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Dermatomyositis or polymyositis as a paraneoplastic syndrome of hepatocellular carcinoma (HCC) is an uncommon event. Few cases have been reported in the literature. We herein report the case of a 55-year-old man with chronic hepatitis B and alcoholism who presented with skin rash. Abdominal computed tomography revealed multiple hypervascular liver tumors consistent with HCC. He subsequently developed dysphagia with proximal limb weakness. Laboratory tests and electromyography demonstrated inflammatory myopathy. We therefore diagnosed the patient with HCC-induced dermatomyositis. Prednisolone and anti-viral therapy were administered; however, the patient died two months later due to the progression of the disease. We review the cases of HCC-induced dermatomyositis and polymyositis in the literature.

Background: Transarterial chemoembolization (TACE) and sorafenib are the therapeutic standard for intermediate and advanced stage hepatocellular carcinoma (HCC) patients respectively. High costs with adverse events (AE) of sorafenib might limit sorafenib dosage, further affecting therapeutic response. To attain greatest benefit, we evaluated the efficacy of different doses and effect of TACE during and after sorafenib discontinuation in patients representing Child-Pugh Classification Class A with venous or extra-hepatic invasion., Methods: A total 156 patients met the criteria and were divided into Groups I (n = 52) accepting 800 mg/day; II (n = 58) accepting 800 mg/day and reduced to 400 mg/day owing to AE; and III (n = 46) accepting 400 mg/day. TACE was performed during and after sorafenib discontinuation and therapeutic response bimonthly to four-monthly was rated thereafter., Results: Median duration of sorafenib treatment and patients' survival were 4.00 ± 0.45 and 7.50 ± 1.44 months in all cases; 2.50 ± 0.90 and 5.00 ± 1.10 months in Group I; 5.50 ± 1.27 and 16.50 ± 1.86 months in Group II; 4.00 ± 0.94 and 6.50 ± 2.49 months in Group III. Group II presented the best response and survival benefit (p = 0.010 and p = 0.011 respectively). Child-Pugh Classification score 5 (Hazard Ratio = 0.492, p = 0.049), absent AE (3.423, p = 0.015), tumor numbers ≤ 3 (0.313, p = 0.009), sorafenib duration ≤ 1 cycle (3.694, p = 0.004), and absent TACE (3.197, p = 0.008) significantly correlated with patient survival. TACE benefit appeared in separate and total cases during (p = 0.002, p = 0.595, p = 0.074, p = 0.002 respectively) and after discontinuation of sorafenib administration (p = 0.001, p = 0.034, p = 0.647, p = 0.001 respectively)., Conclusions: Low-dosage sorafenib not only appeared tolerable and lowered economic pressure but also provided satisfactory results. TACE benefited patient's survival during and after sorafenib discontinuation.

Sorafenib has been approved to increase the survival in patients with advanced hepatocellular carcinoma. Acute pancreatitis is an uncommon complication of sorafenib treatment. Only a few cases of sorafenib-induced acute pancreatitis have been reported in the English literature. We herein present the case of a 56-year-old man with hepatocellular carcinoma treated with sorafenib at 200 mg once daily. After six days of treatment, he suffered epigastric pain. Laboratory tests showed markedly elevated serum amylase and lipase levels. Imaging studies demonstrated negative findings. Sorafenib-induced acute pancreatitis was diagnosed after reviewing his history. The sorafenib treatment was discontinued, and his symptoms were resolved seven days later. To date, this case had the shortest duration and the lowest dosage of sorafenib to have induced acute pancreatitis.

