Evidence map›Paper›PMID 36620914›Full record

ArticleExpert review of hematology2023

Bad players in AL amyloidosis in the current era of treatment.

Natalia Kreiniz, Morie A Gertz

Abstract read
In one paragraph

Article in Expert review of hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Natalia KreinizDivision of Hematology, Bnai Zion Medical Centre, Haifa, Israel.
Morie A GertzDivision of Hematology, Mayo Clinic, Rochester, MN, USA.ORCID 0000-0002-3853-5196

Funding

Project 4: Targeting Resistance to T-Cell Directed Therapy in Multiple MyelomaP50CA186781 · NCI · MAYO CLINIC ARIZONA · PI Yi Lin · 2015 to 2026
$25.5M
NCI NIH HHS P50 CA186781
6 · The paper itself

Abstract

introductionSystemic AL amyloidosis (ALA) is a clonal plasma cell (PC) disease characterized by deposition of amyloid fibrils in different organs and tissues. Traditionally, the prognosis of ALA is poor and is primarily defined by cardiac involvement. The modern prognostic models are based on cardiac markers and free light chain difference (dFLC). Cardiac biomarkers have low specificity and are dependent on renal function, volume status, and cardiac diseases other than ALA. New therapies significantly improved the prognosis of the disease. The advancements in technologies - cardiac echocardiography (ECHO) and cardiac MRI (CMR), as well as new biological markers, relying on cardiac injury, inflammation, endothelial damage, and clonal and non-clonal PC markers are promising. AREAS COVERED: An update on the prognostic significance of cardiac ALA, number of involved organs, response to treatment, including minimal residual disease (MRD), ECHO, MRI, and new biological markers will be discussed. The literature search was done in PubMed and Google Scholar, and the most recent and relevant data are included. EXPERT OPINION: Prospective multicenter trials, evaluating multiple clinical and laboratory parameters, should be done to improve the risk assessment models in ALA in the modern era of therapy.

Indexed as

AmyloidosisImmunoglobulin Light-chain AmyloidosisBiomarkersHumansImmunoglobulin Light ChainsPrognosisProspective StudiesBiomarkersImmunoglobulin Light ChainsAL amyloidosisbiological markersBNPcardiac amyloidosisimmunoglobulin free light chainsprognosissystemic amyloidosistroponin

Identifiers

PMID36620914
PMCPMC9905376

What Socratic holds

Textmetadata
LicenceTDM
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.