Xu J, Li SX, Liu D, Chen LX, Chen X. Diagnostic value of serum pepsinogen, gastrin, and carbohydrate antigens in gastric ulcer and gastric cancer. World J Gastrointest Oncol 2025; 17(6): 105931 [DOI: 10.4251/wjgo.v17.i6.105931]
Corresponding Author of This Article
Xi Chen, MD, PhD, Professor, Senior Researcher, Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei 230022, Anhui Province, China. ayfychenxi@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Retrospective Study
Open-Access Policy of This Article
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/
Juan Xu, Xi Chen, Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, China
Juan Xu, Shao-Xue Li, Dong Liu, Li-Xin Chen, Department of Gastroenterology, The Third People’s Hospital of Hefei, The Third Clinical Medical College of Hefei of Anhui Medical University, Hefei 230022, Anhui Province, China
Author contributions: Chen X and Xu J designed the research study; Xu J, Li SX, Liu D, and Chen LX performed the research; Xu J, Li SX, and Chen X analyzed the data and wrote the manuscript; and all authors have read and approved the final manuscript.
Supported by Chinese Medicine Research Project of Anhui Chinese Medicine Society, No. 2024ZYYXH135.
Institutional review board statement: The study was reviewed and approved by the Third People’s Hospital of Hefei Institutional Review Board (Approval No. 2024 LLWL041).
Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: Technical appendix, statistical code, and dataset available from the corresponding author at ayfychenxi@163.com.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Xi Chen, MD, PhD, Professor, Senior Researcher, Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei 230022, Anhui Province, China. ayfychenxi@163.com
Received: February 11, 2025 Revised: April 9, 2025 Accepted: May 15, 2025 Published online: June 15, 2025 Processing time: 123 Days and 4 Hours
Abstract
BACKGROUND
Emerging evidence suggests that serum levels of pepsinogen (PG), gastrin-17 (G17), carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), and CA72-4 may aid in distinguishing gastric cancer (GC) from gastric ulcer (GU).
AIM
To assess serum PG, G17, CEA, CA19-9, and CA72-4 in diagnosing GU and optimizing GC detection.
METHODS
A retrospective analysis was conducted from 263 patients treated at the Third People’s Hospital of Hefei, who were classified into three groups: Chronic non-atrophic gastritis (CG), GU, and GC. Fasting serum levels of PG, G17, CEA, CA19-9, and CA72-4 were measured and compared across the groups.
RESULTS
Serum levels of PGII and G17 were significantly elevated in both the GU and GC groups compared to the CG group (P < 0.01), whereas the PGI/PGII ratio was markedly decreased (P < 0.01). Levels of CEA, CA19-9, and CA72-4 were significantly higher in the GC group than in the CG and GU groups (P < 0.01). Receiver operating characteristic curve analysis identified the optimal diagnostic cut-off values for GU and GC as follows: PGI (169.855 pmol/L), PGII (30.555 μg/L), PGI/PGII ratio (16.529), G17 (6.435 pmol/L), CEA (2.005 ng/mL), CA19-9 (16.65 U/mL), and CA72-4 (2.075 U/mL). The area under the curve for combined detection was 0.826 (P < 0.001), indicating good diagnostic performance.
CONCLUSION
Serological biomarkers effectively distinguish GC from GU, with combined detection of PGII, PGI/PGII ratio, G17, and tumor markers enhancing diagnostic accuracy.
Core Tip: This study determined that the ratio of pepsinogen I/II was low, and the levels of pepsinogen II, gastrin-17, carbohydrate antigen 19-9, carcinoembryonic antigen and carbohydrate antigen 72-4 were increased as auxiliary serological biomarkers for the differentiation of gastric ulcer and gastric cancer. The diagnostic accuracy of combined application for gastric cancer and gastric ulcer was high, and the area under the curve was 0.826.
Citation: Xu J, Li SX, Liu D, Chen LX, Chen X. Diagnostic value of serum pepsinogen, gastrin, and carbohydrate antigens in gastric ulcer and gastric cancer. World J Gastrointest Oncol 2025; 17(6): 105931
Gastric ulcer (GU) is a prevalent condition affecting the digestive tract, typically marked by mucosal inflammation, necrosis, and erosion, progressing to mucosal damage and ulceration that penetrates through the muscularis mucosa and, in severe cases, may extend to the muscularis propria or deeper layers[1,2]. Various gastric pathologies - such as GU, gastric cancer (GC), and gastric lymphoma - can present with similar endoscopic features. However, the prognosis of GU differs significantly from that of GC. In 2020, GC ranked as the fourth most commonly diagnosed malignancy and the third leading cause of cancer-related death in China[3]. Although early-stage GC is associated with a favorable 5-year survival rate approaching 90%, advanced-stage diagnoses reduce this figure to just 20%-30%[4]. These statistics underscore the critical importance of early diagnosis and intervention to improve outcomes and reduce disease burden.
