Evidence map›Paper›PMID 35610268›Full record

Observational studyScientific reports2022

An exploratory study investigating biomarkers associated with autoimmune pulmonary alveolar proteinosis (aPAP).

Ilaria Campo, Federica Meloni, Martina Gahlemann, Wiebke Sauter, Carina Ittrich, Corinna Schoelch, Bruce C Trapnell, Abhya Gupta

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 2 pooled it
0.6field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 2 syntheses or guidelines pooled it, 4 citations in OpenAlex.

  1. The burden of autoimmune pulmonary alveolar proteinosis: a systematic review.European respiratory review : an official journal of the European Respiratory Society · 2026
    Pooled it
  2. Pooled it
  3. 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

8 authors at 5 institutions in 4 countries.

Ilaria CampoUOS trasnplant center and Pneumology Unit, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.ORCID 0000-0002-4423-2482
Federica MeloniUOS trasnplant center and Pneumology Unit, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy. f.meloni@smatteo.pv.it.ORCID 0000-0003-4014-0617
Martina GahlemannBoehringer Ingelheim (Schweiz) GmbH, Basel, Switzerland.
Wiebke SauterBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Carina IttrichBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Corinna SchoelchBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Bruce C TrapnellTranslational Pulmonary Science Center, Cincinnati Children's Hospital, Cincinnati, OH, USA.
Abhya GuptaBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Boehringer Ingelheim (Germany) · DEBoehringer Ingelheim (Switzerland) · CHCincinnati Children's Hospital Medical Center · USPoliclinico San Matteo Fondazione · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune pulmonary alveolar proteinosis (aPAP) is a rare lung disorder involving production of autoantibodies against endogenous granulocyte-macrophage colony-stimulating factor (GM-CSF). This study aimed to identify biomarkers that could be used to monitor for aPAP, particularly in patients treated with anti-GM-CSF antibodies. This was an exploratory, prospective, observational, single-center study. Pre-specified biomarkers were evaluated between baseline and Day 120 in serum/plasma, whole blood, sputum and exhaled breath condensate from patients with aPAP, healthy volunteers, and patients with chronic obstructive pulmonary disease (COPD) and asthma (not treated with anti-GM-CSF and with no evidence of aPAP). Pulmonary function tests were also performed. Overall, 144 individuals were enrolled (aPAP: n = 34, healthy volunteers: n = 24, COPD: n = 40 and asthma: n = 46). Plasma GM-CSF levels were lower, and Krebs von den Lungen 6 and GM-CSF autoantibody ranges were higher, in patients with aPAP compared with other populations. Surfactant proteins-A and -D, lactate dehydrogenase and carcinoembryonic antigen ranges partially or completely overlapped across populations. Most plasma biomarkers showed high sensitivity and specificity for detection of aPAP; GM-CSF and GM-CSF autoantibody concentrations demonstrated equivalent sensitivity for differentiating aPAP. In addition to characteristic GM-CSF autoantibodies, assessment of plasma GM-CSF may identify individuals at risk of developing aPAP.Trial registration: EudraCT, 2012-003475-19. Registered 23 July 2012- https://eudract.ema.europa.eu/ .

Indexed as

AsthmaAutoimmune DiseasesPulmonary Alveolar ProteinosisPulmonary Disease, Chronic ObstructiveAutoantibodiesBiomarkersGranulocyte-Macrophage Colony-Stimulating FactorHumansProspective StudiesAutoantibodiesBiomarkersGranulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID35610268
PMCPMC9130212
OpenAlexW4281400444

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.