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Background & Aims: Liver resection (LR) in patients with hepatocellular carcinoma (HCC) and clinically significant portal hypertension (CSPH) defined as a hepatic venous pressure gradient (HVPG) ≥10 mmHg is not encouraged. Here, we reappraised the outcomes of patients with cirrhosis and CSPH who underwent LR for HCC in highly specialised liver centres. Methods: This was a retrospective multicentre study from 1999 to 2019. Predictors for postoperative liver decompensation and textbook outcomes were identified. Results: In total, 79 patients with a median age of 65 years were included. The Child-Pugh grade was A in 99% of patients, and the median model for end-stage liver disease (MELD) score was 8. The median HVPG was 12 mmHg. Major hepatectomies and laparoscopies were performed in 28% and 34% of patients, respectively. Ninety-day mortality and severe morbidity rates were 6% and 27%, respectively. Postoperative and persistent liver decompensation occurred in 35% and 10% of patients at 3 months. Predictors of liver decompensation included increased preoperative HVPG (p = 0.004), increased serum total bilirubin (p = 0.02), and open approach (p = 0.03). Of the patients, 34% achieved a textbook outcome, of which the laparoscopic approach was the sole predictor (p = 0.004). The 5-year overall survival and recurrence-free survival rates were 55% and 43%, respectively. Conclusions: Patients with cirrhosis, HCC and HVPG ≥10 mmHg can undergo LR with acceptable mortality, morbidity, and liver decompensation rates. The laparoscopic approach was the sole predictor of a textbook outcome. Lay summary: Patients with cirrhosis, hepatocellular carcinoma, and clinically significant portal hypertension (defined as a hepatic venous pressure gradient ≥10 mmHg) can undergo resection with acceptable mortality, morbidity, liver decompensation rates, and a textbook outcome. These results can be achieved in selected patients with preserved liver function, good general status, and sufficient remnant liver volume.

Introducción. La hidatidosis hepática es endémica en dife - rentes regiones del mundo. Se han propuesto diversos trata - mientos para abordarla. La mejor alternativa terapéutica sigue siendo la cirugía. Los procedimientos quirúrgicos están divididos en radicales y no radicales. El objetivo de nuestro trabajo es evaluar la morbi-mortalidad y el porcentaje de re - cidivas de las resecciones hepáticas como tratamiento radical de la hidatidosis hepática y contrastarlos con las series publi - cadas en la literatura. Material y métodos. Este estudio re - trospectivo fue efectuado en una serie española y argentina y se analizan los siguientes datos: sexo, edad, tipo de resección, gestos quirúrgicos asociados, presencia de hepatopatía, tiem - po operatorio, transfusión de hemoderivados, morbilidad, mortalidad, estancia hospitalaria, re-internación, recidiva y tiempo de seguimiento. Tuvimos en cuenta la clasificación de Dindo - Clavien para las complicaciones y la clasificación de la International Hepato-Pancreato-Biliary Association (IHPBA) de Brisbane para resecciones hepáticas. Se conside - ró mortalidad la ocurrida en los primeros 90 días post-ciru - gía. Para evaluar la recurrencia, solo se incluyeron pacientes seguidos durante más de 6 meses. Resultados. Las indicacio - nes de las resecciones hepáticas se realizaron en pacientes con quistes mayores de 5 cm, quistes múltiples, quistes de gran tamaño, comunicados con la vía biliar o con sospecha de dicha comunicación. Cinco pacientes requirieron transfusio - nes de hemoderivados (10%) con una mediana para esos 5 pacientes de 740 ml cada uno y para el total de la serie de 74 ml. El tiempo operatorio tuvo una mediana de 186 minutos (rango 45 a 1.050 minutos). La estancia hospitalaria tuvo una mediana de 7,7 días. El seguimiento superior a 6 me - ses se realizó en 38 pacientes. Conclusiones. Creemos que la hidatidosis hepática es una patología polifacética y requiere de más de una posibilidad terapéutica. Las hepatectomías, más allá de cumplir con la resección del parásito de manera completa, ofrecen la posibilidad de hacerlo de una manera controlada y segura en manos experimentadas, asegurando buenos resultados en el tratamiento de esta patología.

BACKGROUND:There is still no reliable biomarker for the diagnosis of pancreatic adenocarcinoma. Carbohydrate antigen 19-9 (CA 19-9) is a tumor marker only recommended for pancreatic adenocarcinoma follow-up. One of the clinical problems lies in distinguishing between this cancer and other benign pancreatic diseases such as chronic pancreatitis. In this study we will assess the value of panels of serum molecules related to pancreatic cancer physiopathology to determine whether alone or in combination could help to discriminate between these two pathologies. METHODS:CA 19-9, carcinoembryonic antigen (CEA), C-reactive protein, albumin, insulin growth factor-1 (IGF-1) and IGF binding protein-3 were measured using routine clinical analyzers in a cohort of 47 pancreatic adenocarcinoma, 20 chronic pancreatitis and 15 healthy controls. RESULTS:The combination of CA 19-9, IGF-1 and albumin resulted in a combined area under the curve (AUC) of 0.959 with 93.6% sensitivity and 95% specificity, much higher than CA 19-9 alone. An algorithm was defined to classify the patients as chronic pancreatitis or pancreatic cancer with the above specificity and sensitivity. In an independent validation group of 20 pancreatic adenocarcinoma and 13 chronic pancreatitis patients, the combination of the four molecules classified correctly all pancreatic adenocarcinoma and 12 out of 13 chronic pancreatitis patients. CONCLUSIONS:Although this panel of markers should be validated in larger cohorts, the high sensitivity and specificity values and the convenience to measure these parameters in clinical laboratories shows great promise for improving pancreatic adenocarcinoma diagnosis.

In our previous studies we have described that ST3Gal III transfected pancreatic adenocarcinoma Capan-1 and MDAPanc-28 cells show increased membrane expression levels of sialyl-Lewis x (SLe(x)) along with a concomitant decrease in α2,6-sialic acid compared to control cells. Here we have addressed the role of this glycosylation pattern in the functional properties of two glycoproteins involved in the processes of cancer cell invasion and migration, α2β1 integrin, the main receptor for type 1 collagen, and E-cadherin, responsible for cell-cell contacts and whose deregulation determines cell invasive capabilities. Our results demonstrate that ST3Gal III transfectants showed reduced cell-cell aggregation and increased invasive capacities. ST3Gal III transfected Capan-1 cells exhibited higher SLe(x) and lower α2,6-sialic acid content on the glycans of their α2β1 integrin molecules. As a consequence, higher phosphorylation of focal adhesion kinase tyrosine 397, which is recognized as one of the first steps of integrin-derived signaling pathways, was observed in these cells upon adhesion to type 1 collagen. This molecular mechanism underlies the increased migration through collagen of these cells. In addition, the pancreatic adenocarcinoma cell lines as well as human pancreatic tumor tissues showed colocalization of SLe(x) and E-cadherin, which was higher in the ST3Gal III transfectants. In conclusion, changes in the sialylation pattern of α2β1 integrin and E-cadherin appear to influence the functional role of these two glycoproteins supporting the role of these glycans as an underlying mechanism regulating pancreatic cancer cell adhesion and invasion.