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Hepatitis B
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Laura Felder, Zimeng Gao, Danielle Tholey
Hepatitis D virus: Incomplete RNA virus, which can superinfect 20–25% of chronic HBV-infected patients. As HDV requires the HBV machinery to replicate, the HDV cannot exist without HBV. HDV infection worsens chronic HBV infection, so that 25% may die from disease [2]. If HBV is prevented, HDV infection is prevented, too. HDV has no effect on pregnancy or fetus/neonate.
The digestive system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Hepatitis D Virus (HDV) Blood-borne pathogenCan only coinfect individuals with active hepatitis B infectionTransmitted through contaminated blood and body fluids. Higher incidence in i.v. drug abusersClinical course is similar to HBV
Communicable diseases
Published in Liam J. Donaldson, Paul D. Rutter, Donaldsons' Essential Public Health, 2017
Liam J. Donaldson, Paul D. Rutter
Hepatitis A and E are mainly transmitted by contaminated food or water. Hepatitis D virus is blood-borne but requires the presence of hepatitis B virus for replication; it is therefore always associated with coexisting hepatitis B infection. Infection is usually more severe and fatality rates higher than with simple hepatitis B infection.
Emerging drugs for hepatitis D
Published in Expert Opinion on Emerging Drugs, 2023
Hepatitis D virus (HDV) is the most aggressive form of chronic viral hepatitis for which an effective treatment is still lacking [1]. According to a recent study, it is estimated that approximately 4.5% of hepatitis B surface antigen (HbsAg)-positive individuals are also infected with HDV, which corresponds to 0.16% of the entire world population, and roughly 12 million people are infected with HDV [2]. It needs to be mentioned that two other studies have reported far higher (48–60 million) estimates [3,4]. The most recent figure has been mentioned as 0.44% of the world population (33 million) based on studies in the 2010 to 2019 period [5]. Current global HDV endemic regions include Mongolia, Pakistan, Middle East countries, Uzbekistan and other Central Asian countries in Asia, Cameroon and countries of sub-Saharan Africa in Africa, Western Pacific islands in Oceania, regions close to the Amazon river in South America and some eastern European countries such as Romania, Albania and Turkey [6]. Although there are findings suggesting that its incidence has decreased in Western countries, HDV infection is still a problem in these countries due to recent migration from endemic regions [7].
Pharmacotherapy options for managing hepatitis B in children
Published in Expert Opinion on Pharmacotherapy, 2021
Haruki Komatsu, Ayano Inui, Sachiyo Yoshio, Tomoo Fujisawa
The ESPGHAN guideline is similar to the APALS guideline; expect in cases of decompensated cirrhosis, a liver biopsy is required to determine the initiation of antiviral treatment. The most characteristic feature of the ESPGAHN guideline is the cut-off value used for HBeAg-negative chronic hepatitis: 20,000 IU/mL. The APALS guideline and the U.S. expert opinion use 2,000 IU/mL as the cut-off value of the reactivation phase (HBeAg-negative chronic hepatitis). It is unclear whether this difference in the cut-off value can influence the outcome of antiviral treatment. The difference may simply reflect the cautious stance of the ESPGHAN in the treatment of patients in the reactivation phase (HBeAg-negative chronic hepatitis). Another difference between the APALS and ESPGHAN guidelines is the treatment of children with both a low HBV DNA level (˂2,000 IU/mL) and an elevated ALT level. In the APASL guideline, this group is indicated for antiviral treatment if other causes are excluded and the liver histology is moderate or severe. In the ESPGHAN guideline, other diagnoses should be excluded from this group. Even if other diagnoses are excluded, the eligibility for treatment is unclear in the algorithm of the ESPGHAN guideline (gray zone in Table 1). Antiviral treatment is recommended for children with cirrhosis, HBV-related glomerulonephritis, or co-infection with hepatitis D virus, hepatitis C virus or HIV even if the patient’s ALT, HBV DNA, and liver histology do not meet the guideline’s criteria.
TLR3 and TLR4 SNP variants in the liver disease resulting from hepatitis B virus and hepatitis C virus infection
Published in British Journal of Biomedical Science, 2019
I Sghaier, S Zidi, L Mouelhi, E Ghazoueni, E Brochot, WY Almawi, BY Loueslati
We recruited 100 chronic HBV carriers and 174 chronic HCV carriers at Charles Nicolle Hospital in Tunis, Tunisia. In addition, 360 individuals who were seronegative for both HBV and HCV served as the control group (Table 1). HBV- or HCV-infected patients were sub-grouped into patients with chronic hepatitis, those with liver cirrhosis and those with HCC. Inclusion criteria were HBsAg seropositivity (HBV group), or positive anti-HCV antibodies and HCV RNA (HCV group) for ≥ 6 months, with or without persistently elevated alanine aminotransferase (ALT) levels. Individuals who did not meet these criteria or were co-infected with hepatitis D virus (HDV) and/or HIV were excluded. Additional exclusion criteria included Wilson’s Disease, autoimmune hepatitis and non-alcoholic steatohepatitis in the absence of diabetes, hypertriglyceridemia and related risk factors. Clinical and laboratory evaluation included biochemical [ALT and aspartate aminotransferase (AST)] and serological tests for HBV (HBsAg, HBeAg, anti-HBeAg, anti-HBctotal) and HCV (anti-HCV), and histopathology of liver biopsy. HCC was diagnosed by ultrasound, computerised tomography, magnetic resonance imaging, arteriography and tumour biopsy. Patients were characterised by alpha-fetoprotein (AFP) levels, and further classified by METAVIR score [16]; F0–F2 scores indicated mild fibrosis, while F3 and F4 indicated severe fibrosis. Necro-inflammatory activity was graded on 0–3 scale according to METAVIR activity grading. LFTs and AFP were measured by standard methods in the routine pathology laboratory. The approval of the local research ethics committee was obtained, as was written informed consent from each subject.