Evidence map›Paper›PMID 32071839›Full record

ArticleJIMD reports2020

Early detection of lysosomal diseases by screening of cases of idiopathic splenomegaly and/or thrombocytopenia with a next-generation sequencing gene panel.

Gloria Muñoz, David García-Seisdedos, Crina Ciubotariu, Miguel Piris-Villaespesa, Marta Gandía, Fernando Martín-Moro, Luis G Gutiérrez-Solana, Marta Morado, Javier López-Jiménez, Antonio Sánchez-Herranz and 2 more

Open access · goldAbstract read
In one paragraph

Article in JIMD reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Guideline
  2. Abnormal Splicing ofBiomedicines · 2025
    Article
  3. Article
  4. Article
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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

12 authors at 3 institutions in 1 country.

Gloria MuñozUCA de Genómica Traslacional Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
David García-SeisdedosUCA de Genómica Traslacional Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Crina CiubotariuUCA de Genómica Traslacional Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Miguel Piris-VillaespesaServicio de Hematología Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Marta GandíaUCA de Genómica Traslacional Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Fernando Martín-MoroServicio de Hematología Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Luis G Gutiérrez-SolanaConsulta de Neurodegenerativas, Servicio de Neurología Pediátrica Hospital Infantil Universitario Niño Jesús Madrid Spain.
Marta MoradoServicio de Hematología Hospital Universitario La Paz Madrid Spain.
Javier López-JiménezServicio de Hematología Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Antonio Sánchez-HerranzUCA de Genómica Traslacional Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Jesús VillarrubiaUCA de Genómica Traslacional Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.
Francisco J Del CastilloUCA de Genómica Traslacional Hospital Universitario Ramón y Cajal, IRYCIS Madrid Spain.ORCID https://orcid.org/0000-0003-0467-4320
Instituto Ramón y Cajal de Investigación Sanitaria · ESCentre for Biomedical Network Research on Rare Diseases · ESHospital Universitario La Paz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysosomal diseases (LD) are a group of about 70 rare hereditary disorders (combined incidence 1:5000) in which diverse lysosomal functions are impaired, impacting multiple organs and systems. The first clinical signs and symptoms are usually unspecific and shared by hundreds of other disorders. Diagnosis of LD traditionally relies on performing specific enzymatic assays, if available, upon clinical suspicion of the disorder. However, the combination of the insidious onset of LD and the lack of awareness on these rare diseases among medical personnel results in undesirable diagnostic delays, with unchecked disease progression, appearance of complications and a worsened prognosis. We tested the usefulness of a next-generation sequencing-based gene panel for quick, early detection of LD among cases of idiopathic splenomegaly and/or thrombocytopenia, two of the earliest clinical signs observed in most LD. Our 73-gene panel interrogated 28 genes for LD, 1 biomarker and 44 genes underlying non-LD differential diagnoses. Among 38 unrelated patients, we elucidated eight cases (21%), five with LD (GM1 gangliosidosis, Sanfilippo disease A and B, Niemann-Pick disease B, Gaucher disease) and three with non-LD conditions. Interestingly, we identified three LD patients harboring pathogenic mutations in two LD genes each, which may result in unusual disease presentations and impact treatment. Turnaround time for panel screening and genetic validation was 1 month. Our results underline the usefulness of resequencing gene panels for quick and cost-effective screening of LDs and disorders sharing with them early clinical signs.

Indexed as

genetic screeninglysosomal diseaseNGS resequencing panelssplenomegalythrombocytopenia

Identifiers

PMID32071839
PMCPMC7012743
OpenAlexW2993550451

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.