Endoscopic predictors of iron deficiency in Helicobacter pylori gastritis: a Kyoto classification-based study

Hyun Tak Lee; Ah Young Lee; Hyesun Hong; Jun-young Seo

doi:10.5946/ce.2025.175

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Original Article Endoscopic predictors of iron deficiency in Helicobacter pylori gastritis: a Kyoto classification-based study: Hyun Tak Lee¹, Ah Young Lee², Hyesun Hong¹, Jun-young Seo³; Clinical Endoscopy 2026;59(1):79-88.
DOI: https://doi.org/10.5946/ce.2025.175
Published online: November 6, 2025

¹Department of Gastroenterology, DMC Bundang Jesaeng General Hospital, Seongnam, Korea

²Department of Gastroenterology, CHA Gangnam Medical Center, CHA University, Seoul, Korea

³Department of Gastroenterology, Digestive Disease Center, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea

Correspondence: Jun-young Seo Department of Gastroenterology, Digestive Disease Center, CHA Bundang Medical Center, CHA University School of Medicine, 11 Yatap-ro 65beon-gil, Bundang-gu, Seongnam 13496, Korea E-mail: terryxom11@naver.com

• Received: May 29, 2025 • Revised: July 5, 2025 • Accepted: July 10, 2025

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Abstract
Graphical abstract
INTRODUCTION
METHODS
RESULTS
DISCUSSION
NOTES
REFERENCES

See letter "Endoscopic predictors of iron deficiency in Helicobacter pylori gastritis: a Kyoto classification-based study" in Volume 59 on page 67.

Abstract

Background/Aims
Helicobacter pylori infection is reportedly associated with iron-deficiency anemia. However, little is known about the association between the endoscopic features of H. pylori in the Kyoto classification of gastritis and iron deficiency. Therefore, we analyzed the endoscopic features of H. pylori gastritis and studied the association between these endoscopic features and iron deficiency.
Methods
We retrospectively analyzed patients diagnosed with H. pylori gastritis between May 2022 and June 2023 who also underwent laboratory tests, including anemia profiling. Iron deficiency was defined as a ferritin level below 55 ng/mL. Multivariate analysis was used to assess the association between endoscopic features and iron deficiency.
Results
Of the included patients, 47 had iron deficiency. Female patients were significantly more common in the iron-deficient group (87.2% vs. 33.4%, p<0.001). Endoscopically, nodularity (46.8% vs. 23.4%, p=0.001) and hyperplastic polyps (17.0% vs. 3.7%, p=0.001) were more common in patients with iron deficiency. Multivariate analysis identified younger age, female sex, and larger hyperplastic polyps (≥5 mm) as independent risk factors for iron deficiency.
Conclusions
Younger age, female sex, and larger hyperplastic polyps (≥5 mm) are associated with iron deficiency in patients with H. pylori gastritis. These features may help identify patients at higher risk of iron deficiency.
Keywords: Gastritis; Helicobacter pylori; Iron deficiency; Polyps

Graphical abstract

INTRODUCTION

Helicobacter pylori infection affects more than half of the global population and is a well-established cause of chronic gastritis, peptic ulcers, and gastric cancer.¹^-³ Beyond its gastrointestinal manifestations, accumulating evidence has shown that H. pylori infection is not limited to causing gastric pathologies but is also significantly associated with a range of extra-gastrointestinal conditions. Among these, iron deficiency anemia (IDA) has been most consistently linked to H. pylori infection, with the proposed mechanisms including chronic gastric inflammation leading to impaired iron absorption, gastric hypochlorhydria reducing iron solubility, and occult gastrointestinal bleeding.⁴^-⁷

The Kyoto classification of gastritis offers a standardized endoscopic framework for evaluating gastritis, focusing on features such as atrophy, intestinal metaplasia, nodularity, and hyperplastic polyps, many of which are closely associated with H. pylori infections.⁸^-¹⁰ Despite its widespread use in clinical practice, the relationship between specific endoscopic findings, as classified by the Kyoto system and IDA, has not been thoroughly investigated. Establishing such an association could have practical clinical implications by aiding the identification of high-risk patients through endoscopic examination.

Several studies have reported an association between specific gastric lesions and IDA. A previous study identified the relationship between H. pylori-infected nodular gastritis and iron deficiency, which was potentially mediated by alterations in serum prohepcidin levels.¹¹ In addition, a few studies have described the occurrence of iron deficiency in patients with autoimmune gastritis who had gastric lesions, including hyperplastic polyps.¹²^,¹³ Although these investigations have provided a valuable relationship between individual gastric lesions and iron deficiency, they have primarily focused on limited pathological subtypes or were based on small patient cohorts. To date, no large-scale cohort studies or multivariate risk analyses have systematically investigated the association between a comprehensive range of endoscopic findings, particularly those categorized under the Kyoto classification of gastritis, and IDA.

