Introduction: Since inflammatory cells, such as lymphocytes and plasma cells, normally inhabit the stomach, the border between normal and mild inflammation is difficult to visually determine using the updated Sydney system scale of gastritis. Additionally, eosinophils in the gastric mucosa must be counted to diagnose eosinophilic gastritis. We aimed to determine the normal number of inflammatory cells in patients with endoscopically normal mucosa and without Helicobacter pylori infections. Methods: We assessed patients aged 20–79 years, who had undergone upper gastrointestinal endoscopy at Kawasaki Medical School Hospital between January 2010 and December 2014. Inflammatory cells were counted in 1,000 μm2 fields of pyloric and fundic gland mucosal biopsy specimens. We finally included 325 (male, n = 141; female, n = 184; average age = 49.3 years) patients without inflammation who had H. pylori-negative endoscopic results and negative histological findings interpreted based on the updated Sydney System and the Kyoto classification of gastritis. Results: The average numbers of nucleated cells were 83.3 ± 14.2 and 65.4 ± 12.6/mm2 in the pyloric and fundic gland mucosae, respectively. Inflammatory cells were significantly more abundant in the pyloric mucosa than in the fundic gland mucosa (p < 0.05). Age and sex distribution did not significantly differ. Eosinophils were absent or scanty in the gastric mucosae of both glands in all patients. Conclusion: We determined the absolute values of inflammatory cells, including eosinophils, in normal mucosae of pyloric and fundic glands. These findings could be important in defining gastric mucosal inflammation, including eosinophilic gastritis diagnosis.

Since Warren and Marshall [1] provided the first description of Helicobacter pylori (H. pylori) in 1983, cumulative evidence indicates that H. pylori infections play an important role in the pathogenesis of chronic gastritis [2‒5]. The endoscopic findings of atrophy, erosions, enlarged folds, and nodularity can identify the progression of H. pylori infection into gastritis [3, 6, 7].

A working party at the World Congress of Gastroenterology in Sydney proposed a standardized histological classification of gastritis in 1990 [8] that was subsequently adopted as the updated Sydney System [9]. Consequently, endoscopic and histological gastritis has been conventionally classified based on the updated Sydney System. Inflammatory lymphocytes, plasma cells, and granulocytes within the gastric lamina propria are graded as absent (0), mild (1), moderate (2), or severe (3) according to the visual analog scales of the updated Sydney System. Although the Houston-updated Sydney System guidelines are now widely applied, interobserver agreement among pathologists remains poor [10, 11].

Inflammatory lymphocytes and plasma cells normally inhabit the stomach in the absence of H. pylori infection [9]. Therefore, discrimination of the border between normal tissues (without inflammatory cells) using the updated Sydney System [9] and mild inflammation using a visual analog scale is challenging. Furthermore, the prevalence of eosinophilic gastritis and gastroenteritis has increased, and these need to be differentially diagnosed based on accurate eosinophil counts in the gastric mucosa [12, 13]. Thus, the present study aimed to determine the normal number of inflammatory cells in patients with endoscopically normal gastric mucosae devoid of H. pylori infections.

Patients

We enrolled patients aged 20–79 years who underwent upper gastrointestinal endoscopy at Kawasaki Medical School Hospital between January 2010 and December 2014. The endoscopic findings of the entire gastric mucosa were examined, and the absence of H. pylori infection was confirmed based on the Kyoto classification of gastritis [14]. Biopsies were then taken from the pyloric and fundic gland mucosae, and H. pylori infections and gastritis were histologically evaluated. The number of patients who underwent biopsies of the gastric antrum and corpus during the study period was 1518. Patients who met the exclusion criteria, which included the use of nonsteroidal anti-inflammatory drugs, antacids, H2-­receptor antagonists, proton pump inhibitors, rebamipide (2-(4-chlorobenzoylamino)-3-[2-(1H)-quinolinon-4-yl] propionic acid), immunesuppressors, immunomodulators, or antibiotics during the month preceding endoscopy; a history of gastric surgery; current pregnancy status; a history of systemic conditions, such as collagen disease, inflammatory bowel disease, or eosinophilic gastroenteritis; or a history of treatment for H. pylori infection, were excluded. Non-Japanese patients were excluded because of the perceived variations in the form of gastritis, compared to the Japanese patients. The eventual study population was 325 (male, n = 141; female, n = 184; average age = 49.3 years) patients in whom the presence and extent of non-H. pylori infections could be determined (Fig. 1). Three endoscopists retrospectively assessed endoscopic and histological findings of the gastric mucosae based on the Kyoto classification of gastritis and the updated Sydney System, respectively [9].

