Red cell distribution width as a diagnostic and prognostic biomarker in neonatal sepsis: A scoping review

Abstract

Background

Neonatal sepsis remains a leading cause of infant mortality worldwide, with the greatest burden in low- and middle-income settings. Diagnosis is largely clinical and supported by blood culture, despite being limited by delayed results and suboptimal sensitivity. Red cell distribution width (RDW), a routine parameter in the full blood count, has been explored as a simple and cost-neutral marker of systemic inflammation and sepsis.

Methods

We conducted a scoping review of published research in MEDLINE, EMBASE, Scopus, and the Cochrane Library from inception to December 2025, supplemented by manual screening of reference lists. Studies evaluating RDW as a diagnostic and/or prognostic marker in neonates (≤28 days) with suspected or confirmed sepsis were included.

Results

Fourteen studies involving 2907 participants were included in this review. RDW levels were significantly higher in septic neonates compared to healthy controls, with diagnostic accuracy with Area Under Curve (AUC) ranging from 0.70 to 0.97. Elevated RDW served as a strong independent predictor of mortality, with prognostic AUCs between 0.75 and 0.80; thresholds above 19–20% correlated with an increased risk of mortality. In comparison to CRP and ESR, RDW often matched or exceeded their diagnostic performance. However, significant methodological heterogeneity exists regarding laboratory standards, timing of sampling, and sepsis definitions.

Conclusions

RDW is a promising and accessible marker for early risk stratification, particularly in resource-limited settings. However, current evidence is insufficient to support its use as a standalone tool; therefore, further studies are needed to validate its role in the future clinical settings.

Keywords

mortality neonatal sepsis prognosis red cell distribution width

Introduction

Neonatal sepsis is defined as a bloodstream infection in infants younger than 28 days of life.¹ Clinically, it is categorized as early-onset sepsis (EOS) or late-onset sepsis (LOS) based on age at presentation, with cut-offs commonly set at 72 h or 7 days after birth.² Despite advances in neonatal care, neonatal sepsis continues to be a significant cause of global morbidity and mortality, with a disproportionate impact on low- and middle-income countries.^3,4

Blood culture, the current diagnostic standard, has significant limitations in neonates due to difficulties in obtaining sufficient blood volumes and frequent exposure to antenatal or early postnatal antibiotics. As a result, a negative blood culture does not reliably exclude sepsis.⁵ Additionally, neonatal sepsis often presents with non-specific clinical manifestations, complicating early and accurate diagnosis.⁶ Thus, there is growing interest in identifying reliable and accessible biomarkers to improve diagnosis and risk stratification.

Red cell distribution width (RDW) is a routinely reported parameter in the complete blood count and has emerged as a potential marker of systemic inflammation and sepsis. In adult populations, elevated RDW is consistently associated with inflammation and increased mortality in sepsis.^7,8

In neonates, however, the evidence remains limited and heterogeneous. Existing studies vary considerably in terms of population characteristics (term vs preterm infants), definitions of sepsis (culture-proven vs clinical), timing of RDW measurement, and methods of laboratory reporting of RDW. Furthermore, reported diagnostic thresholds and performance metrics are inconsistent, limiting the clinical applicability of RDW in neonatal sepsis.

Given this heterogeneity and the absence of standardized approaches, we performed a scoping review to map the extent, nature, and characteristics of the available evidence in this topic, to identify key patterns, sources of variation, and methodological gaps that may inform future research and clinical application.

This scoping review therefore aims to systematically map the existing literature on RDW as a diagnostic and prognostic biomarker in neonatal sepsis. Specifically, we seek to (1) describe the range of study designs, populations, and settings in which RDW has been evaluated; (2) summarize reported diagnostic and prognostic performance of RDW; and (3) identify methodological limitations and evidence gaps that hinder its integration into clinical practice. By doing so, this review aims to inform future research directions and support the development of more standardized and context-appropriate use of RDW in neonatal care.

Methods

Study design and reporting

We conducted a scoping review to identify and map the existing literature on the use of RDW as a diagnostic and prognostic marker in neonatal sepsis. The review followed the Arksey and O’Malley framework and is reported in line with the PRISMA Extension for Scoping Reviews (PRISMA-ScR).⁹ A comprehensive protocol and search strategy of the literature was developed in collaboration with librarians from Universiti Sains Islam Malaysia.