Gastroscopy is a reliable method for diagnosing benign and malignant GU[5]. However, this is an invasive and expensive method, and therefore, it is not the preferred method for patients[6]. Besides, some patients with poor tolerance or use of anticoagulants, inhibition of platelet aggregation, and other drugs cannot obtain pathological tissue, often delaying diagnosis and treatment. Malignant ulcers grow to submucosa or heal temporarily after proton pump inhibitor treatment, and biopsies are limited, making it difficult to obtain sufficient submucosa tissue in the early stage[7]. Serum markers, including serum pepsinogen (PG), gastrin-17 (G17), carbohydrate antigens (CAs) are used for screening precancerous lesions of GC[8,9]. The gastric mucosa of GU and GC had different pathological changes, and showed different states and secretory functions, and the concentrations of serum PG and G17 were different, which were helpful in differentiating GU from GC. Serum PG and G17 have become attractive new methods for screening precancerous lesions and GC[10-12]. Nonetheless, limited research exists regarding the potential use of serum PG and G17 detection as supplementary diagnostic tools for GU and GC[13]. Carcinoembryonic antigen (CEA), CA19-9, and CA72-4 are three biomarkers employed in the diagnosis of cancer, with their increased levels strongly associated with cancer onset, recurrence, and metastasis. However, the sensitivity and specificity highlighted in different earlier studies frequently vary[14]. A combined evaluation of CEA, CA19-9, and CA72-4 demonstrates superior diagnostic value for GC[15]. This study assessed the diagnostic performance of PG, G17, the PGI/PGII ratio, CEA, CA19-9, and CA72-4 in identifying GU lesions, aiming to determine optimal thresholds and improve sensitivity and specificity in the context of primary healthcare in China.
MATERIALS AND METHODS
Patients
A retrospective analysis was conducted on 263 patients who received both gastroscopic and pathological evaluations between January 2018 and December 2020. The eligibility criteria included the following aspects: (1) Diagnosis consistent with chronic non-atrophic gastritis (CG), GU, or GC based on established diagnostic criteria; (2) Availability of complete clinical and pathological data; and (3) Histopathological confirmation of diagnosis in all cases. Exclusion criteria included: (1) Presence of other systemic or organ malignancies; (2) Severe hepatic or renal dysfunction; (3) Use of gastric mucosal protectants within the past two weeks; (4) History of gastric surgery; and (5) Pregnancy or lactation. Patients were categorized into three groups: CG (n = 104), GU (n = 88), and GC (n = 71). The Medical Ethics Committee at Hefei Third People’s Hospital reviewed and approved the study protocol (Approval No. 2024 LLWL041).
Serological tests
Serum samples were stored at -20 °C for subsequent analysis. PGI, PGII, and G17 levels were measured using enzyme-linked immunosorbent assay kits provided by BIOHIT (Finland), following the manufacturer’s instructions. Tumor markers were determined using chemiluminescent immunoassay technology, with reagent kits supplied by Jiangsu Sanlian Biotechnology Co., Ltd.
Gastroscopy and histopathology
All patients underwent gastroscopic examination performed by experienced endoscopists, each of whom conducts more than 500 procedures annually. The number of biopsies obtained during the procedure was adjusted according to the size and characteristics of the lesion.
Statistical analysis
All statistical analyses were carried out using SPSS software (version 26.0). The Shapiro-Wilk test was employed to evaluate the distribution of continuous variables. A P value greater than 0.05 indicated a normal distribution. For parameters exhibiting normality, intergroup differences were assessed via one-way analysis of variance, with Bonferroni adjustments applied for post hoc comparisons. Variables not meeting normal distribution criteria were summarized as medians with interquartile ranges (Q25, Q75) and compared using the Mann-Whitney U test or Kruskal-Wallis test as appropriate, also corrected using Bonferroni procedures for multiple testing. Categorical data were described using frequencies and percentages, and differences among groups were tested using the χ2-test with Bonferroni correction. Diagnostic performance for differentiating GC from GU was evaluated using receiver operating characteristic (ROC) curve analysis to identify optimal cutoff values.
