China 
Africa 
Explore chapters and articles related to this topic
Hepatitis C
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Rebecca Pierce-Williams, Neil Silverman, Raja Dhanekula, Jonathan M. Fenkel, Danielle Tholey
Any woman who tests positive for anti-HCV antibody should have HCV RNA quantitative evaluation (via PCR) performed. An HCV genotype is also recommended, as treatment is tailored to the genotype and subtype. She should be screened for co-infection with HIV (HIV antibody) and hepatitis A and B (hepatitis B surface antigen), as well as other STIs. Patients with chronic HCV infection are at high risk of liver failure if they are infected with other forms of viral hepatitis. Screening for immunity to hepatitis A (hepatitis A total antibody) and hepatitis B (hepatitis B surface antibody), and vaccinating if non-immune, is also recommended. Blood tests to measure liver function include aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, platelet count and international normalized ratio (INR). Imaging of the liver to evaluate for cirrhosis can be completed with ultrasound during pregnancy, or liver elastography preconception or postpartum. Patients with cirrhosis should receive the pneumococcal vaccination [5]. A hepatology referral is recommended for assessment of disease severity, counseling on risk reduction behaviors, and treatment.
Hepatic disorders in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Ghassan M. Hammoud, Jamal A. Ibdah
The diagnosis of viral hepatitis is usually made on the basis of serologic testing (Table 2). Although viral hepatitis is not associated with teratogenicity, transmission of viral infection to the fetus may occur, which may result in premature labor. Transmission of infection is believed to occur primarily during the peripartum. For some infections, measures can be taken to prevent or lessen the severity of hepatitis in the newborn.
Human Monoclonal Antibodies and Immune Modulation in Viral Hepatitis, Schistosomiasis, and HTLV Infection
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Thomas F. Kresina, Garry A. Neil, Steven K. H. Foung
Viral hepatitis is a systemic infection in which hepatic cell necrosis and inflammation result in a constellation of hepatic sequelae. The multiple viral agents have distinct immunoserological characteristics, specific epidemiological attributes, and separate causes. No single histopathological lesion in the liver is diagnostic for viral hepatitis. However, there are common inflammatory characteristics apparent in viral hepatitis. Acute portal hepatitis is characterized by edema and an inflammatory infiltrate comprising lymphocytes and histiocytes that enlarge portal tracts. In hepatitis C infection, focal bile duct lesions are common and in chronic infection can result in degenerative changes, including necrosis and periductular fibrosis. Necrosis of periportal hepatocytes and merger of portal and lobular inflammation are characteristic of “piecemeal necrosis” and can occur in either acute or chronic active hepatitis. A further characteristic of viral hepatitis is lobular disarray where spotty necrosis occurs and the inflammatory cells accumulate in areas of hepatocyte necrosis [47]. Thus, infection with hepatitis B virus or hepatitis C virus without subsequent resolution or cure results in hepatic inflammation that progresses to chronic hepatitis, cirrhosis, and primary liver cancer [48].
To boost or not to boost? The long-term protection of people vaccinated in infancy from the perspective of the healthcare worker
Published in Infectious Diseases, 2020
In contrary, Bruce et al. concluded, in the longest cohort study on extended protection after hepatitis B vaccination to date, that hepatitis B booster doses are not currently needed for children, adolescents and adults vaccinated (e.g. healthcare workers) at 30 years out from primary vaccine series [8]. Anderson et al. concluded that paediatric doses of hepatitis B vaccine offers long-term protection against hepatitis B in adolescents up to 15–16 years, and produces a robust ‘anamnestic response’ and robust immune memory, which prevents acute disease and chronic infection [9]. The data presented by Bruce et al. confirm statements from the World Health Organisation (WHO), Centres for Disease Control and Prevention (CDC), and Viral Hepatitis Prevention Board that booster vaccination against hepatitis B for immunocompetent children and adults is not recommended. The Cochrane Database Systemic Review from 2016 concluded that there is no scientific evidence to support or reject the need for booster doses of hepatitis B vaccine in healthy individuals with normal immune status [10].
Severe dengue and liver involvement: an overview and review of the literature
Published in Expert Review of Anti-infective Therapy, 2020
Po Ying Chia, Tun-Linn Thein, Sean Wei Xiang Ong, David Chien Lye, Yee Sin Leo
Moderate liver disease is defined when a patient has all 3 of (i) an acute illness with discrete onset of signs and symptoms consistent with acute viral hepatitis (e.g. fatigue, abdominal pain, loss of appetite, intermittent nausea, vomiting, dark urine, clay-colored or light stools), (ii) alanine aminotransferase (ALT) greater than 10 times upper limit of normal consistent with grade 4 toxicity in the FDA 2007 toxicity tables or ≥400 U/L and (iii) does not meet criteria for acute liver failure (i.e. no mental status changes and international normalized ratio [INR] <1.5) [21]. Severe liver disease is defined when a patient has all 3 of (i) an acute clinical syndrome consistent with acute hepatitis, (ii) change in mental status or any grade of hepatic encephalopathy and (iii) coagulopathy with INR ≥1.5 [21].
Impaired albumin function: a novel potential indicator for liver function damage?
Published in Annals of Medicine, 2019
Lejia Sun, Huanhuan Yin, Meixi Liu, Gang Xu, Xiaoxiang Zhou, Penglei Ge, Huayu Yang, Yilei Mao
Viral hepatitis is an important risk factor for cirrhosis and liver cancer, and it’s one of the leading causes of human death and is becoming an increasingly serious problem of world health. But just like NAFLD, conventional non-invasive measurements cannot detect injury caused by early hepatitis. Impairments in metal- and fatty acid-binding by albumin are found in patients with hepatitis B and C, and these occur before other routine parameters become abnormal (Ge, Liao, et al. 2016). Furthermore, these changes are more severe than in NAFLD patients. A study (Yavuz et al. 2017) of 74 patients with chronic hepatitis B and 25 patients with HBV-induced cirrhosis found that serum IMA concentration and IMAR was higher in these patients than healthy controls, and both groups demonstrated liver fibrosis. Therefore, the authors proposed the use of IMA and IMAR as non-invasive markers of liver fibrosis in HBV patients. Similar results have also been reported for children with chronic liver disease (Cakir et al. 2012).