Therefore, this study aimed to retrospectively analyze the endoscopic findings of patients diagnosed with H. pylori gastritis using the Kyoto classification, and to investigate the association between these features and the presence of IDA. By identifying the endoscopic predictors of IDA, we hope to improve risk stratification and inform future clinical management strategies.

METHODS

Study population

This retrospective study evaluated individuals who underwent screening esophagogastroduodenoscopies, accompanied by rapid urease tests (RUTs), as part of routine health checkups at DMC Bundang Jesaeng General Hospital between May 2022 and June 2023. Of the 1,887 patients initially assessed, those with negative RUT results were excluded. Among the remaining patients with confirmed H. pylori infections (n=578), only those who had completed laboratory tests for anemia were considered for further analysis. After excluding 232 patients without laboratory data, a final cohort of 346 individuals with H. pylori infections was included, as detailed in the patient selection flowchart (Fig. 1). Demographic and clinical data, including age, sex, comorbidities, medication use, and prior H. pylori eradication therapy, were collected from electronic medical records. As this study included individuals undergoing routine health checkups, few patients were receiving acid-suppressive therapy at the time of endoscopy. Furthermore, only patients with positive RUT results were included, minimizing the risk of false-negative RUT results due to proton pump inhibitor use.

Iron deficiency was defined as a serum ferritin level below 55 ng/mL. Anemia was defined according to the World Health Organization criteria (hemoglobin <13.0 g/dL in male patients and <12.0 g/dL in females).¹⁴ Based on the iron status, the patients were categorized into two groups: those with and without IDA.

Endoscopic examination

All patients underwent esophagogastroduodenoscopies conducted by six experienced endoscopists, each with over five years of clinical endoscopy experience and familiarity with the Kyoto classification of gastritis. Conscious sedation with intravenous midazolam was offered as requested if needed. To minimize observer bias, the endoscopists were blinded to each patient’s clinical history, including anemia status, previous H. pylori infection, and treatment history.

Endoscopic findings at the time of examination were documented according to the Kyoto classification of gastritis. High-quality endoscopic images were stored in the institution’s picture archiving and communication system. For retrospective validation, a single endoscopist (J.S.) independently reviewed all the stored images without access to the clinical information.

Assessment of endoscopic findings

The gastric mucosa was systematically assessed using the Kyoto classification of gastritis criteria. Specific features evaluated included the degree of gastric atrophy evaluated endoscopically and categorized based on the Kimura-Takemoto classification, ranging from no atrophy to grades C1–C3 and O1–O3.¹⁵ Intestinal metaplasia was assessed endoscopically and identified by features such as a villous surface or whitish plaques, and its distribution was examined in both the antrum and corpus using white-light endoscopy.¹⁶ Nodularity was defined as the presence of multiple small, uniform, whitish nodules, primarily observed in the gastric antrum. Hyperplastic polyps were identified as protruding mucosal lesions typically characterized by an elongated dilated foveolar epithelium and inflammatory stromal changes. For subgroup analysis, hyperplastic polyps were further categorized by size into two groups: <5 mm and ≥5 mm.

Reflux esophagitis was graded according to the Los Angeles (LA) classification system.¹⁷ LA grade A was defined as the presence of one or more mucosal breaks ≤5 mm in length, whereas LA grade B indicated mucosal breaks of >5 mm. In grade C, the mucosal break involved <75% of the esophageal circumference, whereas grade D involved mucosal damage that affected ≥75% of the circumference.

Peptic ulcers were classified into three stages according to the simplified Sakita-Miwa classification system.¹⁸ The active stage, encompassing both A1 and A2 ulcers, refers to ulcers characterized by a mucus coating and marginal elevation due to edema, often with discrete margins and varying degrees of inflammation. The healing stage, including H1 and H2 ulcers, describes ulcers that are partially or nearly completely covered by regenerating epithelium, with or without remaining mucosal breaks or covering folds. The scar stage, which includes S1 and S2 ulcers, represents lesions with complete or near-complete epithelial healing, presenting as red or white scars, depending on the degree of re-epithelialization.

Additional findings included diffuse redness, enlarged folds, sticky mucus, edema, xanthomas, spotty redness, and map-like redness, consistent with previous infections. The presence or absence of each feature was recorded for all patients. In addition to features specific to H. pylori-associated gastritis, other endoscopic findings potentially related to chronic gastrointestinal blood loss—such as reflux esophagitis, hiatal hernias, gastric ulcers, and duodenal ulcer scarring—were reviewed and included in the analysis. Representative endoscopic images of key findings, including hyperplastic polyps, atrophy, intestinal metaplasia, diffuse redness, nodularity, and enlarged folds, are shown in Figure 2.