Eligibility criteria

The eligibility criteria for this scoping review were defined to include all studies that analyzed red cell distribution width (RDW) in neonates. Studies involving neonates aged ≤28 days who were being evaluated for neonatal sepsis; either suspected, probable, or culture-proven sepsis (as defined by the individual studies) were eligible for inclusion. Only studies published in English were included, and there was no restriction on year of publication.

The articles were eligible if red cell distribution width (RDW), including RDW-coefficient of variation (RDW-CV) and/or RDW-standard deviation (RDW-SD), was evaluated as a diagnostic marker of neonatal sepsis and/or as a prognostic marker for disease severity, disease outcomes, and mortality. The inclusion criteria for this review was formulated according to the “Population–Concept–Context” framework recommended by the Joanna Briggs Institute,¹⁰ this is summarized in Table 1 below.

Table 1.

Inclusion criteria.

Population	Neonates with suspected, probable, or culture-proven sepsis
Concept	• Red cell distribution width (RDW) ◦ RDW-CV and/or RDW-SD • RDW evaluated as: ◦ Diagnostic marker of neonatal sepsis, and/or ◦ Prognostic marker (severity, mortality, outcomes)
Context	• Any healthcare setting ◦ Tertiary NICUs ◦ Secondary hospitals

Information sources

A comprehensive search strategy was developed using a combination of controlled vocabulary (MeSH and EMTREE terms) and free-text keywords related to neonates, sepsis, and red cell distribution width (RDW). The strategy was iteratively refined in consultation with an academic librarian to maximize sensitivity and specificity.

Electronic database searches were conducted in MEDLINE, EMBASE, the Cochrane Library, and Scopus from inception to 25 December 2025. Searches were performed in both title/abstract fields and indexed subject headings, where applicable. Terms within each concept were combined using the Boolean operator “OR,” and the three main concepts (neonates, sepsis, and RDW) were combined using “AND.”

The neonatal concept included terms such as “neonate,” “newborn,” “preterm,” “low birth weight,” “very low birth weight,” and “extremely low birth weight.” The sepsis concept included “sepsis,” “septic,” “bacteraemia,” and “infection.” The RDW concept included “red cell distribution width,” “red blood cell distribution width,” “erythrocyte distribution width,” and “anisocytosis.”

To ensure comprehensive coverage, supplementary search methods were employed, including screening the reference lists of included studies and relevant reviews, forward citation tracking, and targeted searches in Google Scholar.

No restrictions on publication were applied to capture the full scope of available evidence. Only studies published in English were included due to feasibility constraints.

The full search strategy for each database is provided in Table 2.

Table 2.

Search strategy.

1	exp Infant, Newborn
2	neonate or newborn or new born or baby or babies or premature or preterm or infant or low birth weight or LBW or VLBW or ELBW or NICU
3	1 or 2
4	Exp Sepsis
5	sepsis or septic or bacteremia
6	4 or 5
7	Red cell distribution width
8	RDW
9	Anicocytosis
10	7 or 8 or 9
11	3 and 6 and 10

Selection of articles

After duplicate removal, all titles and abstracts were screened for inclusion by two reviewers (AMK and TAMTM) based on the eligibility criteria. Full-text articles were then obtained and reviewed by two reviewers (NAMA and FSA) to confirm eligibility and extract data.

Data charting process

Using a predesigned form, three reviewers (LMY, NAMA, and NWBZ) extracted study metadata, including authorship, setting, and design, alongside neonatal characteristics such as gestational age, birth weight, and the timing of RDW measurements.

Data extracted included sepsis characteristics (early- or late-onset classification), definitions of neonatal sepsis used by authors, and methods of confirmation such as blood culture-proven or clinically diagnosed sepsis. Information on RDW assessment was collected, including RDW type (RDW-CV or RDW-SD), timing of measurement, mean or median RDW values in sepsis and control groups, RDW cut-off values, and the hematology analyzer model when reported.

Where available, diagnostic accuracy measures were extracted, including sensitivity, specificity, positive and negative predictive values, and area under the receiver operating characteristic curve. Prognostic outcomes such as mortality and length of hospital stay were recorded together with effect estimates (odds ratios, relative risks, or hazard ratios with confidence intervals).