Fig. 1.

Enrollment of study participants. NSAIDs, nonsteroidal anti-inflammatory drugs.

Fig. 1.

Enrollment of study participants. NSAIDs, nonsteroidal anti-inflammatory drugs.

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The Ethics Committee of Kawasaki Medical School approved the study (Approval No. 3319-3), which was conducted according to the principles of the Declaration of Helsinki with the procurement. All patients gave written informed consent, and agreements were obtained.

Endoscopic Findings and H. pylori Status

All patients fasted overnight and were assessed via endoscopy without premedication. Three endoscopists (N.S., K.H., and N.M.) who were blinded to the symptoms, laboratory data, histological reports of biopsy specimens, and H. pylori infection status evaluated the endoscopic findings per the Kyoto classification criteria (Table 1) [14]. Inconsistencies were resolved by joint discussion to reach a consensus. The degree of corpus atrophy was categorized from C1 (none) to O3 (extremely severe) per the Kimura-Takemoto classification [15]. Endoscopic findings with corpus atrophy graded as C1 and a regular arrangement of collecting venules indicated a H. pylori-negative status. We excluded patients with H. pylori infections manifesting as atrophy, diffuse redness, and fold swelling visualized by endoscopy (Fig. 2a, b).

Table 1.

Endoscopic findings in 325 H. pylori-negative patients*

 Endoscopic findings in 325 H. pylori-negative patients*
 Endoscopic findings in 325 H. pylori-negative patients*
Fig. 2.

Endoscopic images of the normal gastric mucosa: antrum (a) and corpus (b). Histological images of normal gastric mucosa stained with hematoxylin and eosin. Mucosae of the pyloric (c) and fundic (d) glands. Representative histopathological images of nucleated cells in the gastric mucosa. Mucosae of the pyloric (e) and fundic (f) glands. Arrows, nucleated cells.

Fig. 2.

Endoscopic images of the normal gastric mucosa: antrum (a) and corpus (b). Histological images of normal gastric mucosa stained with hematoxylin and eosin. Mucosae of the pyloric (c) and fundic (d) glands. Representative histopathological images of nucleated cells in the gastric mucosa. Mucosae of the pyloric (e) and fundic (f) glands. Arrows, nucleated cells.

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Assessment of Histological Gastritis and H. pylori Infection

At least 2 gastric biopsy specimens obtained during endoscopy from all patients were histologically assessed. One specimen each was obtained from the greater or lesser curvatures of the antrum and midcorpus. Specimens were fixed in 10% buffered formalin, embedded in paraffin, sliced into 4-µm sections, and stained with hematoxylin and eosin (HE) for histological assessment and Giemsa or Gimenez stains to identify H. pylori. Two pathologists blinded to patient data interpreted all stained biopsy specimens based on the updated Sydney System [9]. Gastric mucosal inflammation was defined as the confirmed infiltration of inflammatory neutrophils, lymphocytes, and plasma cells. Mucosal atrophy was defined as the loss of glandular tissue. Inflammation, mucosal atrophy, and intestinal metaplasia were categorized as none, mild, moderate, or severe. We selected patients in whom inflammation, atrophy, and intestinal metaplasia were evaluated as “none” as per the updated Sydney System (Fig. 2c, d).

The status of H. pylori infection was determined by Giemsa or Gimenez staining together with histologically confirmed inflammation. Patients were determined as uninfected if both Giemsa or Gimenez staining and histological inflammation were assessed as negative or “none.” All 325 patients were confirmed to be negative for H. pylori based on Giemsa or Gimenez staining.

Cell Count

Biopsies from the midcorpus and antrum were stained by HE and analyzed using an Olympus BX51 microscope with a 40× objective and 10× focusing eyepiece containing a calibrated micrometer. Averages of inflammatory cells and eosinophils counted in 3 fields in mucosal strips (standard length: 1,000 μm) were calculated by 1 person (N.S.) (Fig. 2e, f) [16].

The counted cells included mononuclear lymphocytes and plasma cells, neutrophils, and eosinophils. The location for cell count was just beneath the foveolar epithelium in the stomach. These cells were carefully distinguished from fibroblasts, endothelial cells, and epithelial cells. The number of cells and eosinophils counted in the stomach is expressed as mean ± standard deviation. Areas around lymphoid follicles were excluded.