Evaluation of H. pylori infection

H. pylori infection status was assessed using an RUT (Helicobacter test; In Fung). Gastric mucosal samples were collected from non-atrophic regions of the antrum and corpus. A positive RUT result was considered indicative of H. pylori infection, whereas a negative RUT result indicated the absence of infection.

Kyoto classification score

The Kyoto classification score was determined by evaluating five specific endoscopic features: atrophy, intestinal metaplasia, diffuse redness, enlarged folds, and nodularity.¹⁶ Cumulative scores ranged from 0 to 8 points. Atrophy was scored according to its extent, with C–0 or C–I assigned 0 points, C–II or C–III assigned 1 point, and open-type atrophy (O–I, O–II, or O–III) assigned 2 points. Intestinal metaplasia, assessed using white-light endoscopy, was scored as 0 if absent, 1 if confined to the antrum, and 2 if it extended into the corpus. Diffuse redness reflects generalized mucosal erythema in non-atrophic mucosa; mild redness accompanied by the presence of regular arrangement of collecting venules (RAC) was given 1 point, while severe redness without RAC was given 2 points. Enlarged folds, defined as gastric folds measuring >5 mm before air insufflation, were scored one point when present. Nodularity, identified by a mucosal texture resembling goose flesh, was assigned 1 point. The total Kyoto score was calculated by summing the points for all five categories.

Statistical analyses

Data were analyzed using R ver. 4.3.1 (The R Foundation for Statistical Computing). Continuous variables are expressed as medians with interquartile ranges or means±standard deviations, depending on the distribution assessed by the Shapiro–Wilk test. Categorical variables are presented as counts and percentages. Group comparisons were performed using the Mann-Whitney U-test for continuous variables and the chi-squared or Fisher’s exact test for categorical variables, as appropriate.

Logistic regression analysis was conducted to identify independent risk factors for iron deficiency. Variables with a p-value <0.1 in the univariate analysis were included in the multivariate model. The final model was adjusted for potential confounders, including age (<50 years) and sex (female). Odds ratios (ORs) and 95% confidence intervals (CIs) were determined. Statistical significance was set at a two-tailed p-value <0.05.

Ethical statement

The study protocol was approved by the Institutional Review Board of DMC Bundang Jesaeng General Hospital (approval number: DMC 2023-06-007), and the requirement for informed consent was waived.

RESULTS

Baseline characteristics

In total, 346 patients with H. pylori gastritis were included in the analysis. Among them, 47 (13.6%) were classified as having iron deficiency, whereas 299 (86.4%) did not exhibit iron deficiency. The baseline characteristics of the patients are summarized in Table 1.

Patients with iron deficiency were more likely to be female (87.2% vs. 33.4%, p<0.001). The median age was slightly lower in the iron-deficient group, although this difference did not reach statistical significance (47.0 vs. 53.0 years, p=0.171). The prevalence of comorbidities, including hypertension, diabetes mellitus, dyslipidemia, angina, and cerebrovascular accidents, did not differ significantly between the two groups.

Regarding medication use, proton pump inhibitors and H2 receptor blockers were significantly more commonly used in patients with iron deficiency (p<0.001 and p=0.001, respectively).

Laboratory findings showed that anemia was significantly more frequent in the iron-deficient group (23.4% vs. 2.3%, p<0.001). The median ferritin level was substantially lower in patients with iron deficiency (35.7 vs. 180.2 ng/mL, p<0.001), and other iron parameters—including serum iron levels, total iron-binding capacity, and transferrin saturation—also reflected significant differences between the groups (all, p≤0.004). Notably, the mean corpuscular hemoglobin and homocysteine levels were lower in the iron-deficient group (p=0.001 and p<0.001, respectively).

Endoscopic findings

Endoscopic evaluation revealed significant differences in the prevalence of specific mucosal findings between the groups (Table 2). Nodularity was observed more frequently in patients with iron deficiency (46.8% vs. 23.4%, p=0.001). Similarly, hyperplastic polyps were significantly more common in the iron-deficient group (17.0% vs. 3.7%, p=0.001). Larger hyperplastic polyps (≥5 mm) and smaller hyperplastic polyps (<5 mm) were significantly more frequently observed in patients with iron deficiency than in those without (10.6% vs. 1.7% and 6.4% vs. 2.0%, respectively).

Duodenal ulcer scars were more frequently observed in the non-iron-deficient group than in the iron-deficient group (25.1% vs. 14.9%, p=0.245). Similarly, there were no significant differences in the prevalence of reflux esophagitis (7.4% vs. 2.1%, p=0.518), hiatal hernias (35.8% vs. 23.4%, p=0.082), or gastric ulcers (11.4% vs. 6.4%, p=0.697) between the two groups.

