Xie B, Zhang J, Wen YH, Zhao HF. Circulating stem/progenitor cell biomarkers and prognosis in critically ill patients with gastrointestinal bleeding. World J Stem Cells 2026; 18(7): 119749 [DOI: 10.4252/wjsc.119749]
Corresponding Author of This Article
Hui-Feng Zhao, MD, Intensive Care Unit, Jiashan First People’s Hospital, No. 1218 Tiyu South Road, Luoxing Street, Jiashan 314100, Zhejiang Province, China. zhaohf9945@163.com
Research Domain of This Article
Cell Biology
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research-article
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Author contributions: Xie B and Zhang J conceived and designed the study; Xie B was responsible for patient enrollment, data collection, flow cytometric analysis of circulating stem/progenitor cells, and drafted the manuscript; Zhang J and Wen YH performed statistical analyses and interpreted the data; Zhao HF supervised the study, contributed to the study design, interpreted the results, and critically revised the manuscript for important intellectual content. All the authors have read and approved the final version of the manuscript and agree to be accountable for all aspects of the work.
AI contribution statement: All the authors declare that there is no content generated by AI in the manuscript, including language modification, structure optimization, code assistance or literature organization. These contents are reviewed and revised manually by the authors, and confirm that we are fully responsible for the accuracy, originality and integrity of the manuscript according to the guidance of the International Medical Journal Editorial Committee and the publishing ethics committee.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of Jiashan First People’s Hospital in Zhejiang Province, No. 2026-005.
Informed consent statement: Owing to the retrospective nature of the study, the Ethics Committee waived the requirement for informed consent.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: There is no additional data available.
Corresponding author: Hui-Feng Zhao, MD, Intensive Care Unit, Jiashan First People’s Hospital, No. 1218 Tiyu South Road, Luoxing Street, Jiashan 314100, Zhejiang Province, China. zhaohf9945@163.com
Received: April 8, 2026 Revised: May 7, 2026 Accepted: June 9, 2026 Published online: July 26, 2026 Processing time: 107 Days and 4.9 Hours
Abstract
BACKGROUND
Gastrointestinal bleeding (GIB) is a common critical illness, especially in patients in the intensive care unit (ICU), and is often complicated by shock, multiple organ dysfunction, and serious infections, resulting in high mortality. At present, clinical practice mainly relies on the Glasgow-Blatchford, albumin, international normalized ratio, mental status, systolic blood pressure, age ≥ 65 years (AIMS65), and Rockall scoring systems, combined with lactic acid and organ function indicators, to evaluate the condition and prognosis. However, the predictive value of these traditional indicators for short-term mortality in critically ill patients with GIB remains limited, and additional biomarkers are needed to complement, rather than replace, established clinical assessments.
AIM
To explore associations between circulating stem/progenitor cell biomarkers and prognosis in critically ill GIB patients and develop a prognostic model.
METHODS
Overall, 140 GIB patients admitted to the ICU of Jiashan First People’s Hospital (January 2020 and December 2025) were retrospectively included. Flow cytometry analyzed peripheral blood samples within 6 hours of ICU admission, including CD34+ cells, endothelial progenitor cell (EPC) (CD34+KDR+), and EPC (CD34+ CD133+KDR+) subsets. The primary outcome was 28-day all-cause death, and secondary outcomes included 7 days rebleeding, 90-day death and ICU stay. Multivariate logistic regression analyzed factors associated with 28-day all-cause death, and receiver operating characteristic curve analysis evaluated model discrimination.
RESULTS
Twenty-nine (20.71%) patients died within 28 days and 29 (20.71%) experienced rebleeding within 7 days. Patients in the death group were more critically ill, manifested as higher Sequential Organ Failure Assessment score (10.21 ± 2.15 vs 7.96 ± 3.00, P = 0.001), AIMS65 score [4.00 (3.00, 4.00) vs 3.00 (2.00, 3.00), P = 0.008], proportion of cirrhosis [18 (62.07%) vs 27 (24.32%), P < 0.001], and lactic acid levels [4.20 (3.05, 5.35) mmol/L vs 2.95 (2.28, 3.55) mmol/L, P = 0.003]. Among the circulating progenitor cells, lnEPC (CD34+KDR+) levels were significantly lower in the death group [0.85 (0.65, 1.15) vs 1.35 (1.08, 1.60), P < 0.001]. After adjusting for Sequential Organ Failure Assessment score, lactic acid level, AIMS65 score, and cirrhosis, lnEPCs (CD34+KDR+) remained associated with 28-day mortality (odds ratio = 0.557, 95% confidence interval: 0.353-0.879, P = 0.012). The combined model showed moderate discrimination (area under the curve = 0.727); at the optimal predicted-probability cutoff of 0.360, the sensitivity and specificity were 0.483 and 0.937, respectively, with acceptable calibration on the Hosmer-Lemeshow test (P = 0.622).
