Thrombopoietin levels in serum and liver tissue in patients with chronic viral hepatitis and hepatocellular carcinoma

2000 ◽  
Vol 99 (3) ◽  
pp. 207-214 ◽  
Author(s):  
Michiko OKUBO ◽  
Goshi SHIOTA ◽  
Hironaka KAWASAKI

Thrombocytopenia in liver diseases is considered to be due to splenic platelet pooling and accelerated destruction. Since thrombopoietin (TPO), a regulator of thrombopoiesis, is produced mainly in the liver, decreased production of TPO may account for thrombocytopenia in liver diseases. To address this issue, we measured serum TPO, using a sensitive sandwich ELISA, in 108 patients with chronic viral hepatitis, which included chronic hepatitis (CH) and liver cirrhosis (LC), and hepatocellular carcinoma (HCC), and in 29 normal controls. TPO mRNA in 78 liver samples was examined by reverse transcription (RT)-PCR. Platelet counts in CH, LC, HCC and controls were 176±15×109/l, 81±8×109/l, 99±7×109/l and 234±9×109/l respectively. Serum TPO levels in CH, LC and HCC were 2.79±0.4 fmol/ml, 1.49±0.2 fmol/ml and 1.97±0.2 fmol/ml, and were higher than those of controls. Serum TPO levels were positively correlated with prothrombin time and serum albumin (P < 0.05, in each case), and negatively correlated with Indocyanine Green test and Pugh score (P < 0.01 and P < 0.05 respectively). However, RT-PCR and immunohistochemistry showed that expression of TPO mRNA and protein were similar in the different liver diseases, suggesting that serum TPO is a reflection of the total mass of functional liver. Platelet counts were negatively correlated with spleen index, but not with serum TPO. These results suggest that thrombocytopenia in liver disease is not directly associated with serum TPO but is associated with hypersplenism.

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1576 ◽  
Author(s):  
Daisuke Uchida ◽  
Akinobu Takaki ◽  
Atsushi Oyama ◽  
Takuya Adachi ◽  
Nozomu Wada ◽  
...  

Chronic viral hepatitis B and C and non-alcoholic fatty liver disease (NAFLD) have been widely acknowledged to be the leading causes of liver cirrhosis and hepatocellular carcinoma. As anti-viral treatment progresses, the impact of NAFLD is increasing. NAFLD can coexist with chronic viral hepatitis and exacerbate its progression. Oxidative stress has been recognized as a chronic liver disease progression-related and cancer-initiating stress response. However, there are still many unresolved issues concerning oxidative stress, such as the correlation between the natural history of the disease and promising treatment protocols. Recent findings indicate that oxidative stress is also an anti-cancer response that is necessary to kill cancer cells. Oxidative stress might therefore be a cancer-initiating response that should be down regulated in the pre-cancerous stage in patients with risk factors for cancer, while it is an anti-cancer cell response that should not be down regulated in the post-cancerous stage, especially in patients using anti-cancer agents. Antioxidant nutrients should be administered carefully according to the patients’ disease status. In this review, we will highlight these paradoxical effects of oxidative stress in chronic liver diseases, pre- and post-carcinogenesis.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Zenghui Liang ◽  
Yingtang Gao ◽  
Wenxia Shi ◽  
Daokuan Zhai ◽  
Shilei Li ◽  
...  

Objective. In our previous study, we found that some miRNAs were deregulated in hepatocellular carcinoma (HCC), including miR-183. However, the expression of miR-183 in the progression of benign liver diseases to HCC and its correlation with clinicopathologic factors remain undefined.Methods. MiR-183 expression was measured in normal controls (NC) (n=21), chronic viral hepatitis B or C (CH) tissues (n=10), liver cirrhosis (LC) tissues (n=18), HCC tissues (n=92), and adjacent nontumor tissues (NT) (n=92) by quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR).Results. The expression levels of miR-183 were significantly higher in HCC than in NT, LC, CH, and NL (P=0.001,P<0.001,P=0.011,P<0.001, resp.). The upregulated miR-183 in HCC was correlated with TNM stage (P=0.042) and cirrhosis (P=0.025). The Kaplan-Meier survival analysis showed that miR-183 expression was not associated with the survival of HCC patients. However, miR-183 yielded an area under the curve (AUC) of 0.808 with 59.8% sensitivity and 91.8% specificity in discriminating HCC from benign liver diseases (CH and LC) or NC.Conclusions. The upregulated miR-183 may associate with onset and progression of HCC, but not with the patient survival. A further research is needed to determine the potential of miR-183 as biomarker for HCC.


2018 ◽  
Vol 11 (4) ◽  
pp. 1789-1796
Author(s):  
Randa Mohamed MA Farag ◽  
Dujana AlAyobi ◽  
Khalid A Alsaleh ◽  
Hye-Joo Kwon ◽  
Afaf EL-Ansary ◽  
...  