Synthesis of results

Data were synthesized descriptively in accordance with scoping review methodology. Included studies were first mapped according to study design, geographic location, neonatal population characteristics, sepsis type (early-onset or late-onset), and the role of RDW as a diagnostic or prognostic marker.

Findings were then synthesized using a predefined conceptual framework comprising four domains: (1) diagnostic performance, (2) prognostic utility, (3) biological plausibility, and (4) methodological variability.

Within these domains, RDW-related outcomes were summarized narratively, including differences in RDW values between sepsis and control groups, reported cut-off thresholds, and measures of diagnostic accuracy such as sensitivity, specificity, and area under the receiver operating characteristic curve. Associations with clinical outcomes, including illness severity and mortality, were also examined. Composite indices incorporating RDW, such as the RDW-to-platelet ratio, were analyzed separately.

Methodological heterogeneity across studies was explored, including variation in sepsis definitions, timing of RDW measurement, and reporting formats (RDW-CV vs RDW-SD). Due to substantial clinical and methodological heterogeneity, meta-analysis was not undertaken. The synthesis therefore focused on mapping the extent, characteristics, and patterns of the available evidence, as well as identifying key gaps to inform future research.

Results

Selection of articles

The search identified 60 unique records from which 23 articles were screened in full text, and 14 articles were included in the final data collection, as shown in the PRISMA flow diagram of the screening process in Figure 1.

Figure 1.

Prisma flow diagram.

Study characteristics

The included evidence comprised fourteen primary studies. Of the included studies, eight were retrospective cohort studies,^11–18 two were prospective cohort studies,^19,20 two were cross-sectional studies,^21,22 and two were case-control studies.^23,24

The studies were globally distributed but predominantly concentrated in Asia, specifically from China, India, Bangladesh, Nepal, and Indonesia.^{11,15,17,18,20,22,23} Three studies were performed in Africa.^12,21,24 Only two studies utilized data from Western nations: one from Italy and one using the MIMIC-III intensive care database from a medical center in the United States.^13,14

Study settings

The vast majority of the research was conducted in low- and middle-income countries (LMICs) or upper-middle-income economies, highlighting a strong clinical interest in RDW as an accessible and cost-effective biomarker in resource-limited settings.^{11,12,15–24} Only two studies were conducted in high-income settings.^13,14 In terms of clinical settings, almost all studies were hospital-based and conducted in Neonatal Intensive Care Units (NICUs).^11–24

Sample sizes and population characteristics

Sample sizes range from small cohorts to moderately large populations.^19,20 Smaller studies included between 80 and 124 neonates, while the largest studies analyzed cohorts of 300 to 502 neonates.^{12,13,16–21,23,24} Table 3 summarizes characteristics of the included studies.

Table 3.

Characteristics of the included studies.

Study (First Author, Year)	Study design	Geographic distribution and setting	Sample size and population characteristics	Sepsis type studied
Cai (2021)	Retrospective cohort	China (UMIC); NICU	N = 83; Preterm neonates	Late-onset sepsis (LOS)
Dogan (2019)	Retrospective cohort	Turkey (UMIC); NICU	N = 86; Preterm (less than 36 weeks)	Late-onset sepsis (LOS)
Ellahony (2017)	Retrospective observational	Egypt (LMIC); NICU	N = 500; Full-term	Mixed (EOS & LOS)
Garofoli (2014)	Retrospective observational	Italy (HIC); NICU	N = 122; Mixed (Term, Preterm, and IUGR)	Late-onset sepsis (LOS)
Guo (2021)	Retrospective observational	USA database/China authors (HIC setting); Critical Care Units	N = 334; Preterm (Very Low Birth Weight <1500g)	Mixed (Serious bacterial infection)
Huang (2023)	Retrospective cohort	China (UMIC); Neonatal Department	N = 298; Mixed (Term & Preterm)	Mixed (Culture-positive & clinical)
Karabulut (2019)	Retrospective cohort	Turkey (UMIC); Hospital-based	N = 308; Term (37–42 weeks)	Early-onset sepsis (EOS)
Khadka (2022)	Cross-sectional	Nepal (LMIC); NICU and PICU	N = 171; Mixed	Mixed (EOS & LOS)
Lubis (2025)	Retrospective cohort	Indonesia (LMIC); NICU	N = 80; Mixed (Term & Preterm)	Mixed (EOS & LOS)
Martin (2018)	Prospective observational	India (LMIC); Level IIIB NICU	N = 502; Mixed (>28 weeks gestation)	Early-onset sepsis (EOS)
Mousa (2019)	Case-control	Egypt (LMIC); NICU	N = 124; Term neonates	Mixed (Proven & probable)
Nargis (2024)	Case-control	Bangladesh (LMIC); Paediatrics inpatient department	N = 90; Term (37–42 weeks, normal birth weight)	Early-onset sepsis (EOS)
Omer (2021)	Cross-sectional	Sudan (LMIC); NICU	N = 111; Term (1–28 days old)	Mixed (Both early and late)
Xu (2024)	Retrospective observational	China (UMIC); NICU	N = 98; Preterm (<37 weeks, <2.5 kg)	Mixed (Septicemia)

