Evidence map›Paper›PMID 38358415›Full record

ArticleClinical research in cardiology : official journal of the German Cardiac Society2025

Clinical and serological characterization of acute pleuropericarditis suggests an autoinflammatory pathogenesis and highlights risk factors for recurrent attacks.

Dorothee Kaudewitz, Lukas John, Jan Meis, Norbert Frey, Hanns-Martin Lorenz, Florian Leuschner, Norbert Blank

Open access · hybridAbstract read
In one paragraph

Article in Clinical research in cardiology : official journal of the German Cardiac Society, 2025. 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
1.2field-weighted citation impact, top 21% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

7 authors at 1 institution in 1 country.

Dorothee KaudewitzDepartment of Internal Medicine V, Hematology, Oncology and Rheumatology, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany. dorothee.kaudewitz@med.uni-heidelberg.de.ORCID http://orcid.org/0009-0004-2805-2643
Lukas JohnDepartment of Internal Medicine V, Hematology, Oncology and Rheumatology, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Jan MeisInstitute of Medical Biometry, University of Heidelberg, Heidelberg, Germany.
Norbert FreyDepartment of Internal Medicine III (Cardiology, Angiology, and Pneumology), Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Hanns-Martin LorenzDepartment of Internal Medicine V, Hematology, Oncology and Rheumatology, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Florian LeuschnerDepartment of Internal Medicine III (Cardiology, Angiology, and Pneumology), Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Norbert BlankDepartment of Internal Medicine V, Hematology, Oncology and Rheumatology, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWe describe the manifestations and course of patients with pleuropericarditis (PP). Serum parameters were analyzed to evaluate the contribution of autoimmune and autoinflammatory mechanisms to PP pathogenesis. Finally, we outline risk factors for recurrent PP attacks.

methodsElectronic medical records of the University Hospital Heidelberg were screened for PP diagnosis between the years 2009 and 2021. A total of 164 patients were detected and compared to patients suffering from systemic lupus erythematosus (SLE)-associated PP. Follow-up data were collected until January 2023.

resultsIn 57.3% of a total of 164 PP cases, no trigger was identified (idiopathic PP). The clinical manifestations were similar in subgroups with different triggers (idiopathic, post-cardiac injury and post-infectious). None of the patients in the idiopathic-PP (i-PP) group fulfilled the diagnostic criteria of an autoimmune disease and the i-PP group could be clearly discriminated by clinical, epidemiological and serological means from the control cohort of SLE-associated PP. After a median follow-up of 1048 days, the majority of PP patients (72.7%) had at least one PP relapse. Univariate analyses showed that CRP, SAA (serum amyloid A), troponin T, NT-BNP and post-cardiac injury were negatively correlated, while the presence of fever and an idiopathic trigger were positively correlated with recurrence of PP. Multivariate analyses showed that fever, an idiopathic trigger and low SAA values were risk factors for PP recurrence.

conclusionThis study highlights that most cases of PP are idiopathic and PP cases with various triggers have an identical clinical phenotype. Our data suggest that the clinical, epidemiological and serological characteristics of idiopathic PP considerably differ from patients with PP caused by autoimmune disease like SLE. We further demonstrate that PP has a high risk of recurrence and identify factors associated with this risk, allowing for a targeted secondary prophylaxis.

Indexed as

Autoimmune DiseasesPericarditisPleurisyAcute DiseaseAdultAgedBiomarkersFemaleFollow-Up StudiesHumansMaleMiddle AgedRecurrenceRetrospective StudiesRisk FactorsBiomarkersAntinuclear antibodiesAutoinflammationPericarditisPleuritisSerum amyloid A

Identifiers

PMID38358415
PMCPMC12408741
OpenAlexW4391844336

What OpenQuestion holds

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LicenceCC BY
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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.