Evidence map›Paper›PMID 37259144›Full record

SynthesisOrphanet journal of rare diseases2023

New insights in the genetic variant spectrum of SLC34A2 in pulmonary alveolar microlithiasis; a systematic review.

Åsa Lina M Jönsson, Ole Hilberg, Ulf Simonsen, Jane Hvarregaard Christensen, Elisabeth Bendstrup

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in Orphanet journal of rare diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Structures of the sodium-coupled phosphate importer SLC34A2 reveal a distinct architecture and gating mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
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 3 institutions in 1 country.

Åsa Lina M JönssonDepartment of Clinical Genetics, Aarhus University Hospital, Aarhus, Denmark. aasajoen@rm.dk.
Ole HilbergDepartment of Regional Health Research, University of Southern Denmark, Odense, Denmark. Ole.Hilberg@rsyd.dk.ORCID 0000-0002-3075-3463
Ulf SimonsenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Jane Hvarregaard Christensen *Department of Biomedicine, Aarhus University, Aarhus, Denmark.
Elisabeth Bendstrup *Centre for Rare Lung Diseases, Department of Respiratory Diseases and Allergy, Aarhus University Hospital, Aarhus, Denmark.
Aarhus University · DKAarhus University Hospital · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary alveolar microlithiasis (PAM) is a rare autosomal recessive lung disease caused by variants in the SLC34A2 gene encoding the sodium-dependent phosphate transport protein 2B, NaPi-2b. PAM is characterized by deposition of calcium phosphate crystals in the alveoli. Onset and clinical course vary considerably; some patients remain asymptomatic while others develop severe respiratory failure with a significant symptom burden and compromised survival. It is likely that PAM is under-reported due to lack of recognition, misdiagnosis, and mild clinical presentation. Most patients are genetically uncharacterized as the diagnostic confirmation of PAM has traditionally not included a genetic analysis. Genetic testing may in the future be the preferred tool for diagnostics instead of invasive methods. This systematic review aims to provide an overview of the growing knowledge of PAM genetics. Rare variants in SLC34A2 are found in almost all genetically tested patients. So far, 34 allelic variants have been identified in at least 68 patients. A majority of these are present in the homozygous state; however, a few are found in the compound heterozygous form. Most of the allelic variants involve only a single nucleotide. Half of the variants are either nonsense or frameshifts, resulting in premature termination of the protein or decay of the mRNA. There is currently no cure for PAM, and the only effective treatment is lung transplantation. Management is mainly symptomatic, but an improved understanding of the underlying pathophysiology will hopefully result in development of targeted treatment options. More standardized data on PAM patients, including a genetic diagnosis covering larger international populations, would support the design and implementation of clinical studies to the benefit of patients. Further genetic characterization and understanding of how the molecular changes influence disease phenotype will hopefully allow earlier diagnosis and treatment of the disease in the future.

Indexed as

CalcinosisGenetic Diseases, InbornLung DiseasesFrameshift MutationHumansLungPulmonary AlveoliSodium-Phosphate Cotransporter Proteins, Type IIbSLC34A2 protein, humanSodium-Phosphate Cotransporter Proteins, Type IIbGenetic diseasesInbornInterstitial lung diseasePulmonary alveolar microlithiasisPulmonary calcificationSLC34A2SLC34A2 mutationsSLC34A2 variantsSolute carrier family 34 (sodium phosphate), member 2 protein, human

Identifiers

PMID37259144
PMCPMC10230741
OpenAlexW4378902029

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.