RESULTS
Basic information about the subject
The study included 263 participants, of whom 164 (62.36%) were male and 99 (37.64%) were female. Based on gastroscopic and pathological findings, the patients were classified into three groups: 104 cases of CG (39.54%), 88 cases of GU (33.46%), and 71 cases of GC (27.00%) (Table 1).
Table 1 Baseline data and disease composition, n (%).
Variable
Value
n
263
Disease
GC
71 (27.00)
GU
88 (33.46)
CG
104 (39.54)
Age, M (Q25, Q75)
66.00 (54.00, 74.00)
Sex
Male
164 (62.36)
Female
99 (37.64)
Differences in serum PG, G17, CEA, CA19-9, and CA72-4 in different disease states
Table 2 summarizes the laboratory test results for the CG, GU, and GC groups. Statistically significant variations were identified in the serum concentrations of PGI, PGII, G17, CEA, CA19-9, and CA72-4 across the three cohorts. Among them, the GC group demonstrated markedly elevated levels of PGII and G17, followed by those in the GU group, whereas the CG group exhibited the lowest values (P < 0.001). Conversely, the PGI to PGII ratio was lowest in GC patients, moderate in the GU group, and highest in CG individuals (P < 0.001). Additionally, levels of tumor markers CEA, CA19-9, and CA72-4 were substantially higher in the GC group compared with both GU and CG groups (P < 0.001).
Table 2 Differences in pepsinogen, gastrin-17, carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 72-4 in different disease states, M (Q25, Q75).
ROC curve of serum PG, G17, CEA, CA19-9, and CA72-4 in different disease states
To better differentiate between GC and CG, the optimal cutoff values were as follows: PGI (171.205 ng/mL), PGII (15.502 ng/mL), PGI/PGII ratio (27.870), G17 (5.405 pg/mL), CEA (1.610 ng/mL), CA19-9 (18.335 U/mL), and CA72-4 (2.090 U/mL) (Figure 1A). To distinguish GU from CG, the optimal cutoff values were: PGI (115.165 ng/mL), PGII (9.740 ng/mL), PGI/PGII ratio (31.789), G17 (2.245 pg/mL), CEA (6.925 ng/mL), CA19-9 (22.410 U/mL), and CA72-4 (1.440 U/mL) (Figure 1B). To differentiate GC from GU, the best cutoff values were: PGI (169.855 ng/mL), PGII (30.555 ng/mL), PGI/PGII ratio (16.529), G17 (6.435 pg/mL), CEA (2.005 ng/mL), CA19-9 (16.650 U/mL), and CA72-4 (2.075 U/mL) (Figure 1C).
Figure 1 Receiver operating characteristic curve of serum pepsinogen, gastrin-17, carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 72-4 in different disease states.
A: Receiver operating characteristic (ROC) curve of gastric cancer and chronic non-atrophic gastritis; B: ROC curve of chronic non-atrophic gastritis and gastric ulcer; C: ROC curve of gastric ulcer and gastric cancer. ROC: Receiver operating characteristic; PG: Pepsinogen; G17: Gastrin-17; CEA: Carcinoembryonic antigen; CA: Carbohydrate antigen.
Value of serum PG, G17, CEA, CA19-9, and CA72-4 in the diagnosis of GU and GC
The GC group (n = 71) was designated as the case group, while the GU group (n = 88) served as the control. ROC curves were constructed for PGI, PGII, the PGI/PGII ratio, G17, CEA, CA19-9, and CA72-4. The area under the curve (AUC) for PGI was 0.386 [95%confidence interval (CI): 0.294-0.478], with an optimal diagnostic cutoff of 169.855 ng/mL (sensitivity: 29.6%; specificity: 75%). For PGII, the AUC was 0.579 (95%CI: 0.485-0.674), with an optimal cutoff of 30.555 ng/mL (sensitivity: 31.0%; specificity: 49.3%). The PGI/PGII ratio yielded an AUC of 0.298 (95%CI: 0.209-0.387), with an optimal cutoff of 16.529 (sensitivity: 15.5%; specificity: 86.4%). G17 showed an AUC of 0.673 (95%CI: 0.589-0.757), with a cutoff value of 6.435 pmol/L (sensitivity: 66.2%; specificity: 61.4%). CEA had an AUC of 0.722 (95%CI: 0.644-0.801), with a diagnostic threshold of 2.863 ng/mL (sensitivity: 50.7%; specificity: 83.0%). The AUC for CA19-9 was 0.619 (95%CI: 0.530-0.709), with an optimal cutoff of 16.65 U/mL (sensitivity: 32.4%; specificity: 92.0%). Finally, CA72-4 achieved the highest diagnostic performance, with an AUC of 0.778 (95%CI: 0.705-0.850) and a cutoff of 2.075 U/mL (sensitivity: 62.0%; specificity: 79.5%) (Table 3).