Background: The aim of this study was to identify predictors of treatment failure of percutaneous catheter drainage (PCD) in patients with hepatobiliary-pancreatic cancer with pyogenic liver abscess (PLA)., Methods: Medical records of 44 patients with PLA with underlying hepatobiliary-pancreatic cancer who underwent PCD under computed tomographic guidance as primary treatment between January 2001 and December 2010 were collected and reviewed. Included patients were diagnosed with cholangiocarcinoma (n = 16), hepatocellular carcinoma (n = 12), pancreatic carcinoma (n = 9), carcinoma of the ampulla of Vater (n = 6), and gallbladder cancer (n = 1). The clinical factors related to failure of PCD were determined using logistic regression., Results: The median age of the 44 patients with PLA was 68 years, and 48% were men. PCD failed in 15 patients (34%). Of the 15 patients with PCD failure, 12 subsequently required surgical intervention because of either clinical deterioration or imaging that demonstrated failure of abscess resolution with PCD. Three of these patients died with the initial drain in place before resolution of the abscess. In patients requiring surgery after PCD failure, the frequency of cure or abscess resolution reached 67%. Fourteen patients (32%) died during hospitalization. Multivariate analysis identified that multiloculated abscesses (P = .005) and abscesses with biliary communication (P = .036) were associated with failure of PCD., Conclusions: Multiloculated abscesses and lesions with biliary communication pose a greater likelihood of failure of PCD in patients with hepatobiliary-pancreatic cancer with PLA. Early surgical intervention after PCD failure should be considered for these patients., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background/aims: Hepatitis B infection is a well-known cause of hepatocellular carcinoma (HCC). This study aims to investigate the role that the co-stimulatory molecule CD28 and co-inhibitory molecule programmed death-1 (PD-1) play in compromising the function of tumour-infiltrating lymphocytes (TIL) in hepatitis B virus (HBV)-related HCC., Methods: A total of 45 patients with HBV-related HCC were enrolled during the period February 2008 to March 2010. The immune phenotype and the expression of PD-1, CD28 and CD127 in TIL in biopsy specimens and in peripheral blood lymphocytes (PBL) from the same patients were analysed by flow cytometry., Results: Among the 45 patients, there was a male predominance (80%) and the mean age was 50 ± 13.68 years (range: 29-71). The majority of TIL were CD45RO(+) CD69(+). PD-1 expression was higher and CD28 and CD127 expression levels were lower in TIL than in PBL. The prevalence of portal vein thrombosis was 40%. Furthermore, tumour thrombosis invasion into the portal vein correlated with the expression level of the PD-1 co-inhibitory molecule., Conclusion: PD-1(+) tumour-infiltrating lymphocytes correlate with portal vein thrombosis and might serve as a potential prognostic marker of and a novel therapeutic target for HBV-related HCC., (© 2010 John Wiley & Sons A/S.)

Background/aims: The purpose of this study was to examine the roles of tumour necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-18, and alpha-fetoprotein (AFP) in patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC)., Methodology: AFP and cytokine serum concentrations were determined via EIA or ELISA., Results: In total, 81 patients were included, including 9 healthy controls, 36 LC patients, and 36 HCC patients. Significant differences in AFP, TNF-alpha, IL-6, and IL-18 between the three groups were noted (p < 0.001). AFP was lowest in the healthy subjects, intermediate in LC patients and highest in HCC patients (all p < 0.001). 11-6 and 11-18 concentrations were significantly higher in the HCC group than the other two groups. HCC and LC patients with AFP concentration > 7ng/ml had increased IL-18 concentrations compared to both the other groups p < 0.001). In contrast to previously published studies, TNF-alpha was highest in the healthy group, intermediate in the HCC group, and lowest in the LC group (p < 0.001)., Conclusions: IL-18 may be a potential tumour marker in combination with IL-6 and AFP in the diagnosis of HCC, but further research including a larger population of patients is essential. Further research is warranted.

Background/aims: The survival rates of patients with hepatocellular carcinoma (HCC) were investigated over the past 20 years to clarify the long-term survival trend., Methods: A total of 11 312 patients with HCC from seven medical centers from 1986 to 2002 were included. Survival was analyzed by correlating data with the national mortality databank., Results: Multivariate analysis showed that the following factors were associated with shorter survival: male sex, younger age, hepatitis B virus, earlier year of diagnosis, alpha fetoprotein higher than 400 ng/mL, alanine aminotransferase (ALT) higher than two times the upper normal limit, higher aspartate aminotransferase (AST)/ALT ratio, central or southern Taiwan residence, and rural areas residence. Patients diagnosed during 1998-2002 showed the highest survival rate, followed by patients diagnosed during 1994-1997, 1990-1993, and 1986-1989, respectively., Conclusions: There are geographic variations in the survival rates of patients with HCC. Survival has been improving gradually over the past 20 years, probably due to earlier detection of HCC or to improved patient care.