CONCLUSION
A lower early EPC (CD34+KDR+) level was associated with increased short-term mortality in critically ill patients with GIB. The combined EPC-clinical model may complement organ dysfunction assessment and aid supplementary risk stratification.
Core Tip: In this retrospective of intensive care unit patients with gastrointestinal bleeding, early circulating endothelial progenitor cell (CD34+KDR+) levels were lower in patients who died within 28 days and remained associated with mortality after adjusting for clinical variables. The endothelial progenitor cell-clinical model showed moderate discrimination and high specificity, but limited sensitivity; therefore, it should not be interpreted as a standalone early warning tool for high-risk screening. Its current value is mainly hypothesis-generating and may complement organ dysfunction scores and help identify patients with relatively low predicted risk, pending external validation and standardized flow cytometry workflows.
Citation: Xie B, Zhang J, Wen YH, Zhao HF. Circulating stem/progenitor cell biomarkers and prognosis in critically ill patients with gastrointestinal bleeding. World J Stem Cells 2026; 18(7): 119749
Gastrointestinal bleeding (GIB) is a common high-risk emergency in the intensive care unit (ICU)[1]. Compared with patients on the general ward, critically ill patients often present with concomitant infection, shock, coagulation dysfunction, or multiple organ dysfunction syndrome, with a more complex bleeding etiology and a higher risk of rebleeding. In addition, the death outcome is often driven by “bleeding itself” and “underlying disease/organ failure”[2,3]. Clinically, scoring systems such as the albumin, international normalized ratio, altered mental status, systolic blood pressure, and age ≥ 65 years (AIMS65) score, the Glasgow-Blatchford score, and the Rockall score can be used for risk stratification; however, these tools are mostly established based on general emergency/inpatient GIB cohorts, and their generalization ability for ICU scenarios is limited. The vital signs and laboratory indicators of critical patients are significantly affected by sedation, mechanical ventilation, vasoactive drugs, and capacity management[4]. In contrast, organ dysfunction and endothelial damage may play more central pathological roles in ICU-GIB outcomes. Endothelial cells are key nodes for the cross-regulation of the microcirculation barrier and coagulation inflammation[5,6]. Hemorrhagic ischemia/reperfusion and systemic inflammatory reactions can lead to endothelial glycocalyx damage, capillary leakage, microthrombosis, and increased perfusion heterogeneity, thus aggravating tissue hypoxia and organ dysfunction[7,8]. Circulating stem/progenitor cells, especially endothelial progenitor cells (EPCs), are involved in endothelial repair and angiogenesis, and their number and function are considered to reflect the dynamic balance of “injury-repair”[9,10]. Previous studies have linked EPCs to outcomes in sepsis, shock, trauma, and vascular diseases; however, the phenotype, assay protocol, and clinical interpretation of EPCs remain heterogeneous across studies[11,12]. Therefore, this study used a real-world ICU cohort and flow cytometry to quantify EPC-related subsets, explore their association with short-term mortality and rebleeding outcomes, and preliminarily develop a clinical-biological prognostic model, with the aim of providing a hypothesis-generating supplement for risk stratification in critically ill patients with GIB.
MATERIALS AND METHODS
Study design and subjects
This was a single-center retrospective study. Patients admitted to the ICU of Jiashan First People’s Hospital between January 2020 and December 2025 with a diagnosis of GIB were screened. The diagnosis was based on clinical manifestations, such as hematemesis, melena, or bloody stool, and/or objective evidence from gastroscopy, enteroscopy, or computed tomography angiography. The exclusion criteria were as follows: (1) Age < 18 years or pregnancy; (2) Transfer out of the ICU or death within 24 hours after ICU admission; (3) Missing key variables > 30%; and (4) Incomplete circulating cell detection within the pre-specified time window. Ultimately, 140 patients were included in the study. This study was reviewed and approved by the Ethics Committee of the Jiashan First People’s Hospital. Given the retrospective observational design and the use of anonymized clinical data and previously collected blood samples, all study participants, or their legal guardian, provided informed written consent prior to study enrollment. This study was conducted in accordance with the principles of the Declaration of Helsinki.