Table 3 Diagnostic value of pepsinogen, gastrin-17, carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 72-4 for gastric ulcer and cancer.
Cut-off value
GC (n = 71)
GU (n = 88)
χ2
P value
Sensitivity
Specificity
Youden index
Positive predictive value
Negative predictive value
PGI, ng/mL
≥ 169.855
21
22
0.417
0.518
0.296
0.75
0.046
0.488
0.569
< 169.855
50
66
PGII, ng/mL
≥ 30.555
22
5
17.848
< 0.001
0.31
0.943
0.253
0.815
0.629
< 30.555
49
83
PGI/PGII ratio
≥ 16.529
11
12
0.109
0.741
0.155
0.864
0.019
0.478
0.559
< 16.529
60
76
G17, pmol/L
≥ 6.435
47
34
11.944
0.001
0.662
0.614
0.276
0.58
0.692
< 6.435
24
54
CEA, ng/mL
≥ 2.005
36
15
20.433
< 0.001
0.507
0.83
0.337
0.706
0.676
< 2.005
35
73
CA19-9, U/mL
≥ 16.65
23
7
15.333
< 0.001
0.324
0.92
0.244
0.767
0.628
< 16.65
48
81
CA72-4, U/mL
≥ 2.075
44
18
28.473
< 0.001
0.62
0.795
0.415
0.71
0.722
< 2.075
27
70
ROC analysis of combined serum PG, G17, CEA, CA19-9, and CA72-4 for differentiating GC from GU
To evaluate the combined diagnostic performance of serum PG, G17, CEA, CA19-9, and CA72-4 in distinguishing GC from GU, a composite ROC curve was generated using the GU group as the control. The model, incorporating PGI, PGII, the PGI/PGII ratio, G17, CEA, CA19-9, and CA72-4, yielded an AUC of 0.826 (95%CI: 0.759-0.893, P < 0.001), indicating good diagnostic accuracy (Figure 2).
Figure 2 Receiver operating characteristic curve of serum pepsinogen, gastrin-17, carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 72-4 combined diagnosis of gastric ulcer and gastric cancer.
ROC: Receiver operating characteristic.
DISCUSSION
Multiple guidelines and expert consensus recommend non-invasive serological screening in individuals at high risk for GC, followed by targeted endoscopic examination[16]. In this study, we established diagnostic thresholds and improved the sensitivity of detection. Our findings indicate that a low PGI/PGII ratio, as well as elevated levels of PGII, G17, CA19-9, CEA, and CA72-4, are indicative of GC and serve as effective biomarkers for differentiating it from GU. Combined detection of these markers yielded a higher AUC, demonstrating enhanced diagnostic performance. Moreover, serum PGI and PGII levels are elevated in individuals with GU compared to those with chronic gastritis (P < 0.01). In contrast, patients with GC exhibited significantly lower PGI levels (P < 0.01), while PGII levels remained unchanged or were even elevated, resulting in a markedly reduced PGI/PGII ratio. Previous studies have reported that serum PGI levels in patients with non-recurrent GU tend to increase during the active phase and subsequently decline significantly as the ulcer heals. Continuous monitoring of serum PGI during the ulcer healing process can aid in predicting ulcer recurrence[17]. Elevated serum PGI and PGII levels serve as valuable serological markers for both the diagnosis and therapeutic evaluation of peptic ulcers, with important clinical implications[18]. In contrast, reduced PGI levels and a low PGI/PGII ratio warrant heightened suspicion for GC[19]. Patients with GC typically present with decreased serum PGI levels, while PGII levels remain relatively stable. The decline in both PG levels and the PGI/PGII ratio holds significant value for the early detection and monitoring of gastric malignancies[20]. Conversely, individuals with GU exhibit increased PGI and PGII concentrations, whereas those with GC show a marked reduction in PGI and the PGI/PGII ratio. Elevated PGI and PGII levels are more closely associated with benign ulcerative conditions, whereas lower levels may indicate malignant transformation. These findings underscore the importance of proactive endoscopic examination in at-risk patients.
