Evidence map›Paper›PMID 41406505›Full record

SynthesisEBioMedicine2026

A genome- and phenome-wide association study of plasma procalcitonin concentrations in individuals of European ancestry.

Wenbo Zhang, Peter J van der Most, Siqi Wang, Zoha Kamali, Alice Giontella, Sofia Enhörning, Ron T Gansevoort, Pim van der Harst, Stephan J L Bakker, Olle Melander and 3 more

Abstract readMeta-Analysis
In one paragraph

Synthesis in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Heritability of neonatal acute phase protein levels.Brain, behavior, & immunity - health · 2025
    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

13 authors.

Wenbo ZhangDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands; Department of Critical Care, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands. Electronic address: w.zhang01@umcg.nl.
Peter J van der MostDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands.
Siqi WangDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands.
Zoha KamaliDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands; Department of Bioinformatics, Isfahan University of Medical Sciences, Isfahan, 81746-73441, Iran.
Alice GiontellaDepartment of Clinical Sciences Malmö, Lund University, 205 02, Malmö, Sweden.
Sofia EnhörningPerinatal and Cardiovascular Epidemiology, Department of Clinical Sciences Malmö, Lund University, 205 02, Malmö, Sweden; Department of Internal Medicine, Skåne University Hospital, 205 02, Malmö, Sweden.
Ron T GansevoortDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands.
Pim van der HarstDepartment of Cardiology, University Medical Center Groningen, University of Groningen, 9713 GZ, Groningen, the Netherlands; Division of Heart & Lungs, Department of Cardiology, University Medical Center Utrecht, Utrecht, 3584 AA, the Netherlands.
Stephan J L BakkerDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands.
Olle MelanderDepartment of Clinical Sciences Malmö, Lund University, 21428, Malmö, Sweden; Department of Internal Medicine, Skåne University Hospital Lund, 22242, Lund, Sweden.
Frederik KeusDepartment of Critical Care, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands.
Gerton LunterDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands.
Harold SniederDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, the Netherlands. Electronic address: h.snieder@umcg.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProcalcitonin (PCT) is a biomarker used to differentiate between viral and bacterial infections, though the underlying mechanisms are not yet fully understood. This study aimed to identify genetic variants associated with plasma PCT concentrations and explore the associations of genetically predicted PCT with a wide range of disease related traits in a PheWAS.

methodsWe conducted GWAS and meta-analysis using data from the MDCS (n = 4007), MPP (n = 5097), and PREVEND (n = 3344) cohorts. We used fine-mapping to prioritise likely causal variants and explored regulatory effects using eQTL data, summary-data-based Mendelian randomisation (SMR) and colocalisation. To validate the PCT findings, we conducted multi-trait analysis of GWAS (MTAG) combining our results with CALCA data from a large pQTL study. The polygenic risk score (PRS) for PCT was calculated in the UK Biobank (n = 457,418) based on the GWAS summary data, and associations between the PRS and 179 traits were assessed in a PheWAS.

findingsWe identified four independent significant SNPs in three loci associated with plasma PCT: CALCB (rs7119706, rs10832337), PBX4 (rs17217098), and PRDM15 (rs7277773). Fine-mapping prioritised 18 likely causal variants, including rs7119706 (near CALCB) and rs16930609 (mapped to CYP2R1) at the chromosome 11 locus. Our eQTL lookup identified significant results for 13 genes, but SMR and colocalisation analyses did not support their potentially causal effects on plasma PCT. The MTAG identified 28 additional significant SNPs across 14 loci. The PheWAS results revealed that PRS was associated with calcium metabolism-related traits, including calcium concentrations (p = 7.0 × 10

interpretationOur findings suggest that genetically predicted PCT is associated with multiple pathways including calcium metabolism and immune function, and has potential clinical implications for bone health, kidney function, and type 2 diabetes.

fundingChina Scholarship Council (File no. 202006210041 to WZ and 201906010319 to SW, respectively).

Indexed as

European PeopleGenome-Wide Association StudyPhenomicsProcalcitoninWhite PeopleBiomarkersFemaleGenetic Predisposition to DiseaseHumansMalePhenotypePolymorphism, Single NucleotideQuantitative Trait LociBiomarkersProcalcitoninExpression quantitative trait lociGenome-wide association studyPhenome-wide association studyProcalcitonin

Identifiers

PMID41406505
PMCPMC12902255

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Registered trials

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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.