Evidence map›Paper›PMID 31638602›Full record

ArticleThe Journal of clinical investigation2019

Paroxysmal nocturnal hemoglobinuria without GPI-anchor deficiency.

Robert A Brodsky

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. The inflammasomes: crosstalk between innate immunity and hematology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  4. Article
  5. Review
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Robert A Brodsky
Johns Hopkins Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired disorder characterized by hemolysis, thrombosis, and bone marrow failure caused by defective expression of glycosylphosphatidylinositol-anchored (GPI-anchored) complement inhibitors. Most commonly, PNH is caused by loss of function of PIGA, which is required for GPI biosynthesis. In this issue of the JCI, Höchsmann et al. report on 4 PNH patients who also had marked autoinflammatory manifestations, including aseptic meningitis. All 4 patients had a germline mutation of the related gene PIGT and a somatically acquired myeloid common deleted region (CDR) on chromosome 20q that deleted the second PIGT allele. The biochemistry and clinical manifestations indicate that these patients have subtle but important differences from those with PNH resulting from PIGA mutations, suggesting PIGT-PNH may be a distinct clinical entity.

Indexed as

Hemoglobinuria, ParoxysmalComplement System ProteinsGlycosylphosphatidylinositolsHumansInflammasomesMutationComplement System ProteinsGlycosylphosphatidylinositolsInflammasomes

Identifiers

PMID31638602
PMCPMC6877310
OpenAlexW2981711149

What OpenQuestion holds

Textmetadata
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.