Other endoscopic features, including atrophy, intestinal metaplasia, diffuse redness, spotty redness, edema, sticky mucus, enlarged folds, and xanthomas, did not differ significantly between the groups.

Risk factors for iron deficiency

The risk factors for iron deficiency were analyzed using logistic regression analysis, and the results are presented in Table 3. In the univariate logistic regression analysis, younger age (<50 years), female sex, nodularity, and larger hyperplastic polyps (≥5 mm) were identified as significant risk factors for iron deficiency. In the multivariate analysis, female sex was significantly associated with a higher risk of iron deficiency (OR, 15.80; 95% CI, 6.14–47.74; p<0.001). Younger age (<50 years) was also significantly associated with an increased risk of iron deficiency (OR, 4.58; 95% CI, 1.94–11.47; p<0.001). Additionally, the presence of hyperplastic polyps remained an independent risk factor (OR, 4.86; 95% CI, 1.04–23.71; p=0.044).

DISCUSSION

Our study showed that female sex, nodularity, and hyperplastic polyps were independently associated with iron deficiency in patients with H. pylori gastritis. These findings suggest that specific endoscopic features categorized according to the Kyoto classification of gastritis can serve as valuable indicators for identifying patients at an elevated risk of IDA. To the best of our knowledge, this is one of the first studies to systematically examine the relationship between a broad spectrum of Kyoto-defined endoscopic features and iron deficiency using multivariate analysis in a large cohort.

Several studies have shown that nodular gastritis is associated with iron deficiency in patients with H. pylori infections. Sato et al. showed that patients with H. pylori-infected nodular gastritis had higher rates of iron deficiency and elevated serum prohepcidin levels, which decreased after eradication therapy, suggesting a mechanistic link between nodularity and iron metabolism.¹¹ Nahon et al. also identified nodularity as a risk factor for IDA in adults, and previous studies have shown that chronic inflammation and mucosal changes in nodular gastritis can impair iron absorption.⁷^,¹⁹

In our study, we found that nodularity was significantly more prevalent in patients with iron deficiency than in those without iron deficiency (46.8% vs. 23.4%, p=0.001). However, this association was not statistically significant in the multivariate analysis after adjusting for other factors, suggesting that the observed relationship may be confounded by variables such as age and sex. This finding may be explained by the strong association between nodular gastritis and younger female patients, who also represent the demographics most susceptible to iron deficiency. Nodular gastritis is more prevalent in young females, particularly in East Asian populations, where the phenotype is often associated with active H. pylori infection and heightened gastric mucosal immune responses.²⁰ As both age and sex were identified as powerful independent predictors in our multivariate analysis, the initial univariate association between nodularity and iron deficiency was likely driven by these confounding factors rather than by nodularity itself. Additionally, the relatively small number of patients with iron deficiency in our cohort may have limited the statistical power to detect the independent effects of nodularity after adjustment. Small sample sizes reduce the precision of multivariate models and may obscure modest associations.²¹ Thus, although nodularity may reflect a gastric environment prone to disrupted iron metabolism, its role as an independent risk factor may be secondary to the broader host environment.

Although nodularity was not statistically significant after adjustment, hyperplastic polyps emerged as an independent endoscopic risk factor for iron deficiency. Hyperplastic polyps are generally considered benign; however, their presence may reflect chronic gastric inflammation and mucosal damage. This may have contributed to chronic blood loss or impaired iron absorption.²² Previous studies have reported that hyperplastic polyps, especially those located in the gastric antrum, can occasionally cause occult gastrointestinal bleeding, leading to IDA, particularly in older adults.²³ In our study, hyperplastic polyps were significantly more prevalent in patients with iron deficiency than in those without, and this association persisted after controlling for potential confounding variables in the multivariate analysis, with hyperplastic polyps identified as an independent risk factor for iron deficiency. These findings suggest that, beyond their benign histological nature, hyperplastic polyps may serve as clinically relevant markers for identifying patients at increased risk of iron deficiency. The vascular nature of these polyps and their potential for surface erosions appear to increase the likelihood of chronic blood loss.²⁴

Conventional endoscopic lesions, typically associated with chronic gastrointestinal blood loss, such as reflux esophagitis, gastric ulcers, and duodenal ulcers, were not more prevalent in the iron-deficient group. Duodenal ulcer scars and reflux esophagitis were more common in the non-iron-deficient group, and no statistically significant differences were noted across these lesions. These findings imply that occult iron loss in H. pylori-associated gastritis may arise from subtle or chronic mucosal changes such as hyperplastic polyps or inflammation-related alterations, rather than from overt ulcerative lesions. Therefore, further studies involving larger patient populations are warranted to clarify the relationship between various endoscopic lesions and anemia.

