The Effects of Hepatic Artery Chemotherapy on Viral Hepatitis in Patients With Hepatocellular Carcinoma

Abstract Background Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths in Africa. In Africa, the major causes of HCC include chronic infection with hepatitis B virus (HBV) and/or hepatitis C virus (HCV). Knowledge of the changes in the incidence of viral hepatitis-associated HCC over time and the factors responsible for such changes is key in informing policies for the prevention of viral hepatitis-associated HCC in Africa. Aim The study aimed to systematically summarize the changes in the prevalence of viral hepatitis among HCC patients and the overall effect of the prevalence of viral hepatitis on the incidence of HCC over the past four decades in Africa (1980–2019). Methods A literature search was conducted in MEDLINE (PubMed), Google Scholar, Science Direct, Scopus, Web of Science, and African wide web for articles published on viral hepatitis-associated HCC in Africa from 1980 to 2019. The abstracts of the articles were screened for eligibility and those meeting the inclusion criteria were retrieved and reviewed. Results A total of 272 studies were included in the analysis. Viral hepatitis-related HCC incidence changed by 1.17% (95% confidence interval (CI): 0.63–1.71, p < 0.001), 0.82% (95% CI: 0.45–1.18, p < 0.001), and 3.34% (95% CI: 2.44–4.25, p < 0.001) for every 1% change in the prevalence of HBV, HCV, and hepatitis D virus (HDV) respectively, per decade. The incidence of HBV-related HCC decreased by − 0.50% (95% CI: − 0.74 – − 0.25, p < 0.001) over the last 40 years, while HCV-related HCC increased. Conclusion Overall, the incidence of viral hepatitis-associated HCC has not declined, mainly due to no decline in the prevalence of HCV, HDV, and the high number of chronic hepatitis B carriers on the African continent. There is an urgent need for the allocation of resources for the implementation of treatment and preventive programs for HBV, HCV, HDV, and HCC in Africa. This systematic review is registered with PROSPERO®, number CRD42020169723.

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Prophylaxis and treatment of chronic viral hepatitis as the prevention of hepatocellular carcinoma

Orvosi Hetilap ◽

10.1556/oh.2009.28529 ◽

2009 ◽

Vol 150 (1) ◽

pp. 19-26 ◽

Cited By ~ 1

Author(s):

Alajos Pár

Keyword(s):

Hepatocellular Carcinoma ◽

Hepatitis B ◽

Viral Hepatitis ◽

Chronic Viral Hepatitis

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.

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Changes in Hepatic Hemodynamics due to Primary Liver Tumours

HPB Surgery ◽

10.1155/1996/62057 ◽

1996 ◽

Vol 9 (4) ◽

pp. 245-248 ◽

Cited By ~ 9

Author(s):

F. Jakab ◽

Z. Ráth ◽

F. Schmal ◽

P. Nagy ◽

J. Faller

Keyword(s):

Hepatocellular Carcinoma ◽

Blood Flow ◽

Hepatic Artery ◽

Hepatic Blood Flow ◽

Primary Hepatocellular Carcinoma ◽

Portal Venous Flow ◽

Venous Flow ◽

Control Value ◽

Early Results ◽

Total Hepatic Blood Flow

Data regarding the afferent circulation of the liver in patients with primary hepatocellular carcinoma are controversial, we have carried out measurement of hepatic arterial and portal venous flow intraoperatively by transit time ultrasonic volume flowmetry. In patients with primary hepatocellular carcinoma the hepatic artery flow increased to 0.55±0.211 compared with the control value of 0.37±0.102 1/min. (p<0.01). The portal venous flow decreased from 0.61±0.212 l/min, to 0.47±l/min. p<0.01). Due to the opposite changes in the afferent circulation the total hepatic blood flow did not change significantly, compared with controls.The ratio of hepatic arterial flow to portal vein flow increased to 1.239±0.246 in patients with hepatocellular carcinoma, which is double of the control value (0.66±0.259 l/min). After resection this ratio did not change.The resection did not alter hepatic artery or portal venous flow significantly, although the total hepatic blood flow decreased significantly (p<0.01).On the basis of our early results it is possible that the ratio of the two circulations may be to deel measured with doppler ultrasound and provide diagnostic information.

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Combination therapy in the treatment of chronic viral hepatitis and prevention of hepatocellular carcinoma

International Immunopharmacology ◽

10.1016/s1567-5769(03)00012-2 ◽

2003 ◽

Vol 3 (8) ◽

pp. 1169-1176 ◽

Cited By ~ 20

Author(s):

G Rasi ◽

P Pierimarchi ◽

P Sinibaldi Vallebona ◽

F Colella ◽

E Garaci

Keyword(s):

Hepatocellular Carcinoma ◽

Combination Therapy ◽

Viral Hepatitis ◽

Chronic Viral Hepatitis

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

Clinical Science ◽

10.1042/cs0990207 ◽

2000 ◽

Vol 99 (3) ◽

pp. 207-214 ◽

Cited By ~ 17

Author(s):

Michiko OKUBO ◽

Goshi SHIOTA ◽

Hironaka KAWASAKI

Keyword(s):

Hepatocellular Carcinoma ◽

Viral Hepatitis ◽

Liver Diseases ◽

Total Mass ◽

Sandwich Elisa ◽

Chronic Viral Hepatitis ◽

Rt Pcr ◽

Platelet Counts ◽

Indocyanine Green Test ◽

Normal Controls

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.

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