ArticleNeuropsychiatric disease and treatment2025
Feasibility of Serum Peroxiredoxin 2 as a Biochemical Indicator for Reflecting Severity and Prognosticating Stroke-Associated Pneumonia, Early Neurological Deterioration and Poor Neurological Outcomes in Acute Supratentorial Intracerebral Hemorrhage: An Observational Analytical Clinical Study.
Article in Neuropsychiatric disease and treatment, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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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.
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Who cites it
3 citing papers in PubMed.
- Peroxiredoxins in Stroke: Friends and Foes.Cells · 2026Review
- Serum Proteomics Reveals Systemic Responses inPathogens (Basel, Switzerland) · 2025Article
- Serum peroxiredoxin 2 emerges as a predictive biomarker of poor neurological outcome and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage: a prospective cohort study.Neurosurgical review · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Peroxiredoxin 2 (Prdx2) functions as an antioxidant and may be involved in acute brain injury. This study aimed to investigate whether Prdx2 can act as a serological marker for assessing the severity and forecasting stroke-associated pneumonia (SAP), early neurological deterioration (END), and neurological outcomes in acute intracerebral hemorrhage (ICH). Methods: A collective of 167 patients with ICH and 61 controls underwent quantifications for serum Prdx2 levels. In addition, 61 of them allowed Prdx2 measurements on days 1, 3, 5, 7, 10, and 14 post-ICH. Admission National Institutes of Health Stroke Scale (NIHSS) score and hematoma size were documented, and the modified Rankin Scale (mRS) at six-month mark following ICH was registered. Correlations between serum Prdx2 and END, SAP, and poor prognosis (mRS scores of 3-6) were determined using multivariate models. Results: Serum Prdx2 levels of patients rapidly increased after stroke, with the highest levels on day 3, and were substantially higher during the initial 14 days than those of controls. Prdx2 levels were closely related to NIHSS scores, hematoma size, and mRS scores, were linearly relevant to likelihoods of SAP, END, and poor prognosis, and were independently predictive of SAP, END, and poor prognosis. These associations were not markedly affected by age, sex, hypertension, or other factors using subgroup analysis. Moreover, the possibilities of END, SAP, and poor prognosis were efficiently distinguished by Prdx2 levels. Its discrimination efficiency was similar to those of the NIHSS scores and hematoma size. The combination of the three variables displayed a higher predictive ability than the combination of NIHSS scores and hematoma volume for prognosis prediction. Conclusion: A marked increase in serum Prdx2 levels after ICH may accurately mirror hemorrhagic severity and effectively predict END, SAP, and poor neurological outcomes, solidifying serum Prdx2 as a prognosticator of ICH.
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Registered trials
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