Evidence map›Paper›PMID 32487240›Full record

ArticleArthritis research & therapy2020

Interleukin-32 in systemic sclerosis, a potential new biomarker for pulmonary arterial hypertension.

Paola Di Benedetto, Giuliana Guggino, Giovanna Manzi, Piero Ruscitti, Onorina Berardicurti, Noemi Panzera, Nicolò Grazia, Roberto Badagliacca, Valeria Riccieri, Carmine Dario Vizza and 5 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Spatial transcriptomics identifies IL-32 as a lipid droplet-associated cytokine linked to tubular injury in human diabetic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  12. Endothelial Dysfunction in Systemic Sclerosis.International journal of molecular sciences · 2023
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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

15 authors at 5 institutions in 2 countries.

Paola Di BenedettoClinical Pathology Unit, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Giuliana GugginoRheumatology Section, Department of Internal Medicine, University of Palermo, Palermo, Italy.
Giovanna ManziDepartment of Cardiovascular and Respiratory Sciences, Sapienza University of Rome, Rome, Italy.
Piero RuscittiDivision of Rheumatology, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Onorina BerardicurtiDivision of Rheumatology, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Noemi PanzeraClinical Pathology Unit, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Nicolò GraziaClinical Pathology Unit, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Roberto BadagliaccaDepartment of Cardiovascular and Respiratory Sciences, Sapienza University of Rome, Rome, Italy.
Valeria RiccieriDepartment of Internal Medicine and Medical Specialities, Sapienza University of Rome, Rome, Italy.
Carmine Dario VizzaDepartment of Cardiovascular and Respiratory Sciences, Sapienza University of Rome, Rome, Italy.
Ganna RadchenkoSecondary Hypertension Department with Pulmonary Hypertension Center, State Institute National Scientific Center "MD Strazhesko Institute of Cardiology" of Ukrainian National Academy of Medical Science, Kyiv, Ukraine.
Vasiliki LiakouliRheumatology Section, Department of Clinical and Experimental Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.
Francesco CicciaRheumatology Section, Department of Clinical and Experimental Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.
Paola CiprianiDivision of Rheumatology, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Roberto GiacomelliDivision of Rheumatology, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. roberto.giacomelli@cc.univaq.it.ORCID 0000-0003-0670-9638
University of L'Aquila · ITSapienza University of Rome · ITUniversity of Campania "Luigi Vanvitelli" · ITNational Scientific Center "M.D. Strazhesko Institute of Cardiology" · UAUniversity of Palermo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPulmonary arterial hypertension (PAH) is a severe complication of systemic sclerosis (SSc), associated with a progressive elevation in pulmonary vascular resistance and subsequent right heart failure and death. Due to unspecific symptoms, the diagnosis of PAH is often delayed. On this basis, it is of great value to improve current diagnostic methods and develop new strategies for evaluating patients with suspected PAH. Interleukin-32 (IL-32) is a proinflammatory cytokine expressed in damaged vascular cells, and the present study aimed to assess if this cytokine could be a new biomarker of PAH during SSc.

methodsThe IL-32 expression was evaluated in the sera and skin samples of 18 SSc-PAH patients, 21 SSc patients without PAH, 15 patients with idiopathic PAH (iPAH) and 14 healthy controls (HCs), by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC). Receiver-operating characteristic (ROC) curves were performed to evaluate the cut-off of IL-32 in identifying patients with PAH. Furthermore, in SSc patients, correlation analyses were performed between IL-32 sera levels and mean pulmonary artery pressure (mPAP) evaluated by right heart catheterization (RHC) and systolic pulmonary artery pressure (sPAP), obtained by echocardiography. Additionally, the number of skin IL-32+ cells was correlated with modified Rodnan skin score (mRSS).

resultsIn SSc-PAH patients, IL-32 sera levels were significantly higher when compared with SSc patients without PAH and patients affected by iPAH. The analysis of ROC curve showed that IL-32 sera levels above 11.12 pg/ml were able to predict patients with PAH (sensitivity = 90%, specificity = 100%). Furthermore, the IL-32 sera levels of patients with SSc correlated with both mPAP and sPAP. In the skin derived from SSc-PAH patients, the number of IL-32+ cells was significantly increased when compared with the skin derived from SSc patients without PAH, correlating with the mRSS.

conclusionOur study suggested that sera determination of IL-32 may be a promising approach to evaluate the presence of PAH in SSc patients and together with longitudinal future studies could help to increase the understanding how these biomarkers mirror the vascular changes and the inflammatory process during SSc.

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionScleroderma, SystemicBiomarkersHumansInterleukinsBiomarkersIL32 protein, humanInterleukinsIL-32Pulmonary arterial hypertensionSystemic sclerosis

Identifiers

PMID32487240
PMCPMC7268373
OpenAlexW3029845271

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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.