Evidence map›Paper›PMID 35282339›Full record

ReviewFrontiers in cardiovascular medicine2022

Post-transplant Lymphoproliferative Disorder Following Cardiac Transplantation.

Rabea Asleh, Hilmi Alnsasra, Thomas M Habermann, Alexandros Briasoulis, Sudhir S Kushwaha

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  3. Review
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  11. A Comprehensive Landscape ofTransplant international : official journal of the European Society for Organ Transplantation · 2023
    Article
  12. 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 4 institutions in 2 countries.

Rabea AslehDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, United States.
Hilmi AlnsasraDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, United States.
Thomas M HabermannDivision of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, United States.
Alexandros BriasoulisDivision of Cardiovascular Disease, University of Iowa Hospitals and Clinics, Iowa City, IA, United States.
Sudhir S KushwahaDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, United States.
Mayo Clinic in Arizona · USBen-Gurion University of the Negev · ILHadassah Medical Center · ILUniversity of Iowa Hospitals and Clinics · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-transplant lymphoproliferative disorder (PTLD) is a spectrum of lymphoid conditions frequently associated with the Epstein Barr Virus (EBV) and the use of potent immunosuppressive drugs after solid organ transplantation. PTLD remains a major cause of long-term morbidity and mortality following heart transplantation (HT). Epstein-Barr virus (EBV) is a key pathogenic driver in many PTLD cases. In the majority of PTLD cases, the proliferating immune cell is the B-cell, and the impaired T-cell immune surveillance against infected B cells in immunosuppressed transplant patients plays a key role in the pathogenesis of EBV-positive PTLD. Preventive screening strategies have been attempted for PTLD including limiting patient exposure to aggressive immunosuppressive regimens by tailoring or minimizing immunosuppression while preserving graft function, anti-viral prophylaxis, routine EBV monitoring, and avoidance of EBV seromismatch. Our group has also demonstrated that conversion from calcineurin inhibitor to the mammalian target of rapamycin (mTOR) inhibitor, sirolimus, as a primary immunosuppression was associated with a decreased risk of PTLD following HT. The main therapeutic measures consist of immunosuppression reduction, treatment with rituximab and use of immunochemotherapy regimens. The purpose of this article is to review the potential mechanisms underlying PTLD pathogenesis, discuss recent advances, and review potential therapeutic targets to decrease the burden of PTLD after HT.

Indexed as

Epstein-Barr virusheart transplantationimmunosuppressionmTOR inhibitorsPTLDrituximab

Identifiers

PMID35282339
PMCPMC8904724
OpenAlexW4212913021

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.