Evidence map›Paper›PMID 37042947›Full record

ReviewBlood advances2023

Deciphering the genetic basis of immune thrombocytopenia: current evidence for genetic predisposition in adult ITP.

Julia-Annabell Georgi, Jan Moritz Middeke, Martin Bornhäuser, Axel Matzdorff, Karolin Trautmann-Grill

Open access · goldAbstract readReview
In one paragraph

Review in Blood advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
9.6field-weighted citation impact, top 2% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Evaluation ofFrontiers in medicine · 2026
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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

5 authors at 3 institutions in 1 country.

Julia-Annabell GeorgiMedizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus der Technischen Universität, TU Dresden, Dresden, Germany.
Jan Moritz MiddekeMedizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus der Technischen Universität, TU Dresden, Dresden, Germany.
Martin BornhäuserMedizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus der Technischen Universität, TU Dresden, Dresden, Germany.ORCID 0000-0002-5916-3029
Axel MatzdorffAsklepios Klinikum Uckermark, Schwedt, Germany.
Karolin Trautmann-GrillMedizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus der Technischen Universität, TU Dresden, Dresden, Germany.
Klinik und Poliklinik für Psychotherapie und Psychosomatik · DEAsklepios Fachklinikum Brandenburg · DENational Center for Tumor Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune thrombocytopenia (ITP) is the consequence of a complex, still incompletely understood immunological dysregulation. Proposed mechanisms include autoantibody-induced platelet destruction, impaired platelet production as well as abnormalities in T-cell immunity, such as T helper cells (Th1) polarization, a high proportion of Th17 cells, and a reduced number of regulatory T cells. Although the etiology of ITP is incompletely understood and considered multifactorial in most cases, genetic variants are thought to play a key role in susceptibility to ITP, especially in persistent or chronic ITP. Efforts are currently underway to uncover possible predisposing genetic factors for the development of ITP. Single-nucleotide polymorphisms and copy number variations have been identified in several immune-related genes, such as cytokine genes, Fcγ receptor genes or T-cell costimulation genes, and have been associated with patients' susceptibility to ITP. However, because of the clinical heterogeneity and low incidence of ITP it remains challenging to perform genetic analyses with sufficiently large sample size within informative patient populations, highlighting the need for collection of well-annotated biomaterials in clinical trials or registry projects. Another significant challenge is to go beyond performing association studies alone and to establish genotype-phenotype associations, thus proving causality between a genetic alteration and ITP pathogenesis. This review summarizes our current knowledge on genetic alterations identified as potential predisposing factors for the development of ITP in adults, thereby addressing signaling pathways considered critical for ITP pathogenesis.

Indexed as

Purpura, Thrombocytopenic, IdiopathicThrombocytopeniaDNA Copy Number VariationsGenetic Predisposition to DiseaseHumansPolymorphism, Single Nucleotide

Identifiers

PMID37042947
PMCPMC10368779
OpenAlexW4365136444

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.