Statistical Analysis

All statistical analyses were nonparametric. Comparisons between groups and among 3 groups (such as age differences) were analyzed using the Mann-Whitney U test and the Kruskal-Wallis test, respectively. The Spearman correlation coefficient was used to evaluate the correlation between the number of nucleated cells in the mucosae of the pyloric and the fundic glands. Data were statistically analyzed using EZR [17], a modified version of R commander designed to add statistical functions frequently used in biostatistics. Values with p < 0.05 were considered statistically significant.

Endoscopic Findings in the Study Population

The endoscopic findings of all 325 patients were normal and H. pylori negative. Based on the Kyoto classification [14], red streaks were found in 41 (12.6%) patients, fundic gland polyps in 126 (38.8%), raised erosions in 35 (10.8%), hematin in 26 (8.0%), and depressive erosions in 30 (9.2%). The other 98 patients were completely normal (Table 1).

Relationship between the Number of Nucleated Cells in the Mucosae of Pyloric and Fundic Glands

Figure 3 shows the relationship between the average number of nucleated cells in the pyloric and fundic glands. The range of nucleated cells in the pyloric glands and fundic glands was 38.3–138.0 and 31.7–110.3 cells/mm2, respectively. The data revealed a positive correlation between the number of cells in the mucosae of the pyloric and fundic glands (Spearman Rs = 0.476; p = <0.05) in the normal gastric mucosa (Fig. 3).

Fig. 3.

Correlation between the number of nucleated cells in the mucosae of the pyloric and fundic glands. The dotted line indicates linear approximation. There was a significant positive correlation (Spearman’s rank correlation: Rs = 0.476, p = <0.05).

Fig. 3.

Correlation between the number of nucleated cells in the mucosae of the pyloric and fundic glands. The dotted line indicates linear approximation. There was a significant positive correlation (Spearman’s rank correlation: Rs = 0.476, p = <0.05).

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Nucleated cells in pyloric and fundic glands did not differ by age or gender. The average number of nucleated cells was significantly higher in the pyloric glands than in the fundic glands (83.3 ± 14.2 vs. 65.4 ± 12.6/mm2; p < 0.05).

Figures 4and5 compare the number of nucleated cells in the pyloric and fundic glands according to age and sex. Patients were allocated to 3 age groups as follows: 20–39, 40–59, and 60–79 years. These 3 age groups are referred to as young, middle-aged, and elderly. The mean nucleated cell counts in the pyloric and fundic glands in the 3 age groups were 84.0 ± 15.3, 83.3 ± 12.7, and 82.6 ± 14.9/mm2, respectively, and 66.5 ± 13.5, 65.0 ± 12.9, and 64.9 ± 11.0/mm2, respectively. Average cell counts in the pyloric and fundic glands of males and females were 82.7 ± 13.4 and 83.8 ± 14.8/mm2; 64.9 ± 13.1 and 65.8 ± 12.1/mm2, respectively. These findings show that age or sex did not result in significant differences in mean nucleated cell counts in the pyloric and fundic glands (Fig. 4, 5).

Fig. 4.

Comparison of nucleated cells between pyloric (a) and fundic gland mucosae (b) according to age. Patients (n = 325) aged 20–39 (n = 100), 40–59 (n = 123), and 60–79 (n = 102) years are, respectively, described as young, middle-aged, and elderly. Boxes, interquartile range; lines, median. The width of the violin plots indicates the proportion of cases with the average number of nucleated cells.

Fig. 4.

Comparison of nucleated cells between pyloric (a) and fundic gland mucosae (b) according to age. Patients (n = 325) aged 20–39 (n = 100), 40–59 (n = 123), and 60–79 (n = 102) years are, respectively, described as young, middle-aged, and elderly. Boxes, interquartile range; lines, median. The width of the violin plots indicates the proportion of cases with the average number of nucleated cells.

Close modal
Fig. 5.

Comparison of nucleated cells between pyloric (a) and fundic gland mucosae (b) according to sex. Patients (n = 325) comprised 184 females (F) and 141 males (M). Boxes, interquartile range; lines, median. The width of the violin plots indicates the proportion of cases with the average number of nucleated cells.

Fig. 5.

Comparison of nucleated cells between pyloric (a) and fundic gland mucosae (b) according to sex. Patients (n = 325) comprised 184 females (F) and 141 males (M). Boxes, interquartile range; lines, median. The width of the violin plots indicates the proportion of cases with the average number of nucleated cells.

