A novel, bedside, etiology specific prognostic model (Peds-HAV) in hepatitis A induced pediatric acute liver failure

Lal, Bikrant Bihari; Sood, Vikrant; Snehavardhan, Pandey; Khanna, Rajeev; Pasupuleti, Samba Siva Rao; Siloliya, Manish K; Kumar, Guresh; Alam, Seema

doi:10.1007/s12072-020-10050-0

Cited by 21 publications

(19 citation statements)

References 23 publications

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“…HAV infection is the leading cause of pediatric acute liver failure in Asian countries (5), although the use of the HAV vaccine can prevent symptomatic hepatitis A, acute liver failure is still caused by HAV infection, and liver transplantation is required in many cases (6). Therefore, anti-HAV drugs should be developed.…”

mentioning

confidence: 99%

Additive Effects of Zinc Chloride on the Suppression of Hepatitis A Virus Replication by Interferon in Human Hepatoma Huh7 Cells

Kanda

Sasaki

Masuzaki

et al. 2020

In Vivo

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Background/Aim: Hepatitis A virus (HAV) infection is still one of the serious health problems worldwide, despite the existence of effective vaccines for HAV. Zinc compounds have antiviral activities against various DNA and RNA viruses. Therefore, we investigated the effects of zinc compounds on the antiviral activity of interferon against HAV. Materials and Methods: The effects of zinc compounds with or without interferon on HAV genotype IIIA HA11-1299 replication were examined in human hepatoma Huh7 cells. Cell viability was examined by the MTS assay. Inflammasome associated gene expression was examined by real-time reverse transcription-polymerase chain reaction. Results: Both zinc sulfate and zinc chloride had an inhibitory effect on HAV replication. Zinc sulfate tended to enhance while zinc chloride significantly enhanced the anti-HAV effect induced by interferon-alpha-2a. Zinc chloride significantly up-regulated mitogen-activated protein kinase 12 (MAPK12) and downregulated 6 related genes [baculoviral IAP repeat containing 3 (BIRC3), interleukin 1 beta (IL1B), proline-serine-threonine phosphatase interacting protein 1 (PSTPIP1), prostaglandinendoperoxide synthase 2 (PTGS2), PYD and CARD domain containing (PYCARD), and tumor necrosis factor (TNF)]. Conclusion: Zinc chloride inhibits HAV replication and has additive effects on the anti-HAV activities of interferon.

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mentioning

confidence: 99%

Additive Effects of Zinc Chloride on the Suppression of Hepatitis A Virus Replication by Interferon in Human Hepatoma Huh7 Cells

Kanda

Sasaki

Masuzaki

et al. 2020

In Vivo

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“…HAV accounted for 45.9% of the total PALF of 285 people. 27 The coexistence of dengue and HAV ALF has also been reported from India and may present clinical scenarios that are difficult to manage due to the complex course of the disease. 28 Unlike many countries in the Asia Pacific region, HAV rarely causes acute hepatitis-related deaths in Japan.…”

Section: Hepatitis Amentioning

confidence: 99%

“…34 In a Korean study, MELD and SIRS scores of >23.5 and >3 and above, respectively, were also associated with the development of ALF. 27 For paediatric HAV ALF, the PedsHAV model is a simple dynamic bedside prognostic model based on three objective parameters: (1) the presence of grade 3-4 HE, (2) an INR greater than 3.1 and (3) jaundice to HE interval >10 days a simple bedside dynamic HAV specificity based on jaundice. 35 In a large study by Jung et al from South Korea, post-transplant outcomes for HAV ALF patients were worse than for HBV ALF patients.…”

Section: Hepatitis Amentioning

confidence: 99%

Epidemiology of liver failure in Asia‐Pacific region

Jindal

Sarin

2022

Liver International

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It is important to understand the concept of liver failure because it can manifest in a number of phenotypes. If the onset of liver dysfunction or jaundice is accompanied by encephalopathy within days or weeks, it is called acute liver failure (ALF). 1 If chronic liver disease is rapidly worsened (within 4 weeks) by an acute event such as a hepatitis B or autoimmune flare or excessive alcohol intake, this is called acute-on-chronic liver failure (ACLF). [2][3][4] Early recognition of ACLF before the onset of sepsis and extrahepatic insults (such as renal, circulatory and respiratory failure) is important to help prioritize organ-specific interventions. 5 The syndrome of ACLF is potentially reversible 2 and with early attenuation of acute precipitating event, liver reserve improves, fibrosis regresses and portal pressure decreases. The clinical course and outcomes of ACLF patients are well differentiated from decompensated cirrhosis patients

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“…Infections are the leading cause of PALF in low and middleincome countries (41,42). In these countries, the lack of effective water sanitation facilities, of hygienic requirements for food processing and a sound sanitary system with adequate vaccination programs is responsible for the high incidence of hepatitis A virus (HAV) and hepatitis E virus (HEV) infections.…”

Section: Infections and Acute Liver Failurementioning

confidence: 99%

Proceedings of ESPGHAN Monothematic Conference 2020

Zellos

Debray

Indolfi

et al. 2021

J. pediatr. gastroenterol. nutr.

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Objectives:The Hepatology Committee of the European Society for Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) aims to educate pediatric gastroenterologists, members of ESPGHAN and professionals from other specialties promoting an exchange of clinical expertise in the field of pediatric hepatology. Herewith we have concentrated on detailing the recent advances in acute liver failure in infants and children.Methods:The 2020 ESPGHAN monothematic three-day conference on pediatric hepatology disease, entitled “acute liver failure” (ALF), was organized in Athens, Greece. ALF is a devastating disease with high mortality and most cases remain undiagnosed. As knowledge in diagnosis and treatment of ALF in infants and children has increased in the past decades, the objective was to update physicians in the field with the latest research and developments in early recognition, curative therapies and intensive care management, imaging techniques and treatment paradigms in these age groups.Results:In the first session, the definition, epidemiology, various causes of ALF, in neonates and older children and recurrent ALF (RALF) were discussed. The second session was dedicated to new aspects of ALF management including hepatic encephalopathy (HE), coagulopathy, intensive care interventions, acute on chronic liver failure, and the role of imaging in treatment and prognosis. Oral presentations by experts in various fields are summarized highlighting key learning points.Conclusions:The current report summarizes the major learning points from this meeting. It also identifies areas where there is gap of knowledge, thereby identifying the research agenda for the near future.

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A novel, bedside, etiology specific prognostic model (Peds-HAV) in hepatitis A induced pediatric acute liver failure

Cited by 21 publications

References 23 publications

Additive Effects of Zinc Chloride on the Suppression of Hepatitis A Virus Replication by Interferon in Human Hepatoma Huh7 Cells

Additive Effects of Zinc Chloride on the Suppression of Hepatitis A Virus Replication by Interferon in Human Hepatoma Huh7 Cells

Epidemiology of liver failure in Asia‐Pacific region

Proceedings of ESPGHAN Monothematic Conference 2020

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