Etiological determination of hemorrhage
The etiology of hemorrhage was determined preferentially according to endoscopic findings; for patients who did not undergo endoscopy, imaging results and clinical judgment were used. Bleeding was classified as variceal or non-variceal, and the main cause was recorded. The diagnosis and treatment of portal hypertension were implemented according to the Baveno VII consensus and relevant guidelines[13,14].
Detection of circulating stem/progenitor cells
Peripheral venous blood (2 mL, anticoagulated with ethylenediaminetetraacetic acid) was collected within 6 hours of ICU admission and processed within 2 hour of collection. Flow cytometry was performed using a BD FACSCanto II system or an equivalent four-color platform with daily instrument calibration and fluorescence compensation before sample analysis. The antibody panels included anti-CD34 (BD, clone 581), anti-CD133 (Miltenyi, clone AC133), anti-KDR/VEGFR-2 (R&D Systems, clone 89106), and CD45 antibodies to exclude mature leukocytes. After red blood cell lysis and direct staining, EPC-related events were identified sequentially using forward/side scatter, singlet gating, CD45dim/negative exclusion, and CD34/KDR or CD34/CD133/KDR co-expression. Isotype or fluorescence-minus-one controls were used to define positive thresholds, and counting beads were used to calculate absolute counts (cells/μL). All assays were performed by trained laboratory personnel blinded to the clinical outcomes, and samples with delayed processing, clotting, inadequate cell events, or failed compensation were excluded from the analysis. The main indicators were: (1) CD34+ cells; (2) EPC (CD34+KDR+); and (3) EPC (CD34+CD133+KDR+).
Observation indicators and outcomes
Baseline demographic information, comorbidities, bleeding type, key laboratory indicators (hemoglobin, platelets, international normalized ratio, albumin, lactic acid, etc.), severity scores [Sequential Organ Failure Assessment (SOFA), Acute Physiology and Chronic Health Evaluation II, and AIMS65] were collected. The primary outcome was 28-day all-cause death, and the secondary outcomes included 7-day rebleeding (requiring additional hemostasis, transfusion, intervention, or re-endoscopy), ICU stay, and 90-day death.
Statistical analysis
Statistical analysis were performed using SPSS version 22.0 (IBM Corp., Armonk, NY, United States). Normally distributed continuous variables were expressed as mean ± SD and compared using the t-test. Non-normally distributed variables were expressed as medians (quartiles) and compared using the Mann-Whitney U test. Categorical variables are expressed as n (%) and were compared using the χ2 test or Fisher’s exact test. A multivariable logistic regression model was established with 28-day mortality as the dependent variable, and clinically relevant variables with univariate P < 0.100 were considered for inclusion; β, standard error, odds ratio and 95% confidence interval were reported. Model discrimination was evaluated using the area under the receiver operating characteristic curve (AUC), and the sensitivity and specificity at the optimal cutoff point based on the Youden index were calculated. Calibration was evaluated using the Hosmer-Lemeshow test. Statistical tests were two-sided, and P < 0.050 indicated statistical significance.
RESULTS
Baseline characteristics
A total of 140 patients were included in this study. There were 78 males (55.70%), and the mean age was 61.77 ± 13.06 years. There were 48 (34.30%) patients with variceal hemorrhage and 45 (32.14%) with cirrhosis. The overall 28-day mortality rate was 20.71%, and the 7-day rebleeding rate was 20.71%. The SOFA score in the death group was higher than that in the survival group (10.21 ± 2.15 vs 7.96 ± 3.00, P = 0.001), and the platelets showed a declining trend (P = 0.073). In terms of the circulating progenitor cell index, the lnEPC (CD34+KDR+) value in the death group was lower [0.85 (0.65, 1.15) vs 1.35 (1.08, 1.60), P < 0.001]. This finding indicates an association between lower early EPC (CD34+KDR+) levels and poor short-term outcomes without establishing functional impairment of repair capacity (Table 1).
Table 1 Baseline characteristics (grouped by 28 days outcome), n (%)/mean ± SD/median (quartile).
