Chronic hepatitis B (CHB) infection is responsible for 40% of the global burden of hepatocellular carcinoma (HCC) with a high case fatality rate. The risk of HCC differs among CHB subjects owing to differences in host and viral factors. Modifiable risk factors include viral load, use of antiviral therapy, co-infection with other hepatotropic viruses, concomitant metabolic dysfunctionassociated steatotic liver disease or diabetes mellitus, environmental exposure, and medication use. Detecting HCC at early stage improves survival, and current practice recommends HCC surveillance among individuals with cirrhosis, family history of HCC, or above an age cut-off. Ultrasonography with or without serum alpha feto-protein (AFP) every 6 months is widely accepted strategy for HCC surveillance. Novel tumor-specific markers, when combined with AFP, improve diagnostic accuracy than AFP alone to detect HCC at an early stage. To predict the risk of HCC, a number of clinical risk scores have been developed but none of them are clinically implemented nor endorsed by clinical practice guidelines. Biomarkers that reflect viral transcriptional activity and degree of liver fibrosis can potentially stratify the risk of HCC, especially among subjects who are already on antiviral therapy. Ongoing exploration of these novel biomarkers is required to confirm their performance characteristics, replicability and practicability.
The most significant risk factor for hepatocellular carcinoma (HCC) is the presence of cirrhosis or advanced fibrosis of the liver. Liver biopsy was traditionally considered the gold standard for assessing the liver fibrosis burden. Recently, non-invasive methods, particularly transient elastography (TE), have proven effective at measuring fibrosis and determining cirrhosis. Clinical application of TE ranges from measuring fibrosis to predicting long-term prognosis and treatment response. Here, we focus on recent studies on the prognostic value of TE for predicting HCC.
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Metabolic dysfunction associated fatty liver disease and the risk of hepatocellular carcinoma Byeong Geun Song, Sung Chul Choi, Myung Ji Goh, Wonseok Kang, Dong Hyun Sinn, Geum-Youn Gwak, Yong-Han Paik, Moon Seok Choi, Joon Hyeok Lee, Seung Woon Paik JHEP Reports.2023; : 100810. CrossRef
Lee, Joo Ho , Jun, Mi Jung , Shim, Ju Hyun , Song, Gi Won , Tak, Eunyoung , Oh, Bora , Yu, Eunsil , Choi, Sang Woon , An, Jihyun , Lee, Danbi , Kim, Kang Mo , Lim, Young Suk , Lee, Han Chu , Chung, Young Hwa , Lee, Yung Sang
J Liver Cancer. 2018;18(1):33-43. Published online March 31, 2018
Background/Aims Because there is a lack of effective biomarkers, we aimed to discover proteomic candidate markers for hepatocellular carcinoma (HCC) in cirrhotic patients at the highest-risk of HCC, and to validate the markers. Methods: We collected tumor tissue from 5 cirrhotics with HCC, and from 5 cirrhotics without HCC, who underwent liver resection or transplantation. These tissue samples were analyzed by 2-dimensional difference gel electrophoresis coupled with matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), and potential markers were validated at the transcriptional and translational levels. We also performed western blot assays using other blood samples from 10 cirrhotics with HCC and 10 without HCC. Results: Among the 66 distinguishable spots on 2-D gel images, we identified 15 proteins overexpressed more than 1.5 fold in terms of volume ratio in the tumors. Ten of the over-expressed proteins were identified by MALDI-TOF MS; of those, only methionine adenosyltransferase 1 (MAT1), a protein specific for liver, and acyl-CoA dehydrogenase were significantly up-regulated in tumors in further immunoblotting analyses (Ps<0.05). There was no between-pair difference in MAT1 mRNA measured by real-time polymerase chain reaction (P=0.96). However, in western blots of serum samples, distinct MAT1 bands were observed in all 10 HCC patients, but in only 2 of the non-HCC patients. Conclusions: MAT1 is a potential marker for surveillance in cirrhotic patients with and without prior HCC.
The reported prevalence of PVT is in the range of 0.6-15.8% in patient with liver cirrhosis
or portal hypertension. If the patient has hepatocellular carcinoma, thrombus is likely to be
malignant thrombus. Malignancy, frequently of hepatic origin, is responsible for 21-24% of
over all cases. The overall mortality rate of chronic PVT has been reported to be less than
10%, but is increased to 26% when associated with hepatocellular carcinoma and cirrhosis.
However, no treatment guideline has been established on anticoagulant therapy for PVT in
patients with concomitant hepatocellular carcinoma and cirrhosis. Because actually it is not
easy to distinguish between malignant thrombus and benign thrombus in clinical aspect, PVT
in hepatocellular carcinoma are still debatable whether or not treatment when it diagnosed.
We present 3 cases of portal vein thrombosis successfully treated with anticoagulation in
hepatocellular carcinoma and liver cirrhosis, and we include a literature review.
