Evidence map›Paper›PMID 36428959›Full record

ReviewCells2022

Treatment of Chronic Hepatitis D with Bulevirtide-A Fight against Two Foes-An Update.

Peter Ferenci, Thomas Reiberger, Mathias Jachs

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Peter FerenciDivision of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-2306-1992
Thomas ReibergerDivision of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria.
Mathias JachsDivision of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria.
Medical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HDV infection frequently causes progression to cirrhosis and hepatocellular carcinoma (HCC). In summer 2020, the first potentially effective drug Bulevirtide (BLV) has been approved for the treatment of HDV by the EMA. BLV is a synthetic N-acylated pre-S1 lipopeptide that blocks the binding of HBsAg-enveloped particles to the sodium taurocholate co-transporting polypeptide (NTCP), which is the cell entry receptor for both HBV and HDV. In this review, we discuss the available data from the ongoing clinical trials and from "real world series". Clinical trials and real-world experiences demonstrated that BLV 2 mg administered for 24 or 48 weeks as monotherapy or combined with pegIFNα reduces HDV viremia and normalizes ALT levels in a large proportion of patients. The combination of BLV and pegIFNα shows a synergistic on-treatment effect compared with either one of the monotherapies.

Indexed as

Carcinoma, HepatocellularHepatitis DHepatitis D, ChronicLiver NeoplasmsSymportersAntiviral AgentsHepatitis Delta VirusHumansLipopeptidesOrganic Anion Transporters, Sodium-DependentVirus InternalizationAntiviral AgentsbulevirtideLipopeptidesOrganic Anion Transporters, Sodium-DependentSymportersbulevirtidehepatitis Binterferon-alfatreatment hepatitis D

Identifiers

PMID36428959
PMCPMC9688382
OpenAlexW4308507717

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.