The etiological composition of the hemorrhage was determined using endoscopy and/or imaging. Non-variceal hemorrhages are mainly caused by peptic ulcers and stressed mucosal lesions, whereas variceal hemorrhages are mainly caused by the rupture of esophageal and gastric varices. The 28-day mortality rate varied numerically among bleeding causes (12.5% to 42.9%), but the difference was not statistically significant (χ2 = 9.189, P = 0.239) (Table 2).
Table 2 Etiological distribution of hemorrhage and 28-day mortality.
The ICU stay was longer in the death group [8.00 (5.00, 12.00) days vs 6.00 (4.00, 9.00) days, P = 0.031], mechanical ventilation was used more frequently (65.52% vs 32.43%, P = 0.001), and vasoactive drugs were used more frequently (72.41% vs 41.44%, P = 0.003) than in the survival group. The 7-day rebleeding rates in the two groups were 21.62% and 17.24%, respectively, and the difference was not statistically significant (P = 0.604), suggesting that short-term rebleeding alone could not fully explain the observed mortality risk (Table 3).
Table 3 Comparison of outcomes and critical treatment measures, n (%).
After SOFA score, lactic acid, AIMS65 score, cirrhosis and lnEPC (CD34+KDR+) were entered into the logistic regression model, lnEPC (CD34+KDR+) remained associated with 28-day mortality (β = -0.586, odds ratio = 0.557, 95% confidence interval: 0.353-0.879, P = 0.012) (Table 4). The combined model has an AUC of 0.727, indicating moderate discrimination. At the optimal predicted probability cutoff of 0.360, the sensitivity and specificity were 0.483 and 0.937, respectively. Thus, the model showed higher specificity than sensitivity, and should be interpreted more as a supplementary stratification tool than as a stand-alone screening model for early high-risk warnings. Calibration was acceptable, with Hosmer-Lemeshow test χ2 = 6.221 (df = 8) and P = 0.622 (Figure 1).
Figure 1 Discrimination and calibration curve analysis of the combined model.
A: Receiver operating characteristic curve for predicting 28 days mortality rate using a combination model; B: Calibration curve of composite model. ROC: Receiver operating characteristic; AUC: Area under the receiver operating characteristic curve.
The patients were divided into high (n = 55) and low (n = 85) groups based on the median absolute count of lnEPCs (CD34+KDR+) in the early stages of their ICU stay. After the 90-day follow-up, eight patients (14.54%) died in the high lnEPC group and 22 patients (25.88%) died in the low lnEPC group. The Kaplan-Meier curve showed a difference in the cumulative survival rate between the two groups (log-rank test, P = 0.038) (Figure 2).
Figure 2 Kaplan-Meier curve of cumulative survival probability stratified by the median endothelial progenitor cell count.
KDR: Kinase insert domain receptor; lnEPC: Natural log-transformed endothelial progenitor cell count.
DISCUSSION
Adverse outcomes in patients with ICU-GIB are often not determined entirely by the amount of bleeding itself[15,16]. Shock reperfusion can trigger systemic inflammatory reactions, microcirculatory perfusion disorders, and endothelial barrier destruction, which in turn aggravate coagulation disorders and organ failure[17,18]. EPCs are related to endothelial repair, angiogenesis, and maintenance of microvascular homeostasis; however, the lower EPC count in the present study should be interpreted as a repair-related biomarker signal rather than direct evidence of impaired repair function[19,20]. In patients with ICU-GIB, hemodynamic fluctuations, infection or sepsis, vasoactive drugs, transfusion, and coagulation management may influence EPC mobilization and measurement. These factors may partly explain the association between lower EPC levels and mortality[21-23]. Given the observational design, the present results support a correlation between early EPC levels and prognosis but do not prove that EPC depletion causally drives organ deterioration. Notably, the phenotypic definition of EPC varies significantly between different studies. In this study, CD34+KDR+ cells were selected as core endothelial-related markers, and their specificity was improved by the CD45 exclusion strategy, emphasizing progenitor cells with vascular repair potential rather than the pure CD34+ cell count. Because no universally accepted EPC phenotype exists, these findings should be compared cautiously with those of studies using different marker combinations, gating strategies, or functional assays.