In our sub-analysis, we further stratified hyperplastic polyps by size to explore their clinical relevance. Interestingly, larger hyperplastic polyps (≥5 mm) were observed more frequently in the iron-deficient group than in the non-iron-deficient group (10.6% vs. 1.7%). The predominance of larger lesions in patients with iron deficiency suggests a size-dependent contribution to mucosal blood loss, particularly through surface erosions or vascular fragility. Although both small and large polyps were more common in the iron-deficient group, the disproportionate presence of larger polyps underscores the need for careful endoscopic assessment of polyp morphology and size in clinical practice. Future studies incorporating histological confirmation and endoscopic hemostasis markers may help clarify the clinical importance of hyperplastic polyp size in the pathogenesis of iron deficiency.

Our study also revealed that younger age and female sex were significantly associated with iron deficiency in patients with H. pylori gastritis. This is consistent with previous findings that nodular gastritis, a common endoscopic finding in our iron-deficient group, tends to occur more frequently in younger individuals, particularly females.²⁰ Although physiological factors, such as menstruation, may partially explain the higher prevalence of iron deficiency in younger females,⁵ the concurrent presence of mucosal abnormalities, including nodularity and hyperplastic polyps, suggests that gastric mucosal factors also play an important role in iron loss and impaired iron absorption.

The findings of our study have important clinical implications for the management of patients with H. pylori gastritis. The identification of nodularity and hyperplastic polyps during endoscopic examinations should prompt clinicians to consider the possibility of concurrent iron deficiency, particularly in younger female patients who appear to be at a higher risk. Routine assessment of the iron status, including serum ferritin levels and complete blood counts, may be warranted for patients exhibiting these mucosal features. Early detection of iron deficiency can facilitate timely intervention with iron supplementation and, where appropriate, H. pylori eradication therapy. Furthermore, recognizing these endoscopic features as potential markers of iron deficiency may enhance risk stratification in clinical practice. This approach could lead to improved patient outcomes by preventing the progression of subclinical iron deficiency to overt anemia, which can significantly affect quality of life. Future guidelines should consider incorporating endoscopic predictors, such as nodularity and hyperplastic polyps, into algorithms for the evaluation and management of iron deficiency in patients with H. pylori infections.

Our study has a few limitations. First, its retrospective design limits its ability to establish causal relationships. Second, the study was conducted at a single center, which may affect the generalizability of the results to other populations. Third, although we adjusted for many clinical variables, nongastrointestinal causes of iron deficiency, such as dietary iron intake, menstrual blood loss, and other systemic conditions, could not be fully accounted for. Finally, we did not assess changes in iron status after H. pylori eradication, which could provide further insights into the reversibility of iron deficiency associated with endoscopic findings.

Future prospective multicenter studies are needed to validate our findings and explore the underlying mechanisms linking specific endoscopic features to iron deficiency. Studies assessing the impact of H. pylori eradication on iron parameters in patients with nodular and hyperplastic polyps are particularly valuable. Additionally, detailed histopathological analyses of hyperplastic polyps and nodular lesions may help clarify their roles in mucosal iron loss and guide targeted management strategies.

Conflicts of Interest

The authors have no potential conflicts of interest.

Funding

None.

Author Contributions

Conceptualization: JS; Data curation: all authors; Methodology: HH, JS; Writing–original draft: HTL, HH, AYL; Writing–review & editing: all authors.

Fig. 1.

Flowchart of patients with Helicobacter pylori-current infection according to the presence of iron deficiency.

Fig. 2.

Endoscopic images. (A) Hyperplastic polyp. (B) Atrophy. (C) Intestinal metaplasia. (D) Diffuse redness. (E) Nodularity. (F) Enlarged folds.

Table 1.

Baseline characteristics of patients who were diagnosed with Helicobacter pylori gastritis according to presence of iron deficiency

