Evidence map›Paper›PMID 28070238›Full record

ReviewWorld journal of cardiology2016

Hematological disorders and pulmonary hypertension.

Rajamma Mathew, Jing Huang, Joseph M Wu, John T Fallon, Michael H Gewitz

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Hemolysis-induced Lung Vascular Leakage Contributes to the Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018
    Article
  17. Article
  18. Myeloid-Derived Suppressor Cells and Pulmonary Hypertension.International journal of molecular sciences · 2018
    Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Rajamma MathewRajamma Mathew, Department of Physiology, New York Medical College, Valhalla, NY 10595, United States.
Jing HuangRajamma Mathew, Department of Physiology, New York Medical College, Valhalla, NY 10595, United States.
Joseph M WuRajamma Mathew, Department of Physiology, New York Medical College, Valhalla, NY 10595, United States.
John T FallonRajamma Mathew, Department of Physiology, New York Medical College, Valhalla, NY 10595, United States.
Michael H GewitzRajamma Mathew, Department of Physiology, New York Medical College, Valhalla, NY 10595, United States.
New York Medical College · USCreative Research Enterprises (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH), a serious disorder with a high morbidity and mortality rate, is known to occur in a number of unrelated systemic diseases. Several hematological disorders such as sickle cell disease, thalassemia and myeloproliferative diseases develop PH which worsens the prognosis. Associated oxidant injury and vascular inflammation cause endothelial damage and dysfunction. Pulmonary vascular endothelial damage/dysfunction is an early event in PH resulting in the loss of vascular reactivity, activation of proliferative and antiapoptotic pathways leading to vascular remodeling, elevated pulmonary artery pressure, right ventricular hypertrophy and premature death. Hemolysis observed in hematological disorders leads to free hemoglobin which rapidly scavenges nitric oxide (NO), limiting its bioavailability, and leading to endothelial dysfunction. In addition, hemolysis releases arginase into the circulation which converts L-arginine to ornithine, thus bypassing NO production. Furthermore, treatments for hematological disorders such as immunosuppressive therapy, splenectomy, bone marrow transplantation, and radiation have been shown to contribute to the development of PH. Recent studies have shown deregulated iron homeostasis in patients with cardiopulmonary diseases including pulmonary arterial hypertension (PAH). Several studies have reported low iron levels in patients with idiopathic PAH, and iron deficiency is an important risk factor. This article reviews PH associated with hematological disorders and its mechanism; and iron homeostasis and its relevance to PH.

Indexed as

AnemiaHemolysisIron homeostasisMyelofibrosisPulmonary hypertension

Identifiers

PMID28070238
PMCPMC5183970
OpenAlexW2567597526

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.