AIMS65 and Glasgow-Blatchford score are useful for stratifying upper GIB in emergency settings. However, ICU-GIB is often complicated by infection, respiratory and circulatory support, liver and kidney dysfunction, and other conditions. Scoring variables may be strongly affected by treatment processes, and it is difficult for these scores to fully reflect the pathological axis of endothelial injury and repair[24-26]. In this study, SOFA score was more closely related to outcome differences in the univariate comparison (Table 1), suggesting that organ failure remains a fundamental determinant of mortality risk. After lnEPCs (CD34+KDR+) were added, the model achieved an AUC of 0.727 with acceptable calibration (Figure 1 and Table 4). However, this level of discrimination should be regarded as moderate rather than strong. More importantly, the sensitivity was only 0.483, whereas the specificity was 0.937, indicating that the model is not suitable as a standalone screening tool for identifying high-risk patients. Its potential clinical application may be to complement clinical judgment, help recognize patients with a relatively low predicted risk, and provide a basis for future dynamic monitoring studies, rather than to replace established severity scores.
In ICU-GIB management, risk stratification can help clinicians consider endoscopic or interventional timing, transfusion strategy, infection control, and organ support intensity[27-30]. At the current stage, the combined EPC-clinical model should be viewed as an exploratory aid rather than an immediately deployable decision tool. If EPC testing is available, the SOFA score, lactic acid, and EPC (CD34+KDR+) may be assessed together during early ICU evaluation to form a clinical-biological profile; however, the results should be interpreted together with bleeding control, hemodynamics, and organ support status[31,32]. For patients with variceal hemorrhage, routine management of portal hypertension should remain a priority, while infection control and liver function fluctuations may still influence the endothelial and coagulation status. For patients with low EPC levels, closer clinical observation and more careful evaluation of microcirculation-related risk may be reasonable. However, the current study could not determine whether EPC-guided interventions improve outcomes. It should also be emphasized that EPC testing relies on flow cytometry, standardized gating, counting beads, and experienced operators. Many ICUs do not have rapid testing capacity, and the 6-hour sampling window may be affected by emergency treatment, transfusion, or delayed sample transport. Therefore, accessibility, turnaround time, and interlaboratory reproducibility should be carefully evaluated before this biomarker can be generalized to routine critical care practice.
Limitations and prospects of this study: First, this was a single-center retrospective study with potential selection bias and residual confounding factors. The model was evaluated internally only, and multicenter prospective cohorts are required for external validation and threshold recalibration. Second, there is no unified gold standard for the EPC phenotype, and antibody clones, gating strategy, pretreatment time, and counting methods may affect reproducibility and external comparability. Future studies should establish standardized quality control systems and report inter-batch calibration, repeatability, event thresholds, and absolute count methods in detail. Third, this study measured EPCs only once within 6 hours of ICU admission. Because EPC is a dynamically changing biomarker, inflammatory burden, hemodynamic support, vasoactive drugs, transfusion, and coagulation management may rapidly alter its level; repeated measurements may better reflect the disease trajectory and treatment response. Fourth, this study did not perform functional validation, such as migration, tube formation, or transfer experiments; therefore, the mechanistic interpretation should remain at the association level. Fifth, the sample size of the bleeding subgroups was limited, and the heterogeneity between variceal and non-variceal bleeding may have influenced the effect estimates. Future studies should verify the applicability in stratified populations, such as those with cirrhosis and chronic kidney disease, and further explore the associations with rebleeding, microcirculatory indicators, and infectious complications.
CONCLUSION
In this single-center retrospective of critically ill patients with GIB, low early EPC (CD34+KDR+) levels were associated with 28-day mortality. The combined EPC-clinical model provided moderate discrimination with high specificity and limited sensitivity; therefore, it should be used only as a supplementary, hypothesis-generating risk stratification tool, rather than as a stand-alone screening model. Prospective multicenter studies with standardized flow cytometry quality control, repeated EPC measurements, and functional validation are needed to determine the stability, threshold, and dynamic clinical value of EPC-related indicators.
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Footnotes
Peer review: Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Cell and tissue engineering
Country of origin: China
Peer-review report’s classification
Scientific quality: Grade B, Grade C
Novelty: Grade B, Grade C
Creativity or innovation: Grade B, Grade C
Scientific significance: Grade B, Grade C
P-Reviewer: Liberman M, PhD, Canada; Tang CC, PhD, Taiwan S-Editor: Wang JJ L-Editor: A P-Editor: Zhao YQ
