Portal hypertension caused by pancreatic cancer: Multidetector computed tomography diagnosis and multivariate analysis of variceal hemorrhage.

CONTEXT: Pancreatic cancer portal hypertension (PCPH) is a rare cause of gastrointestinal bleeding. This study retrospectively assessed gastrointestinal bleeding risk factors in 57 PCPH patients diagnosed via multidetector computed tomography (MDCT). MATERIALS AND METHODS: The data of patients with pancreatic cancer from January 2008 to January 2018 at Qingdao Municipal Hospital were reviewed. PCPH patients were screened with MDCT and followed up. MDCT findings (e.g., the location of the venous obstruction, type of variceal veins pathway, and splenomegaly) were recorded. Variceal hemorrhage was recorded. The MDCT findings and clinical data of the PCPH patients were used in this analysis to explore the risk factors of variceal hemorrhage using binary logistic regression and multivariate logistic regression model. RESULTS: Fifty-seven of the 182 patients were diagnosed with PCPH. A total of 7 draining routes and 11 types of varices were found. Of these patients, eight experienced variceal hemorrhage. Univariate analysis showed that splenomegaly (odds ratio [OR] = 10.364, P = 0.003) was significantly associated with an increased risk of variceal hemorrhage. Multivariate analysis showed that splenomegaly (OR = 66.491, 95% confidence interval: 2.790-1584.643, P = 0.009) was an independent influencing factor for variceal hemorrhage in PCPH patients. CONCLUSIONS: Patients with pancreatic cancer have high morbidity of PCPH. The splenomegaly is more prone to hemorrhage. Splenomegaly was an independent risk factor of variceal hemorrhage. MDCT can provide insight into the stenosis and occlusion of the portal vein system and the drainage routes of variceal veins and is one of the best ways to diagnose PCPH.

Acute liver failure and infarction complicating TIPS placement.

Here in we report a case of acute liver failure with hepatic infarction after transjugular intrahepatic portosystemic shunt (TIPS). An upper gastrointestinal hemorrhage patient with a medical history of alcoholic cirrhosis underwent a TIPS procedure. One day after TIPS, his alanine aminotransferase and aspartate aminotransferase levels increased to 1214 U/L and 1511 U/L, respectively. Two days after TIPS, they peaked at alanine aminotransferase 8389 U/L and aspartate aminotransferase >7500 U/L, respectively. An emergent stent occlusion was performed on the second day. Portography showed that there were no portal vein branches or parenchymal stains on the edge of the right liver lobe. A CT scan demonstrated diffuse hepatic parenchyma, homogeneous hypodense lesion, and bilateral pleural effusion. The patient died of liver failure and multiple organ dysfunction syndrome 6 hours after the stent occlusion.

FoxM1 promotes epithelial-mesenchymal transition of hepatocellular carcinoma by targeting Snai1.

Forkhead box protein M1 (FoxM1) is aberrantly expressed in several types of human malignancy, and serves an important role in tumor metastasis. Epithelial­mesenchymal transition (EMT) of cancer cells has been associated cancer metastasis; however, the implication of FoxM1 in EMT and its putative roles in the regulation of cancer metastasis remain to be elucidated. In the present study, the expression of FoxM1, Snai1 and E­cadherin in hepatocellular carcinoma (HCC) cell lines with various metastatic potentials, and in normal liver cells, was investigated using western blot analysis and reverse transcription­quantitative polymerase chain reaction. The effects of FoxM1 on the invasive and migratory capabilities of HCC cells were evaluated using wound healing and Transwell migration assays. The present results demonstrated that FoxM1 expression was significantly upregulated in HCC cells compared with in normal hepatocytes (P<0.05). In addition, FoxM1 expression was significantly increased in MHCC­LM3 cells, characterized by higher metastatic potential, compared with in SMMC­7721 cells, which have a lower metastatic potential. Furthermore, overexpression of FoxM1 was demonstrated to be negatively correlated with E­cadherin (P<0.05) and positively associated with Snai1 (P<0.05) expression. These observations suggested that FoxM1 may enhance the invasion and migration of cancer cells, and thus promotes their EMT, in a mechanism that may involve the regulation of Snai1. Therefore, it may be hypothesized that FoxM1 has potential as a novel diagnostic marker and therapeutic target for the treatment of patients with HCC.

Extensive calcifications in portal venous system in a patient with hepatocarcinoma.

Calcification of the portal venous system is a rare entity that can be incidentally discovered during computed tomography (CT). We describe a case of extensive calcifications in the portal venous system in a middle-aged male patient with hepatocellular carcinoma (HCC). This patient presented with epigastric pain that had no obvious origin prior to admission. Laboratory examinations were positive for hepatitis B surface antigen and α-fetoprotein, and severe esophageal and gastric varices were detected during gastroscopy. Abdominal X-ray plain film showed well-defined linear and track-like calcification, with irregular margins directed along the course of the portal venous system. CT revealed extensive calcifications along the course of the portal, splenic, superior mesenteric and gastroesophageal veins. He underwent splenectomy 22 years ago due to splenomegaly and partial hepatectomy seven months before because of HCC of low-grade differentiation, confirmed by pathology. Finally, the patient was diagnosed with postoperative recurrent HCC and extensive portal venous system calcification after selective hepatic angiography under digital subtraction angiography.