In Saudi Arabia AFP considered the main serum marker for diagnostic Hepatocellular carcinoma (HCC), due to the continuous detection of HCC in Saudi Arabia, using new biomarkers for early surveillance are essential to control in prevalence of HCC. The present study depend on compare the significant between serum and mRNA Glypican-3 (GPC-3) as newly identified diagnostic and prognostic biomarkers for HCC between study cases. And combined sensitivity of AFP and GPC-3. Three hundred study cases, divided into: 250 blood samples were 145 samples from HCC , 105 samples from chronic liver cirrhosis (CLC) and 50 normal controls were investigated for serum GPC-3 (sGPC-3) by Sandwich ELISA. Glypican-3 mRNA from whole blood cells was detected by quantitative RT-PCR. The comparison between two techniques was by sensitivity and specificity. The results of sGPC-3 showed higher significant in HCC group than CLC and normal controls (p<0.001). sGPC-3 sensitivity was 95% and specificity was 100%, while in GPC-3 mRNA were 100% and 94% respectively. The combination of sensitivity between AFP and sGPC-3 was 80% and 95% respectively. The data demonstrated that, can depend on sGPC-3 and Glypican-3 mRNA as tumor biomarkers for detection and surveillance of Hepatocellular carcinoma in Saudi patients. The sensitivity of Reverse Transcriptase-PCR is high accurate (100%) than estimating sGPC-3 by ELISA (95%).


2021 ◽  
Author(s):  
Cortlandt M. Sellers ◽  
Johannes Uhlig ◽  
Johannes M. Ludwig ◽  
Jeffrey S. Pollak ◽  
Tamar H. Taddei ◽  
...  

2009 ◽  
Vol 150 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Alajos Pár

Mivel a hepatitis B- és C-vírus- (HBV-, HCV-) fertőzés döntő szerepet játszik a hepatocellularis carcinoma (HCC) keletkezésében, a HBV és HCV okozta hepatitis és cirrhosis megelőzése és kezelése egyben a HCC prevencióját is jelentheti. A HCC primer prevencióját képviseli a HBV elleni vakcináció és a donorok szűrése HBV- és HCV-markerekre. A szekunder prevencióhoz sorolható az interferonalapú és/vagy nukleozidanalóg anti-HBV- és anti-HCV-terápia, a cirrhosisos betegek HCC irányában történő alfa-foetoprotein + ultrahang szűrése, valamint a HCC kuratív reszekciója/ablatiója utáni adjuváns antivirális kezelés. Várható, hogy a HBV-vakcináció világszerte történő széles körű alkalmazása, továbbá az optimalizált individuális antivirális kezelésmódok, az új nukleozidanalógok és HCV-specifikus proteáz- és polimerázgátlók révén előrelépés történik nemcsak a vírushepatitisek megelőzésében és terápiájában, hanem a HCC prevenciójában is a nem túl távoli jövőben.


2003 ◽  
Vol 3 (8) ◽  
pp. 1169-1176 ◽  
Author(s):  
G Rasi ◽  
P Pierimarchi ◽  
P Sinibaldi Vallebona ◽  
F Colella ◽  
E Garaci

2015 ◽  
Vol 1 (1) ◽  
pp. 18 ◽  
Author(s):  
Omar Abdel-Rahman

Hepatocellular carcinoma (HCC) is a commonly occurring cancer worldwide. The aetiology of HCC, often associated with different molecular carcinogenic pathways, differs geographically; with chronic viral hepatitis being the main cause in most localities. Different driving mutations resulting from distinct carcinogenic pathways potentially impact the choice of effective therapies for HCC.


2022 ◽  
Vol 23 (1) ◽  
pp. 500
Author(s):  
Francesco Paolo Russo ◽  
Alberto Zanetto ◽  
Elisa Pinto ◽  
Sara Battistella ◽  
Barbara Penzo ◽  
...  

Hepatocellular carcinoma (HCC) is one of the major causes of cancer-related death. Although the burden of alcohol- and NASH-related HCC is growing, chronic viral hepatitis (HBV and HCV) remains a major cause of HCC development worldwide. The pathophysiology of viral-related HCC includes liver inflammation, oxidative stress, and deregulation of cell signaling pathways. HBV is particularly oncogenic because, contrary to HCV, integrates in the cell DNA and persists despite virological suppression by nucleotide analogues. Surveillance by six-month ultrasound is recommended in patients with cirrhosis and in “high-risk” patients with chronic HBV infection. Antiviral therapy reduces the risks of development and recurrence of HCC; however, patients with advanced chronic liver disease remain at risk of HCC despite virological suppression/cure and should therefore continue surveillance. Multiple scores have been developed in patients with chronic hepatitis B to predict the risk of HCC development and may be used to stratify individual patient’s risk. In patients with HCV-related liver disease who achieve sustained virological response by direct acting antivirals, there is a strong need for markers/scores to predict long-term risk of HCC. In this review, we discuss the most recent advances regarding viral-related HCC.


1994 ◽  
Vol 29 (5) ◽  
pp. 610-615 ◽  
Author(s):  
C. Pramoolsinsap ◽  
N. Promvanit ◽  
S. Komindr ◽  
P. Lerdverasirikul ◽  
S. Srianujata

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