Evidence map›Paper›PMID 42410852›Full record

ArticleMedicine2026

The predictive value of the systemic immune-inflammation index in chronic thromboembolic pulmonary hypertension.

Hatice Solmaz, Burcu Uludag, Ayse Colak

Abstract read
In one paragraph

Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Hatice SolmazDepartment of Cardiology, University of Health Sciences, Izmir City Hospital, Izmir, Turkey.ORCID 0000-0002-8474-1214
Burcu UludagDepartment of Cardiology, University of Health Sciences, Izmir City Hospital, Izmir, Turkey.ORCID 0000-0003-2178-6308
Ayse ColakDepartment of Cardiology, Dokuz Eylul University Faculty of Medicine, Izmir, Turkey.ORCID 0000-0002-1958-6158

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The systemic immune-inflammation index (SII) is associated with the severity and progression of vascular disorders. However, the relationship between SII and chronic thromboembolic pulmonary hypertension (CTEPH) remains unclear. This study aimed to investigate for the first time the predictive value of SII for the development of CTEPH in patients with a history of unprovoked acute pulmonary embolism (PE). This retrospective case-control study included 62 patients with unprovoked acute PE for the first time. Thirty patients with CTEPH and 32 without CTEPH were compared in terms of baseline and follow-up clinical, echocardiographic, and laboratory parameters obtained at least 3 months after the index event. Univariate and multivariate logistic regression analyses were performed to determine predictors of CTEPH. The diagnostic performance of the SII was evaluated using receiver operating characteristic curve analysis. Among the baseline laboratory parameters related to SII, only platelet count (308 [237-339] vs 259 [207-283], P = .028) was significantly higher in the CTEPH group, whereas SII did not differ significantly between the groups. During follow-up beyond 3 months, neutrophil count (5.4 [3.6-6.4] vs 4 [3.3-4.8], P = .01), platelet count (313 [219-376] vs 251 [201-295], P = .02), and SII (1614 [607-2147] vs 566 [417-727], P < .001) were significantly higher, whereas lymphocyte count (1.4 ± 0.5 vs 1.9 ± 0.5, P < .001) was significantly lower in the CTEPH group. Multivariate logistic regression analysis demonstrated that the SII was an independent predictor of CTEPH (odds ratio 1.003 [1.000-1.005], P = .02). Receiver operating characteristic curve analysis showed that the SII had moderate diagnostic performance for predicting CTEPH (area under the curve = 0.797; 95% confidence interval, 0.682-0.912; P < .001), with an optimal cutoff value of 626.7. The SII may represent a practical and easily accessible biomarker for identifying patients at risk of developing CTEPH during follow-up after the first episode of unprovoked acute PE.

Indexed as

Hypertension, PulmonaryInflammationPulmonary EmbolismAgedCase-Control StudiesChronic DiseaseEchocardiographyFemaleHumansMaleMiddle AgedPlatelet CountPredictive Value of TestsRetrospective StudiesROC CurveSeverity of Illness Indexchronic thromboembolic pulmonary hypertensioninflammationpulmonary embolismsystemic immune-inflammation index

Identifiers

PMID42410852
PMCPMC13336930

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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.