Characteristic	Without iron deficiency (n=299)	With iron deficiency (n=47)	p-value
Age (yr)	53.0 (43.0–60.0)	47.0 (43.5–55.5)	0.171
Old age (>65)	43 (14.4)	9 (19.1)	0.528
Sex (male/female)	199 (66.6)/100 (33.4)	6 (12.8)/41 (87.2)	<0.001
Underlying disease
Hypertension	93 (31.1)	13 (27.7)	0.760
DM	46 (15.4)	5 (10.6)	0.527
Dyslipidemia	84 (28.1)	10 (21.3)	0.424
Angina	8 (2.7)	3 (6.4)	0.368
CVA	3 (1.0)	1 (2.1)	1.000
Medication
Antiplatelet	22 (7.4)	6 (12.8)	0.329
NSAID	14 (4.7)	2 (4.3)	1.000
H2 blocker	4 (1.3)	5 (10.6)	0.001
PPI	5 (1.7)	6 (12.8)	<0.001
PCAB	2 (0.7)	2 (4.3)	0.160
Laboratory findings
Anemia	7 (2.3)	11 (23.4)	<0.001
Hb (g/dL)	14.8(13.9–15.7)	13.1 (12.1–13.8)	<0.001
Hct (%)	44.1 (41.3–46.3)	39.2 (36.5–41.2)	<0.001
Plt (×10³/mm³)	241.0 (205.5–266.5)	243.0 (206.0–289.0)	0.409
MCV (fL)	92.6 (89.8–94.8)	91.3 (86.5–94.8)	0.067
MCH (pg)	31.2 (30.5–32.1)	30.7 (29.2–31.8)	0.001
ESR	8.0 (5.0–14.0)	9.0 (4.0–17.5)	0.539
hs-CRP	0.1 (0.0–0.1)	0.1 (0.0–0.1)	0.087
Ferritin (ng/mL)	180.2 (113.0–252.2)	35.7 (13.9–41.8)	<0.001
Iron (μg/dL)	120.0 (100.0–150.0)	103.0 (60.0–140.0)	0.004
TIBC (μg/dL)	310.0 (290.0–339.0)	352.0 (323.5–373.0)	<0.001
Transferrin saturation (%)	40 (30–50)	30 (20–40)	0.001
Homocysteine (μmol/L)	10.2 (8.4–12.1)	7.9 (6.9– 9.4)	<0.001

Values are presented as median (interquartile range) or number (%).

DM, diabetes mellitus; CVA, cerebrovascular accident; NSAID, non-steroidal anti-inflammatory drug; PPI, proton pump inhibitor; PCAB, potassium competitive acid blocker; Hb, hemoglobin; Hct, homocysteine; Plt, platelet; MCV, mean corpuscular volume; MCH, mean corpuscular hemoglobin; ESR, erythrocyte sedimentation rate; hs-CRP, high-sensitivity C-reactive protein; TIBC, total iron-binding capacity; transferrin saturation TIBC, transferrin saturation iron/TIBC.

Table 2.

Endoscopic findings of the patients who were diagnosed with Helicobacter pylori gastritis according to the presence of iron deficiency

	Without iron deficiency (n=299)	With iron deficiency (n=47)	p-value
RAC	18 (6.0)	4 (8.5)	0.742
Raised erosion	94 (31.4)	10 (21.3)	0.214
Hematin	32 (10.7)	4 (8.5)	0.841
Atrophy			0.350
Absent or C1	5 (1.7)	0 (0)
C2 or C3	33 (11.0)	8 (17.0)
Open type	261 (87.3)	39 (83.0)
Intestinal metaplasia			0.071
Antrum	22 (7.4)	4 (8.5)
Corpus	202 (67.6)	24 (51.1)
Diffuse redness			0.282
With partial RAC	10 (3.3)	0 (0)
Severe	238 (79.6)	36 (76.6)
Spotty redness	195 (65.2)	26 (55.3)	0.250
Edema	194 (64.9)	25 (53.2)	0.167
Sticky mucus	78 (26.1)	14 (29.8)	0.722
Enlarged folds	71 (23.7)	12 (25.5)	0.934
Nodularity	70 (23.4)	22 (46.8)	0.001
Xanthoma	22 (7.4)	4 (8.5)	1.000
Hyperplastic polyp			0.001
None	288 (96.3)	39 (83.0)
<5 mm	6 (2.0)	3 (6.4)
≥5 mm	5 (1.7)	5 (10.6)
Reflux esophagitis			0.518
No erosion	277 (92.6)	46 (97.9)
LA–A	12 (4.0)	0 (0)
LA–B	9 (3.0)	1 (2.1)
LA–C	1 (0.3)	0 (0)
Hiatal hernia	107 (35.8)	11 (23.4)	0.134
Gastric ulcer			0.697
Active	17 (5.7)	2 (4.3)
Healing	12 (4.0)	1 (2.1)
Scar	5 (1.7)	0 (0)
Duodenal ulcer			0.245
Active	6 (2.0)	0 (0)
Healing	3 (1.0)	0 (0)
Scar	75 (25.1)	7 (14.9)
Kyoto score	6 (4–6)	5 (4–6)	0.515

Values are presented as number (%) or median (interquartile range). Endoscopic atrophy was assessed by Kimura-Takemoto classification and classified into six grades: close (C)–I, C–II, C–III; and open type, Los Angeles (LA) classification.

RAC, regular arrangement of collecting venules.

Table 3.