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Eosinophil Counts

Eosinophils were essentially absent on the surface of the gastric mucosa of the pyloric and fundic glands. The average (range) peak density of eosinophils was 0.4 (0–11.5)/mm2 in pyloric and 0.4 (0–10)/mm2 in fundic mucosae.

The numbers of eosinophils on the gastric mucosal surface among the young, middle-aged, and elderly age groups were 0.28 ± 0.83, 0.49 ± 1.50, and 0.29 ± 0.82/mm2, respectively, in the pyloric gland, and 0.44 ± 1.39, 0.34 ± 0.90, and 0.47 ± 1.34/mm2, respectively, in the fundic gland. The numbers of eosinophils were 0.51 ± 1.51 and 0.25 ± 0.71/mm2 in the pyloric glands and 0.46 ± 1.43 and 0.37 ± 1.01/mm2 in the fundic glands of males and females, respectively. Thus, the number of eosinophils on the surface of the gastric mucosa of the pyloric and fundic glands did not significantly differ regardless of age or sex.

This is the first report on the numbers of inflammatory cells that normally inhabit the stomach without H. pylori infections. Our study demonstrates that a normal stomach contains very few eosinophils (<0.4/mm2).

Although defining a normal stomach is difficult, we selected patients with stomachs deemed normal according to endoscopic findings and the Kyoto classification [14], which has recently been established in Japan, where it is clinically applied. Our previous study has shown that the Kyoto classification is a useful method for the diagnosis of H. pylori infections and gastritis based on endoscopic findings in young Japanese individuals [18]. Others have shown that endoscopic findings of atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness are closely associated with histological gastritis [3, 6, 19].

The grading system for histological gastritis is based on the updated Sydney System [9]. Gastritis is classified in the updated Sydney System as absent (0), mild (1), moderate (2), and severe (3) according to the density of stained inflammatory lymphocytes, plasma cells, and granulocytes within the lamina propria. However, this is a visual analog scale, and consistency varies among pathologists [9]. Guarner et al. [20] evaluated the concordance rate of histological findings of the gastric mucosa reported by 2 pathologists during 2 periods. Concordance was low during the first period (Kappa score: H. pylori, 0.59; acute inflammation, 0.22; intestinal metaplasia, 0.60; atrophy, 0.04) but better during the second period. However, concordance in the evaluation of acute inflammation remained low in both studies (Kappa score: 0.22 and 0.50). Therefore, it is important to understand the absolute numbers of inflammatory cells in a normal stomach in the absence of H. pylori infections.

We found that the mean (range) number of inflammatory cells was 74.4 (31.7–138/mm2), with significant differences noted in the pyloric and the fundic gland mucosae. Although the reason for this is unclear, the pyloric gland mucosa is readily influenced by duodenogastric reflux, which introduces bile acids and pancreatic enzymes into the stomach that can cause mucosal inflammation [21, 22]. Moreover, acid and pepsin secretion from the fundic gland may protect the gastric mucosa. The reason for the wide range of inflammatory cell numbers remains unclear. Besides H. pylori infection, alcohol consumption, cigarette smoking, medications, underlying diseases, and BMI can influence immune cell infiltration into the gastric mucosa [21, 23, 24]. Although we excluded patients with a history of H. pylori treatment, medication, or underlying diseases, other factors might be associated with increased numbers of inflammatory cells. Several recent studies have found an association between obesity and gastritis [24, 25]. Chakhachiro et al. [26] found markedly few plasma cells (2.15 per high power field [HPF]) in H. pylori-negative stomachs of patients who underwent sleeve gastrectomy for obesity. The present study found no age- or sex-based differences in the number of inflammatory cells, although they are thought to influence the gastric mucosa.

The prevalence of eosinophilic gastroenteritis has recently increased in Western countries, although it has not reached similar incidence rates in Japan [12, 27‒30]. A diagnosis of eosinophilic gastroenteritis requires the infiltration of >20 eosinophils/HPF in the stomach, duodenum, and intestine [13, 31]. Matsushita et al. [32] reported that the average number of eosinophils in the normal gastric mucosa of Japanese individuals was 12.18 ± 11.39/HPF (range: 0.00–39.60). The mean (range) eosinophil count in H. pylori-negative patients with normal mucosa in the present study was 0.36 ± 1.1 (0–11.5) eosinophils/mm2. Since eosinophil infiltration can be caused by several factors, including allergic responses, H. pylori infection, or parasitic infections, understanding the numbers of eosinophils that inhabit the normal stomach may be useful for further investigations into allergies and infections.