In individuals with GU, serum PGI and PGII levels were significantly elevated compared to those in healthy controls. PGI levels at or below 70 μg/L are indicative of a lower likelihood of developing GU. In a study by Cao et al[21], serum PGI levels and the PGI/PGII ratio were markedly lower in patients with GC than in those with atrophic gastritis or healthy individuals. The optimal threshold for diagnosing GC using PGI was determined to be 57.15 μg/L (sensitivity: 99.3%; specificity: 84.5%), while the optimal PGI/PGII ratio threshold was 2.99 (sensitivity: 92.5%; specificity: 89.0%). However, the definition of appropriate cut-off values for PGI and the PGI/PGII ratio in screening for GU lesions remains unclear. In our study, both serum PGI levels and the PGI/PGII ratio were reduced in the GC group when compared to patients with GU, which served as the control. The optimal cut-off values for distinguishing GC from GU were 169.855 ng/mL for PGI (sensitivity: 29.6%; specificity: 75.0%) and 16.529 for the PGI/PGII ratio (sensitivity: 15.5%; specificity: 86.4%). Additionally, the optimal PGII threshold for diagnosing GC was 30.555 ng/mL, with a sensitivity of 31.0% and specificity of 94.3%. The corresponding positive and negative predictive values for PGII were 81.5% and 62.9%, respectively, suggesting that PGII may serve as a more effective biomarker in this context.
Our study demonstrates that serum G17 levels are significantly elevated in the GC group compared with both the GU and chronic gastritis groups (P < 0.01). Gastrin plays a pivotal role in regulating digestive function, and serum G17 levels serve as a marker of gastric mucosal activity. Elevated G17 concentrations may reflect pathological changes such as gastric body mucosal atrophy, antral gastritis, erosions, ulcers, and potentially GC[22]. Shen et al[23] reported an optimal diagnostic cut-off value of 3.89 pmol/L for GC, using patients with benign gastric lesions as controls (sensitivity 83.3%; specificity 51.8%). Similarly, other studies have found significantly higher G17 levels in GC patients compared to those with precancerous lesions and healthy controls (P < 0.05), although specific diagnostic thresholds were not provided[24]. In our study, using the GU group as a control, the optimal cut-off value for diagnosing GC based on serum G17 was 6.435 pmol/L, yielding a sensitivity of 66.2% and a specificity of 61.4%.
In patients diagnosed with GC, serum levels of CEA, CA19-9, and CA72-4 were significantly elevated compared with those in individuals with GU and chronic superficial gastritis (P < 0.01). Each marker demonstrated strong diagnostic performance, with well-defined optimal cutoff values for GC detection: 2.005 ng/mL for CEA, 16.65 U/mL for CA19-9, and 2.075 U/mL for CA72-4. While single-marker testing holds clinical relevance, consistent with previous reports, combining multiple markers may enhance diagnostic accuracy. Studies have shown that CEA, CA19-9, and CA72-4 are not only useful for diagnosis but are also closely associated with disease progression, recurrence, and metastasis[25]. However, the individual diagnostic value of these markers remains controversial, with significant variability reported across studies. Based on these parameters, individuals were stratified into low-, medium-, and high-risk groups. Gastroscopy was performed in the medium- and high-risk groups, yielding detection rates of 70.8% and 70.3%, respectively. The predictive model demonstrated good discriminatory power, with an AUC of 0.76 (P < 0.001)[26]. Recent research has also highlighted the potential of serum circRNAs as novel biomarkers for GC. For instance, serum hsa_circ_0000702 achieved an AUC of 0.745 (95%CI: 0.669-0.821) in GC diagnosis[27]. Despite its valuable insights, this study is constrained by certain limitations, notably being conducted at a single center with a relatively small cohort and a retrospective design. To enhance the robustness and generalizability of these findings, future investigations involving larger, multi-center populations from diverse regions are warranted.
CONCLUSION
Patients with GC exhibited significantly elevated serum PGII levels alongside a reduced PGI/PGII ratio. Moreover, marked increases were observed in serum G17, CEA, CA19-9, and CA72-4 levels. These results underscore the potential of serological markers as valuable tools for differentiating GU from GC.
ACKNOWLEDGEMENTS
During the process of writing my thesis, I encountered several difficulties and obstacles, which were overcome through the collaboration of my supervisor and co-authors. For this, I express my sincere gratitude. Additionally, this paper cites the research literature of numerous scholars, and I would like to thank all the scholars involved.
Footnotes
Provenance and peer review: Unsolicited article; Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Oncology
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: Pan SJ; Türkmen U S-Editor: Wei YF L-Editor: A P-Editor: Guo X
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