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Cancer
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The cause of hepatocellular carcinoma is primarily cirrhosis of the liver. However, the presence of the hepatitis B virus increases risks by 100 times in people who carry HBV. The risk factors include alcoholic cirrhosis, hemochromatosis, and chronic HCV infection. In some areas of the world, hepatocellular carcinoma is of higher incidence because of ingesting foods that are contaminated with fungal aflatoxins. Liver cancer in diabetic patients may be related to medications being taken to control blood glucose. People with type 2 diabetes may develop fatty liver, which is a trigger for cirrhosis, fibrosis, and cancer. Fatty liver disease is the most common cause of hepatocellular carcinoma. However, people with type 1 diabetes do not have an increased risk of liver cancer.
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Epidemiologic studies have shown a strong correlation between hepatitis B virus infection and the development of hepatocellular carcinoma.14,29,30–32,364,446,461 A relationship has also been found with related viruses.451 Infection with hepatitis B virus may have several consequences. Transient infection can cause subclinical disease, anicteric hepatitis, acute icteric hepatitis, or fulminant hepatitis. Persistent infections may lead to chronic conditions, such as chronic persistent hepatitis, chronic active hepatitis, or postnecrotic cirrhosis. Any of these conditions may lead to liver neoplasia. There is, however, a long incubation period lasting from 20 to 40 years between the onset of persistent hepatitis B virus infection and the development of primary hepatocellular carcinoma.356,365
Disease Prediction and Drug Development
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
The liver develops cancer through two types of infection HBV (Hepatitis B infection) and HCV (Hepatitis C infection). HBV is caused by Hepatitis B virus and is transmitted through a bodily fluid such as semen or blood contaminated through interaction with the contaminated fluid of another person. HCV is a viral infection caused by the Hepatitis C virus that causes liver inflammation and spreads through contaminated blood. Upregulation and downregulation of many genes vary for HBV and HCV. Identifying these genes separates the infection and act as a biomarker for cancer.
CpG DNA-triggered upregulation of TLR9 expression affects apoptosis and immune responses in human plasmacytoid dendritic cells isolated from chronic hepatitis B patients
Published in Archives of Physiology and Biochemistry, 2023
Bin Zhu, Tianbao Wang, Xiaoxia Wei, Yancai Zhou, Jiansheng Li
Human peripheral blood was obtained from three healthy donors aged 45.6 ± 5.23 (two males and one female) and three chronic hepatitis B patients aged 47.2 ± 3.68 (two males and one female) in The First Affiliated Hospital of Xinxiang Medical University with the approval of Health Ethic Committee (No.2016–09-11). Inclusion criteria: patients with chronic hepatitis B had different degrees of systemic fatigue, fatigue, loss of appetite and jaundice, and were diagnosed with chronic hepatitis B by liver function, histological diagnosis, hepatitis B virus markers and hepatitis B virus deoxyribonucleic acid (HBV-DNA). The diagnosis of patients with chronic hepatitis B was consistent with the “relevant diagnostic criteria of chronic hepatitis” in the Guidelines for Prevention and Treatment of Chronic Hepatitis B. Exclusion criteria: patients who were positive for HBeAg and anti-Hbe; patients co-infected with hepatitis C virus, hepatitis D virus, or human immunodeficiency virus, hepatic decomposition; patients who had other liver diseases (alcohol liver disease, fatty liver, autoimmune liver disease, metabolic liver disease, or liver cancer), or fibrosis and cirrhosis of the liver which was determined by transient elastography. This study conformed to the ethical guidelines of the 1975 Declaration of Helsinki. All patients provided written informed consent before the participation into the study.
Long-term durability of immunogenicity induced by standard and triple-dose hepatitis B vaccine in patients receiving methadone maintenance treatment
Published in Expert Review of Vaccines, 2020
Tian Yao, Yuanting Wu, Shuang Dong, Linying Gao, Shan Shi, Zhihong Shao, Lina Wu, Dan Feng, Jing Shi, Yawei Zhang, Yongliang Feng, Xiaofeng Liang, Suping Wang
Hepatitis B virus (HBV) infection is a major global health problem, with an estimated global prevalence of 3.5%. Worldwide, approximately 257 million people live with chronic HBV infection [1], a major contributing factor to liver cirrhosis and hepatocellular carcinoma (HCC) [2,3]. Use of the hepatitis B vaccine is an effective measure to prevent HBV infection [4]. China introduced the hepatitis B vaccine into routine immunization management as a comprehensive strategy in 1992. In response, the HBV prevalence rate in adults dropped from 9.8% in 1992 to 6.1% in 2016 [5,6]. However, the rate of HBV infection remains high in specific population groups, particularly in patients receiving methadone maintenance treatment (MMT) [7–11], a widely used alternative treatment for opioid dependence in drug users [12,13].
Antagonism of RIP1 using necrostatin-1 (Nec-1) ameliorated damage and inflammation of HBV X protein (HBx) in human normal hepatocytes
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Hepatitis B virus (HBV) infection is recognized as one of the major causes of chronic liver diseases, which have become a global health problem and affect millions of people worldwide [1]. HBV X protein (HBx), a protein containing 154 amino acids, is encoded by the smallest open reading frame of the DNA genome of HBV [2]. Studies have shown that HBx acts as a regulatory protein with pleiotropic effects. HBx plays an important role in enhancing HBV replication and causing various damages to hepatocytes [3]. HBx has recently been reported to induce autophagosome formation by increasing the production of reactive oxygen species (ROS) and activation of JNK [4]. Importantly, HBx causes apoptosis of hepatocytes through promoting the translocation of Bax from the cytoplasm to mitochondria, reducing mitochondrial membrane potential (MMP), and stimulating the release of cytochrome C [5]. Additionally, HBx treatment causes excessive production of several pro-inflammatory cytokines, such as interleukin-6 (IL-6), IL-8, chemokine (C-X-C motif) ligand 2 (CXCL2), and transforming growth factor-β (TGF-β), which have been considered as essential contributors to chronic liver inflammation and fibrosis [6]. Importantly, HBx could transactivate multiple intracellular signalling pathways including AP1 and NF-κB [7], which act as key regulators of inflammatory reactions in various tissue and cell types. However, the underlying molecular mechanisms are still needed to be elucidated.