UMIC = Upper-Middle-Income Country, LMIC = Lower-Middle-Income Country, HIC = High-Income Country).

Baseline RDW values

The baseline RDW values varied widely across the included studies, generally ranging from around 14% to nearly 22%. Several studies which studied neonates with sepsis reported mean RDW in their studies, such as Nargis et al. (21.83 ± 2.39%),²³ Omer & Muhammad (19.3%),²¹ and Mousa et al. (17.64 ± 2.72%).²⁴ Other studies reported the median RDW value, ranging from 17.0%¹⁴ to 19.9%.²⁰ Three studies by Karabulut & Argacok,¹⁶ Khadka et al.,²² and Huang et al.¹⁵ compared between culture-proven sepsis versus probable sepsis, with higher reported mean and median RDW values in the culture-proven sepsis group (Median: 16% (IQR: 15.0–17.0)–18% (IQR 16.9–20), Mean: 19.2%) as compared to the probable sepsis group (Median: 15.0% (IQR: 14.0–16.0)–15.6% (IQR 11.5–17%), Mean 18.6 ± 2.1).^15,16,22

Diagnostic performance of RDW

Across multiple study designs, neonates presenting with sepsis exhibit significantly higher RDW levels compared to healthy control groups. Specifically, mean RDW was shown to be 21.83% versus 15.23% in early-onset sepsis (EOS),²³ 17.64% versus 12.55% in mixed sepsis cohorts,²⁴ and 19.90% versus 18.90% in another study by Martin et al.²⁰ Furthermore, RDW successfully differentiates the certainty of infection; values are significantly higher in culture-proven sepsis cases than in culture-negative (probable or clinical) cases.^15,22 A summary of the RDW cut-off values reported across included studies is presented in Figure 2.

Figure 2.

Summary of the RDW cut-off values reported across included studies.

Furthermore, RDW demonstrates strong but variable diagnostic accuracy, with Area Under the Curve (AUC) values ranging from 0.70 to 0.967 depending on the clinical context and specific cut-off used.^19,22,23 For example, one cohort reported a high AUC of 0.967 for diagnosing EOS specifically, achieving 86.6% sensitivity and 95% specificity using a cut-off of ≥20.60%.²³ For general sepsis diagnosis, other studies report moderate accuracy, such as an AUC of 0.760 using a >16.8% cut-off.²² Tracking dynamic changes also enhances accuracy; combining a baseline RDW >17% with a subsequent increase (ΔRDW) of >2% yielded an AUC of 0.81 for serious bacterial infections.¹⁴

The utility of RDW was reported similarly in EOS and LOS. In EOS, RDW functioned as a highly accurate early screening tool, correlating strongly with initial inflammatory responses in the first 12–24 h of life.^16,23 Similarly, preterm infants developing LOS showed significant RDW elevations precisely at the onset of the clinical episode.¹³ Crucially, RDW aided the differentiation of specific pathogens in LOS; values increased significantly during Gram-negative episodes (AUC 0.89) but remained relatively unchanged during Gram-positive infections, providing vital guidance for empiric antibiotic selection.¹⁹

Prognostic utility of RDW

Separate from its diagnostic capabilities, increased RDW served as a strong, independent predictor of mortality and poor clinical outcomes. The prognostic AUCs for predicting mortality were tightly grouped between 0.75 and 0.80 across several studies.^12,18,24 For instance, a cut-off of ≥18% was identified as the most sensitive hematological marker for predicting mortality (77.8% sensitivity, AUC 0.80) in a prospective cohort.²⁴ Other cohorts suggested higher thresholds of RDW in predicting mortality, such as >19.85% or ≥20%.^19,20,23