Background/aims: Our previous study showed that male hepatocellular carcinoma (HCC) patients below 40 years of age had the worst survival in the initial several years, but had the best prognosis thereafter. Thus, it seems that age has a paradoxical influence on the prognosis. To further clarify the issue of age on HCC prognosis, we initiated this study., Methods: A total of 11,312 HCC cases from seven medical centers from 1986 to 2002 were included. We analyzed the 1-year survival and survival after 1 year., Results: Male gender, age younger than 40 years old and hepatitis B virus (HBV) were associated with worse 1-year survival. In contrast, male gender, age younger than 40 years old and HBV were associated with better survival after 1 year. Higher percentage of the young HCC patients had a tumor size larger than 3 cm. 83.7% of HCC patients below 40 years of age were male and 89.8% of them were HBV carriers., Conclusions: If we encountered a young HCC patient, the patient will probably be a male HBV carrier. He would probably have larger tumor and is more likely to expire within 1 year than the older HCC patients. However, if the young HCC patient can survive for more than 1 year, he would probably have better survival in the following years than the older patients.

Metastatic hepatocellular carcinoma (HCC) in the sinonasal region is rare. We report the case of a 45-year-old male hepatitis B carrier who had metastatic HCC 2 years after resection of the primary tumor. The patient died of terminal hepatic failure 6 weeks after the discovery of nasal septal metastasis. The clinical and histopathologic characteristics of the primary and metastatic hepatocellular tumors are described. This is the first reported case of nasal septal metastasis from HCC.

This study was performed to examine the immunohistochemical expression of fibroblast growth factor-1 and fibroblast growth factor-2 in normal liver and a total of 31 cases of hepatocellular carcinoma (HCC). Reactivity for both types of angiogenic factor did not exist in any cellular component of normal liver. For HCC, variable amounts of fibroblast growth factor-1 were detected in 6 of 31 cases (19.4%). There was no apparent relationship between the expression pattern and clinicopathologic factors (P > 0.1, respectively), except a positive correlation with histologic grading (P = 0.04). No tumor showed reactivity for fibroblast growth factor-2 in their cancer cells. However, both types of peptide could be demonstrated in the pericellular stroma of HCC. With a mean follow-up at 60 months, fibroblast growth factor-1 expression did not correlate with patients' outcome (P > 0.1). Our study suggested that fibroblast growth factor-1 appears to play a certain role in hepatocarcinogenesis.

Angiogenesis is of vital importance during the development and progression of solid tumors. To examine the role of vascular endothelial growth factor (VEGF) in hepatocarcinogenesis, we evaluated the expression of peptide in normal human liver (n = 6) and in 36 cases of hepatocellular carcinoma (HCC). Immunoreactivity for VEGF was present in the extracellular matrix of the portal tracts in the normal and nontumor part of liver, but not in hepatocytes and bile duct epithelium. For HCC, variable amounts of VEGF were expressed in 13 cases (36.1%) of tumor cells. Using a logistic regression model, expression of VEGF was significantly associated with a higher proliferative index (P = .01) and sonographic portal vein thrombosis (P = .05). However, VEGF expression did not correlate with a biochemical liver profile, alpha-fetoprotein levels, histological grading, gender, or clinical stage of cirrhosis (P > 0.1, respectively). Log-rank test showed that evaluation of VEGF did not provide more prognostic information (P > .5) than that from tumor volume and portal vein thrombosis (P < .01, respectively). In addition, VEGF was always present in the fibrovascular stroma or pericellular matrix of HCC, although no strong relationship was observed with the expression of VEGF in tumor cells (P > .5). Our data suggested that expression of VEGF may characterize a progression toward higher proliferation in hepatocarcinogenesis in vivo. The relevance of VEGF existing in the extracellular matrix of the normal liver and HCC remains to be clarified.