Logistic regression analysis for risk factors of iron deficiency in patients who were diagnosed with Helicobacter pylori current infection

	Univariate analysis				Multivariable analysis
	OR	95% CI		p-value	OR	95% CI		p-value
	OR	Lower	Upper	p-value	OR	Lower	Upper	p-value
Young age (<50 yr)	2.14	1.15	4.05	0.017	4.58	1.94	11.47	<0.001
Female	13.60	6.00	36.65	<0.001	15.80	6.14	47.74	<0.001
Hypertension	0.85	0.41	1.64	0.634
DM	0.65	0.22	1.60	0.396
Dyslipidemia	0.69	0.31	1.41	0.331
CVA	2.14	0.10	17.16	0.513
Antiplatelet	1.84	0.65	4.57	0.212
Hematin	0.78	0.22	2.08	0.648
Atrophy (open type)	0.50	0.27	0.94	0.029	0.82	0.38	1.79	0.616
Diffuse redness	0.84	0.41	1.81	0.638
Spotty redness	0.66	0.35	1.24	0.191
Edema	0.61	0.33	1.15	0.125	0.65	0.30	1.40	0.272
Enlarged folds	1.10	0.52	2.18	0.790
Nodularity	2.88	1.52	5.42	0.001	1.26	0.53	2.92	0.590
Xanthoma	1.17	0.33	3.24	0.781
Active peptic ulcer	1.68	0.59	4.12	0.288
Hiatal hernia	0.55	0.26	1.09	0.100	0.76	0.31	1.75	0.527
Hyperplastic polyp (≥5 mm)	7.00	1.88	26.16	0.003	4.86	1.04	23.71	0.044

OR, odds ratio; CI, confidence interval; DM, diabetes mellitus; CVA, cerebrovascular accident.

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Endoscopic predictors of iron deficiency in Helicobacter pylori gastritis: a Kyoto classification-based study
Na Rae Lim, Woo Chul Chung
Clinical Endoscopy.2026; 59(1): 67. CrossRef

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Endoscopic predictors of iron deficiency in Helicobacter pylori gastritis: a Kyoto classification-based study

Clin Endosc. 2026;59(1):79-88. Published online November 6, 2025

DOI: https://doi.org/10.5946/ce.2025.175

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Endoscopic predictors of iron deficiency in Helicobacter pylori gastritis: a Kyoto classification-based study

Fig. 1. Flowchart of patients with Helicobacter pylori-current infection according to the presence of iron deficiency.

Fig. 2. Endoscopic images. (A) Hyperplastic polyp. (B) Atrophy. (C) Intestinal metaplasia. (D) Diffuse redness. (E) Nodularity. (F) Enlarged folds.

Graphical abstract

Fig. 1.

Fig. 2.

Graphical abstract

Endoscopic predictors of iron deficiency in Helicobacter pylori gastritis: a Kyoto classification-based study

Characteristic	Without iron deficiency (n=299)	With iron deficiency (n=47)	p-value
Age (yr)	53.0 (43.0–60.0)	47.0 (43.5–55.5)	0.171
Old age (>65)	43 (14.4)	9 (19.1)	0.528
Sex (male/female)	199 (66.6)/100 (33.4)	6 (12.8)/41 (87.2)	<0.001
Underlying disease
Hypertension	93 (31.1)	13 (27.7)	0.760
DM	46 (15.4)	5 (10.6)	0.527
Dyslipidemia	84 (28.1)	10 (21.3)	0.424
Angina	8 (2.7)	3 (6.4)	0.368
CVA	3 (1.0)	1 (2.1)	1.000
Medication
Antiplatelet	22 (7.4)	6 (12.8)	0.329
NSAID	14 (4.7)	2 (4.3)	1.000
H2 blocker	4 (1.3)	5 (10.6)	0.001
PPI	5 (1.7)	6 (12.8)	<0.001
PCAB	2 (0.7)	2 (4.3)	0.160
Laboratory findings
Anemia	7 (2.3)	11 (23.4)	<0.001
Hb (g/dL)	14.8(13.9–15.7)	13.1 (12.1–13.8)	<0.001
Hct (%)	44.1 (41.3–46.3)	39.2 (36.5–41.2)	<0.001
Plt (×10³/mm³)	241.0 (205.5–266.5)	243.0 (206.0–289.0)	0.409
MCV (fL)	92.6 (89.8–94.8)	91.3 (86.5–94.8)	0.067
MCH (pg)	31.2 (30.5–32.1)	30.7 (29.2–31.8)	0.001
ESR	8.0 (5.0–14.0)	9.0 (4.0–17.5)	0.539
hs-CRP	0.1 (0.0–0.1)	0.1 (0.0–0.1)	0.087
Ferritin (ng/mL)	180.2 (113.0–252.2)	35.7 (13.9–41.8)	<0.001
Iron (μg/dL)	120.0 (100.0–150.0)	103.0 (60.0–140.0)	0.004
TIBC (μg/dL)	310.0 (290.0–339.0)	352.0 (323.5–373.0)	<0.001
Transferrin saturation (%)	40 (30–50)	30 (20–40)	0.001
Homocysteine (μmol/L)	10.2 (8.4–12.1)	7.9 (6.9– 9.4)	<0.001