RDW levels closely mirrored established clinical severity scoring systems, reflecting the magnitude of systemic instability. RDW shared a significant positive correlation with the Score for Neonatal Acute Physiology-II (SNAP-II), and elevated RDW accurately matches the mortality prediction of a severe SNAP-II score ≥40.²⁴ Furthermore, an increment of RDW value during the course of hospital stay was shown to be highly accurate for predicting neonatal death.^13,14,18

Figure 3 demonstrates the AUC of RDW used as a diagnostic and prognostic marker across the studies. While RDW showed high diagnostic accuracy for EOS (Blue cluster), its prognostic performance for mortality (green cluster) was more tightly grouped between 0.75 and 0.78.

Figure 3.

AUC of RDW as diagnostic and prognostic marker.

Comparison with other biomarkers

RDW frequently matched or outperformed traditional inflammatory markers like C-reactive protein (CRP) and Erythrocyte Sedimentation Rate (ESR), while offering the advantage of being a “free” metric automatically generated in standard complete blood count. In direct comparisons, RDW achieved a higher diagnostic accuracy (AUC 0.760) than both CRP (AUC 0.675) and ESR (AUC 0.596).²² Prognostically, RDW has demonstrated superiority; one study found RDW to be a highly sensitive mortality predictor while CRP showed no statistically significant prognostic value for survival.²⁴ In other cohorts, the baseline prognostic accuracy of RDW (AUC 0.751) was nearly identical to CRP (AUC 0.745).¹²

When compared to Procalcitonin (PCT), the findings were mixed. While both RDW and PCT respond sensitively to disease severity, PCT generally maintained a higher predictive value for overall clinical prognosis.¹⁸ When compared with CRP and PCT in the early hours of life, derived indices like the RDW-to-platelet ratio (RPR) offered higher diagnostic specificity and positive predictive value.¹⁶ However, Immature to Total neutrophil (I/T) ratio showed a higher overall AUC (0.947–0.955) compared to RPR (0.786–0.816) in their cohort.¹⁶ Thus, combining RDW into diagnostic nomograms with other parameters like I/T ratio, PCT and CRP may enhance their ability to distinguish true proven sepsis from clinical mimicry.

Ultimately, because traditional markers like CRP are constrained by delayed hepatic synthesis and high false-positive rates from non-infectious perinatal stressors,¹⁵ RDW serves as a highly valuable, rapid complementary adjunct rather than a standalone replacement for existing biomarkers.

Biological and pathophysiological plausibility

The physiological mechanism linking elevated RDW to neonatal sepsis is primarily rooted in the body’s systemic inflammatory response and oxidative stress, which disrupt normal erythrocyte homeostasis.^19,20 During a septic episode, the massive release of pro-inflammatory cytokines impairs bone marrow function by inhibiting erythropoietin-induced erythrocyte maturation and downregulating erythropoietin receptor expression.^16,24 This acute inflammatory stress forces the premature release of larger, immature red blood cells (reticulocytes) into the peripheral circulation, thereby increasing the variability in cell size, known clinically as anisocytosis.^19,24 Furthermore, sepsis generates high levels of reactive oxygen species that damage red blood cell membranes, reduce cellular deformability, and shorten overall erythrocyte survival.^16,24 Consequently, an elevated RDW serves as an integrative biological marker reflecting the severity of unstable erythropoiesis, inflammation, and oxidative stress.^13,20,24

Methodological variability

Despite its clinical promise, substantial methodological and clinical heterogeneity limits the immediate universal application of RDW. First, there is a lack of standardization in laboratory determination. Studies utilize a variety of automated hematology analyzers (e.g., Sysmex, Mindray, and Cell-Dyn) with differing algorithmic calculations.^{13,15,19,22,24} Furthermore, RDW is inconsistently reported as either a coefficient of variation (RDW-CV), a standard deviation (RDW-SD), or a generic percentage.