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Evaluation of Low-Molecular-Weight Heparin for Treatment of Portal Vein Thrombosis in Liver Cirrhosis Patients Ji Min Han, Youngil Koh, Sung Hwan Kim, Sung Yun Suh, Yoon Sook Cho, Jeong-Hoon Lee, Su Jong Yu, Jung-Hwan Yoon, Hye Sun Gwak Medicina.2023; 59(2): 292. CrossRef
Most cases of hepatocellular carcinoma (HCC) occur in the Asia-Pacific region and in patients
with underlying hepatitis B and C viral infection. Although surgical resection is the gold
standard for treatment of HCC, only a few patients are surgical candidates because of their
lack of hepatic reserve. Liver transplantation, which eradicates HCC and replaces damaged
noncancerous hepatic parenchyma, is regarded as the best treatment for HCC in patients
with decompensated liver cirrhosis. However, the shortage of donors limit its widespread
use. Furthermore, the long waiting time for liver transplantation allow for tumor progression
and reduce patient survival. Given this long wait, there is a reasonable clinical need in the
meantime for minimally invasive methods to avoid progression of HCC in patients with
decompensated liver cirrhosis. We herein offer our experiences of therapeutic efficacy and
complications of the procedure and the changes in liver function before and after TACE and
radiofrequency ablation in patients with HCC and decompensated liver cirrhosis, defined as a
Child-Pugh-Turcotte score above 7. (J Liver Cancer 2014;14:139-142)
Treatment of hepatocellular carcinoma is often very challenging when the underlying liver
function is decompensated. Recent experimental and clinical studies showed that some
chelating agents, including deferoxamine, display anti-proliferative actions against tumor
cells, thereby exhibiting anti-cancer effect in certain cancers, including hepatocellular
carcinoma. Based on previous studies, we herein offer our experience of positive tumor
marker response after intra-arterial deferoxamine infusion in a patient presenting with
advanced hepatocellular carcinoma with decompensated hepatic function. Validation of
the efficacy of intra-arterial deferoxamine therapy in the setting of advanced hepatocellular
carcinoma with underlying decompensated hepatic function is warranted. (J Liver Cancer
2014;14:127-130)
Background/Aims The aim of the study is to investigate efficacy and safety of sorafenib
combined with transarterial chemoembolization (TACE) in Child-Pugh (CP) class-B patients
with hepatocellular carcinoma (HCC). Methods A total of 12 CP class-B patients who were initially treated with sorafenib combined
with TACE were retrospectively reviewed. At 14 days after the first TACE, patients were
continuously treated with sorafenib until unacceptable adverse events (AEs) or diseaseprogression.
Consecutive TACEs were also performed, if patients were tolerable. Results Of 12 patients, 8, 3 and 1 patients had CP-score 7, 8, and 9, respectively. The median
overall survival was 85 days. Patients underwent median 2 sessions of TACE (range 1-4) and
the median duration of sorafenib was 48days (range, 12-92 days). Three patients refused
repeated TACEs and 4 patients required delay of the consecutive TACE due to AEs of sorafenib.
Six patients required transient or permanent discontinuation of sorafenib, due to its AEs (grade
1/2 AEs, 2 patients; grade 3/4 AEs, 4 patients). High CP score (score 8/9 vs. 7) was tended to
be association with interruption of sorafenib (P=0.061) and requirement of refusal/ delay of
consecutive TACE (P=0.081). Conclusions Sorafenib combined with TACE were frequently interrupted or delayed in CP
class-B patients, mostly because of its side effects, even though there were not serious. Our
experiences suggest that combination with sorafenib and TACE might interface with each
other due to its side effects in CP class-B patients, especially patients with CP score 8/9 liver
cirrhosis.
Background/Aims Hepatocellular carcinoma (HCC) is common cause of liver related death in Korea, and the importance of alcohol as an etiology of chronic liver disease including cirrhosis is emphasized recently. We investigated the epidemiologic changes of HCC during last 10 years in single tertiary center in Gangneung, Korea.
Methods We retrospectively reviewed the medical records of admitted patients diagnosed as HCC in year 2002 and 2012 respectively, and their clinical characteristics were compared.
Results A total of 214 patients were enrolled. Mean age was 60.1 years and 179 (83.6%) was male. Number of patient with cirrhosis was 160 (74.8%) and with viral hepatitis was 164 (74.8%). Chronic hepatitis B (CHB) was the most common cause of HCC patients with liver cirrhosis (61.9%), and alcohol was 14.4%. The possible curative group (by BCLC stage 0 or A) was only 36.4% (n=78), and had not decreased during the study periods (36.3 % vs. 36.6%, P=0.144), and other clinical variables also had no statistical differences.
Conclusions The clinical characteristics of HCC including clinical stage at the time of diagnosis were not changed over the last 10 year period, and CHB was still the most common etiology of HCC in Gangneung, Korea.
Young Joon Yoon, Ki Tae Yoon, Jun Yong Park, Hyun Woong Lee, Hwa Sook Kim, Jae Kyung Kim, Young Nyun Park, Kwang-Hyub Han, Chae Yoon Chon, Young Myung Moon, Mi-Suk Park, Sang Hoon Ahn
Journal of the Korean Liver Cancer Study Group. 2007;7(1):41-44. Published online June 30, 2007
Focal nodular hyperplasia (FNH) usually occurs in non-cirrhotic livers and was defined as a nodule composed
of benign appearing hepatocytes occurring in a liver that is otherwise histologically normal or nearly normal.
However, due to improvements in imaging techniques and pathological evaluation of explant livers, a focal lesion
that is very similar to the classic form of focal nodular hyperplasia that occurs in cirrhotic liver has been
described by several reports. Therefore, the term FNH-like nodules has been proposed. In this report, we report
a case of focal nodular hyperplasia-like nodules in cirrhosis. A 59 year old woman with known hepatitis B virus
infection visited our institution for routine check up. She was diagnosed as having liver cirrhosis and 3.5 cm sized
liver mass on abdomen ultrasonography (US). Because tumor marker was negative and US findings are not
compatible with hepatocellular carcinoma, other imaging modalities were performed. Magnetic resonance imaging
(MRI) documented a 3.5 cm sized hypervascular nodule with internal aberrant vascular structure and multiple
small sized nodules in remaining liver. Needle biopsy was targeted to the liver main mass. Microscopic finding
revealed FNH-like nodule and underlying liver cirrhosis.