Evidence map›Paper›PMID 38920981›Full record

ReviewCurrent issues in molecular biology2024

Genetics and Epigenetics in Acquired Hemophilia A: From Bench to Bedside.

Nikolaos Evangelidis, Nikolaos Kotsiou, Paschalis Evangelidis, Vlasios I Alevizopoulos, Iasonas Dermitzakis, Sofia Chissan, Sofia Vakalopoulou, Eleni Gavriilaki

Abstract readReview
In one paragraph

Review in Current issues in molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. The Epigenetic Landscape of Hemophilia.Current molecular medicine · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. 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

8 authors.

Nikolaos EvangelidisHematology Unit-Hemophilia Centre, 2nd Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.ORCID 0000-0003-0519-1670
Nikolaos KotsiouHematology Unit-Hemophilia Centre, 2nd Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.ORCID 0009-0004-2919-5179
Paschalis EvangelidisHematology Unit-Hemophilia Centre, 2nd Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.ORCID 0000-0003-1783-5111
Vlasios I AlevizopoulosHematology Unit-Hemophilia Centre, 2nd Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
Iasonas DermitzakisMedical School, Faculty of Health Sciences, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.ORCID 0000-0002-9134-1083
Sofia ChissanHematology Unit-Hemophilia Centre, 2nd Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
Sofia VakalopoulouHematology Unit-Hemophilia Centre, 2nd Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
Eleni GavriilakiHematology Unit-Hemophilia Centre, 2nd Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.ORCID 0000-0002-8883-8208

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquired hemophilia A (AHA) is a bleeding disorder characterized by the immunological inhibition of factor VIII (FVIII) of the hemostatic pathway leading to hemorrhagic events. Different domains of FVIII are the target of autoantibodies (mainly immunoglobulin (Ig) G) leading to the deficiency of FVIII. Several factors have been associated with the activation of the auto-immunity towards FVIII. Emerging evidence implicates CD4+ T cell activation in mediating this autoimmune response, with their involvement like that observed in congenital hemophilia A. Several genes such as HLA II DRB*16, DQB1*0502, and CTLA-4 + 49 are responsible for the pathogenesis of AHA. Epigenetic modifications and mainly long-coding RNAS (lncRNAs) are potentially contributing to the pathogenesis of AHA. The treatment approach of AHA includes the management of acute bleeding events and the administration of immunosuppressive medications. This review aimed to summarize the published data on the genetics and epigenetics of AHA. The severity and the mortality of this disease are creating an emerging need for further research in the field of the genetics and epigenetics of acquired hemorrhagic disorder.

Indexed as

acquired hemophiliableeding disordersepigeneticsgeneticshematology

Identifiers

PMID38920981
PMCPMC11201880

What OpenQuestion holds

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Registered trials

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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.