Second, the timing of blood sampling fluctuates widely across the literature, ranging from the first hours of life to the exact onset of clinical symptoms, or tracked over multiple hospital days.^11,14,18,20 It is known that RDW fluctuates with gestational and postnatal age. However, in the included studies, there was notable variation in how control groups were adjusted for postnatal age. Martin et al. is the only study to strictly standardize this comparison by hours, collecting all blood samples for both sepsis cases and healthy controls precisely at 6 hours of life to account for rapid early physiological changes.²⁰ Two studies by Mousa et al.²⁴ and Nargis et al.²³ successfully matched their sepsis and control cohorts based on postnatal age measured in days rather than hours. The vast majority of the remaining studies did not employ a healthy control group, opting instead to compare subgroups within cohorts of already infected neonates, such as evaluating survivors versus non-survivors, differing pathogen types, or proven versus clinical sepsis cases.

Finally, diagnostic definitions of neonatal sepsis vary, heavily blending culture-proven cases with clinical/probable cases, which introduces confounding from non-infectious perinatal stressors.^{12,15–17,20,22–24}

Evidence gaps

Despite the promising diagnostic and prognostic potential of RDW in neonatal sepsis, this review identifies several key evidence gaps that limit its clinical translation. These include the predominance of retrospective single-center studies, the absence of standardized RDW cut-off values, inadequate adjustment for confounding variables, and limited evaluation of longitudinal RDW trends.

First, the current evidence base is largely derived from retrospective, single-center observational studies, which restrict generalizability and introduce potential selection bias. There is a need for large, prospective, multicenter studies to validate the diagnostic accuracy and prognostic utility of RDW across diverse populations and healthcare settings.

Second, no universal RDW cut-off values have been established for diagnosing neonatal sepsis or predicting outcomes. This is particularly important given that RDW varies with gestational age, birth weight, and early postnatal physiological changes, such as reticulocytosis. In conditions with ineffective erythropoiesis, such as prematurity, there are abnormal erythrocyte sizes causing an increase in RDW values. Conversely, in conditions with increased erythropoiesis, such as chronic intrauterine hypoxia, there is an increase in the RDW value.^25,26 Therefore, future development of gestational-age- and postnatal-age-specific reference ranges is essential for meaningful clinical interpretation.

In addition, most studies do not adequately adjust for confounding factors that influence erythrocyte indices, including maternal iron status, timing of umbilical cord clamping, and prior blood transfusions. Failure to account for these variables may bias the observed association between RDW and sepsis. Finally, existing studies predominantly assess RDW as a single time-point measurement. There is limited evidence on the utility of longitudinal or dynamic changes in RDW (ΔRDW) over the course of illness. Evaluating RDW trajectories may provide more informative insights into disease progression and treatment response than isolated baseline values.

Conclusion

Taken together, these limitations highlight that RDW, while promising, remains an under-defined biomarker in neonatal sepsis. Its widespread availability and low cost make it an attractive candidate for early risk stratification, particularly in resource-limited settings; however, current evidence is insufficient to support its use as a standalone diagnostic or prognostic tool.

Future research must move beyond small, heterogeneous observational studies towards well-designed, prospective, multicenter investigations with standardized definitions, harmonized RDW reporting, and robust adjustment for confounding variables.

Importantly, integrating RDW into composite clinical and laboratory models, rather than evaluating it in isolation, may better reflect the complex pathophysiology of neonatal sepsis and enhance predictive performance. Addressing these priorities will be critical to determine whether RDW can transition from a readily available laboratory parameter to a clinically actionable tool in neonatal care.

Footnotes

ORCID iDs

Nur `Afifah Mohamad Asri

Hani Ajrina Zulkeflee

Alina Md Fauzi

Tengku Amatullah Madeehah Tengku Mohd

Lidiya Mohd Yusof

Nur Wahidah Batrisya Zahidi

Fadzlin Syazani Binti Azizi

Aliyyah Mohammad Khuzaini

Authors contribution

AMK: Conceptualization, methodology, formal analysis, data curation, writing—original draft, visualization, and project administration. HAZ: Conceptualization, methodology, and writing—review and editing. TAMTM: Methodology, validation, and formal analysis (Title/Abstract screening). AMF: Data curation, validation and writing—review and editing. NAMA: Investigation (full-text review), data curation, and writing—review and editing. LMY: Investigation and data curation. NWBZ: Investigation and data curation. FSZ: Investigation (Full-text review), data curation, validation, and writing—review and editing.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

All data generated or analyzed during this study are included in this published article. No primary datasets were generated.*

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