	Without iron deficiency (n=299)	With iron deficiency (n=47)	p-value
RAC	18 (6.0)	4 (8.5)	0.742
Raised erosion	94 (31.4)	10 (21.3)	0.214
Hematin	32 (10.7)	4 (8.5)	0.841
Atrophy			0.350
Absent or C1	5 (1.7)	0 (0)
C2 or C3	33 (11.0)	8 (17.0)
Open type	261 (87.3)	39 (83.0)
Intestinal metaplasia			0.071
Antrum	22 (7.4)	4 (8.5)
Corpus	202 (67.6)	24 (51.1)
Diffuse redness			0.282
With partial RAC	10 (3.3)	0 (0)
Severe	238 (79.6)	36 (76.6)
Spotty redness	195 (65.2)	26 (55.3)	0.250
Edema	194 (64.9)	25 (53.2)	0.167
Sticky mucus	78 (26.1)	14 (29.8)	0.722
Enlarged folds	71 (23.7)	12 (25.5)	0.934
Nodularity	70 (23.4)	22 (46.8)	0.001
Xanthoma	22 (7.4)	4 (8.5)	1.000
Hyperplastic polyp			0.001
None	288 (96.3)	39 (83.0)
<5 mm	6 (2.0)	3 (6.4)
≥5 mm	5 (1.7)	5 (10.6)
Reflux esophagitis			0.518
No erosion	277 (92.6)	46 (97.9)
LA–A	12 (4.0)	0 (0)
LA–B	9 (3.0)	1 (2.1)
LA–C	1 (0.3)	0 (0)
Hiatal hernia	107 (35.8)	11 (23.4)	0.134
Gastric ulcer			0.697
Active	17 (5.7)	2 (4.3)
Healing	12 (4.0)	1 (2.1)
Scar	5 (1.7)	0 (0)
Duodenal ulcer			0.245
Active	6 (2.0)	0 (0)
Healing	3 (1.0)	0 (0)
Scar	75 (25.1)	7 (14.9)
Kyoto score	6 (4–6)	5 (4–6)	0.515

	Univariate analysis				Multivariable analysis
	OR	95% CI		p-value	OR	95% CI		p-value
	OR	Lower	Upper	p-value	OR	Lower	Upper	p-value
Young age (<50 yr)	2.14	1.15	4.05	0.017	4.58	1.94	11.47	<0.001
Female	13.60	6.00	36.65	<0.001	15.80	6.14	47.74	<0.001
Hypertension	0.85	0.41	1.64	0.634
DM	0.65	0.22	1.60	0.396
Dyslipidemia	0.69	0.31	1.41	0.331
CVA	2.14	0.10	17.16	0.513
Antiplatelet	1.84	0.65	4.57	0.212
Hematin	0.78	0.22	2.08	0.648
Atrophy (open type)	0.50	0.27	0.94	0.029	0.82	0.38	1.79	0.616
Diffuse redness	0.84	0.41	1.81	0.638
Spotty redness	0.66	0.35	1.24	0.191
Edema	0.61	0.33	1.15	0.125	0.65	0.30	1.40	0.272
Enlarged folds	1.10	0.52	2.18	0.790
Nodularity	2.88	1.52	5.42	0.001	1.26	0.53	2.92	0.590
Xanthoma	1.17	0.33	3.24	0.781
Active peptic ulcer	1.68	0.59	4.12	0.288
Hiatal hernia	0.55	0.26	1.09	0.100	0.76	0.31	1.75	0.527
Hyperplastic polyp (≥5 mm)	7.00	1.88	26.16	0.003	4.86	1.04	23.71	0.044

Table 1. Baseline characteristics of patients who were diagnosed with Helicobacter pylori gastritis according to presence of iron deficiency

Values are presented as median (interquartile range) or number (%).

Table 2. Endoscopic findings of the patients who were diagnosed with Helicobacter pylori gastritis according to the presence of iron deficiency

RAC, regular arrangement of collecting venules.

Table 3. Logistic regression analysis for risk factors of iron deficiency in patients who were diagnosed with Helicobacter pylori current infection

OR, odds ratio; CI, confidence interval; DM, diabetes mellitus; CVA, cerebrovascular accident.