Evidence map›Paper›PMID 34649277›Full record

ArticleBlood advances2022

A clinical, histopathological, and molecular study of two cases of VEXAS syndrome without a definitive myeloid neoplasm.

Peng Li, Shobi Venkatachalam, Daniela Ospina Cordona, Lorena Wilson, Tibor Kovacsovics, Karen A Moser, Rodney R Miles, David B Beck, Tracy George, Srinivas K Tantravahi

Open access · goldAbstract readCase Reports
In one paragraph

Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. VEXAS Syndrome-Review.Global medical genetics · 2023
    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

10 authors at 2 institutions in 1 country.

Peng LiDivision of Hematopathology, Department of Pathology, University of Utah Health, Salt Lake City, UT.
Shobi VenkatachalamDivision of Hematology and Hematologic Malignancies, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT; and.
Daniela Ospina CordonaNational Human Genome Research Institute, Bethesda, MD.ORCID 0000-0003-0865-6891
Lorena WilsonNational Human Genome Research Institute, Bethesda, MD.
Tibor KovacsovicsDivision of Hematology and Hematologic Malignancies, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT; and.
Karen A MoserDivision of Hematopathology, Department of Pathology, University of Utah Health, Salt Lake City, UT.
Rodney R MilesDivision of Hematopathology, Department of Pathology, University of Utah Health, Salt Lake City, UT.
David B BeckNational Human Genome Research Institute, Bethesda, MD.
Tracy GeorgeDivision of Hematopathology, Department of Pathology, University of Utah Health, Salt Lake City, UT.ORCID 0000-0001-5478-7847
Srinivas K TantravahiDivision of Hematology and Hematologic Malignancies, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT; and.
University of Utah · USNational Human Genome Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is caused by somatic mutations in UBA1 and is identified by a genotype-driven method. This condition affects unrelated men with adultonset inflammatory syndromes in association with hematologic manifestations of peripheral cytopenia and bone marrow myeloid dysplasia. Although bone marrow vacuolization restricted to myeloid and erythroid precursors has been identified in patients with VEXAS, the detailed clinical and histopathological features of peripheral blood and bone marrows remain unclear. The current case report describes the characteristic hematologic findings in patients with VEXAS, including macrocytic anemia, thrombocytopenia, marked hypercellular bone marrow with granulocytic hyperplasia, megaloblastic changes in erythroid precursors, and the absence of hematogones in addition to prominent vacuoles in myeloid and erythroid precursor cells. Characterizing the clinical and hematologic features helps to raise awareness and improve diagnosis of this novel, rare, but potentially underrecognized disease. Prompt diagnosis expands the general knowledgeable and understanding of this disease, and optimal management may prevent patients from developing complications related to this refractory inflammatory syndrome and improve the overall clinical outcome.

Indexed as

Myelodysplastic SyndromesMyeloproliferative DisordersNeoplasmsHumansMaleMutationUbiquitin-Activating EnzymesUbiquitin-Activating Enzymes

Identifiers

PMID34649277
PMCPMC8791569
OpenAlexW3205777762

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.