient elastography is a promising non-invasive predictor of portal hypertension. In a prospective study by our group in 97 patients with compensated cirrhosis, no oesophageal varices, bilirubin <1.0 mg/ml and potentially resectable liver tumours, LS <13.6 kPa and LS above 21.1 kPa, respectively, reliably excluded and diagnosed CSPH evaluated by HVPG measurement 19. Interestingly, in an independent study performed in patients undergoing surgery for HCC, none of those with pre-operatory LS <14.2 kPa (very close to that excluding CSPH according to our data) developed post-operative liver failure 20. However, according to our study 19, LS was not technically measurable in 18% of cases, and indeterminate values (those between 13.6 and 21.1 kPa) were found in a further 29% of cases, so that even accepting LS as potential surrogate of CSPH, around 50% of patients in this clinical scenario require further investigation by HVPG measurement. All these comments serve to frame the information provided in this study by Giannini et al. published in this issue of Liver International. They did not detect a correlation between portal hypertension and outcome, but the authors themselves acknowledge the limitation of their data: retrospective investigation, assessment of portal hypertension by splenomegaly and reduced platelet count, and lack of prospective definition of the criteria to recommend surgery in an individual patient. In addition, they did not take into account parameters that have a major impact in overall survival of patients with HCC as is the case for performance status and/or tumour stage. Clearly, prospective studies with well-defined criteria to recommend surgery and accurate assessment of portal pressure are needed to validate or refute the impact of portal hypertension in long-term outcome after resection. However, it would be highly unexpected that this would not be the case when it is well established that portal hypertension is a major predictor of survival in patients without HCC. It would be difficult to guess by which mechanism hepatic surgery would abrogate the value of portal hypertension as a surrogate of a more evolved liver disease. Indeed, a reduction in liver parenchyma has been shown to induce an increase in portal pressure 21 and the ischaemia reperfusion phenomena associated with surgery or the mere cytokine release owing to laparotomy results in a further stress of the mechanisms involved in the progression of fibrotic deposition 22, 23. Financial support: This study was supported by a grant from the Instituto de Salud Carlos III (PI11/01830). CIBERehd is funded by Instituto de Salud Carlos III." @default.
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• W2039235091 title "If portal hypertension predicts outcome in cirrhosis, why should this not be the case after surgical resection?" @default.
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