This retrospective study has several limitations. First, interpretations often differed among the 3 evaluators; consequently, we adopted the majority opinion. Secondly, biopsy specimens were obtained only from the greater or lesser curvature of the antrum and corpus. Thus, our histological findings of gastritis might not be representative of the entire stomach. However, inflammation appears as diffuse changes and can be diagnosed by spot biopsies. Further, H. pylori infection was diagnosed using histological Giemsa or Gimenez staining. The sensitivity and specificity of these staining methods are 88 and 98%, respectively [33, 34]. Finally, we could not exclude patients with previous infections that have been accidentally completely eradicated. We evaluated for H. pylori eradication from the results of past questionnaires and medical records. In case of a previous infection, endoscopic findings can show atrophy of the antrum and corpus, and therefore we confirmed that there was no atrophy through endoscopy. In addition, we could visually count the number of inflammatory cells in our patients because none had histological gastritis.

In conclusion, we determined the absolute values of inflammatory cells, including eosinophils, in both the antrum and corpus of H. pylori-negative patients with endoscopically normal mucosa, which is important for defining gastric mucosal inflammation. This may be useful in clinical practice when assessing endoscopic findings and biopsy specimens.

We are grateful to the previous and present staff at the gastroenterology and pathology laboratories, as well as our laboratory, for their valuable support during this study.

The research protocol was approved by the Ethics Committee of Kawasaki Medical School (Approval No. 3319-3). All patients gave written informed consent, and agreements were obtained.

The authors have no conflicts of interest to disclose.

No funding was received for this study.

N.S., K.H., T.K., and N.M. conceived and designed the study. N.S., K.H., M.S., N.M., Y.Y., S.F., and T.T. analyzed and interpreted data. K.H. and T.A. provided pathology reviews. N.S., K.H., and T.T. wrote the manuscript. N.S., K.H., T.K., N.M., and A.S. contributed to the materials and patients. K.H. and T.T. contributed to study supervision. All authors approved the final version of the manuscript for submission.

1.
Warren
JR
,
Marshall
B
.
Unidentified curved bacilli on gastric epithelium in active chronic gastritis
.
Lancet
.
1983 Jun
;
1
(
8336
):
1273
5
.
2.
Kawaguchi
H
,
Haruma
K
,
Komoto
K
,
Yoshihara
M
,
Sumii
K
,
Kajiyama
G
.
Helicobacter pylori infection is the major risk factor for atrophic gastritis
.
Am J Gastroenterol
.
1996 May
;
91
(
5
):
959
62
.
3.
Mihara
M
,
Haruma
K
,
Kamada
T
,
Komoto
K
,
Yoshihara
M
,
Sumii
K
,
.
The role of endoscopic findings for the diagnosis of Helicobacter pylori infection: evaluation in a country with high prevalence of atrophic gastritis
.
Helicobacter
.
1999 Mar
;
4
(
1
):
40
8
.
4.
Komoto
K
,
Haruma
K
,
Kamada
T
,
Tanaka
S
,
Yoshihara
M
,
Sumii
K
,
.
Helicobacter pylori infection and gastric neoplasia: correlations with histological gastritis and tumor histology
.
Am J Gastroenterol
.
1998 Aug
;
93
(
8
):
1271
6
.
5.
Haruma
K
,
Okamoto
S
,
Sumii
K
,
Yoshihara
M
,
Tari
A
,
Teshima
H
,
.
Helicobacter pylori infection and gastroduodenal disease: a comparison of endoscopic findings, histology, and urease test data
.
Hiroshima J Med Sci
.
1992 Sep
;
41
(
3
):
65
70
.
6.
Kato
T
,
Yagi
N
,
Kamada
T
,
Shimbo
T
,
Watanabe
H
,
Ida
K
.
Diagnosis of Helicobacter pylori infection in gastric mucosa by endoscopic features: a multicenter prospective study
.
Dig Endosc
.
2013 Sep
;
25
(
5
):
508
18
.
7.
Kamada
T
,
Haruma
K
,
Sugiu
K
,
Nagashima
Y
,
Qian
DM
,
Koga
H
,
.
Case of early gastric cancer with nodular gastritis
.
Dig Endosc
.
2004 Jan
;
16
(
1
):
39
43
.
8.
Price
AB
.
The Sydney system: histological division
.
J Gastroenterol Hepatol
.
1991 May–Jun
;
6
(
3
):
209
22
.
9.
Dixon
MF
,
Genta
RM
,
Yardley
JH
,
Correa
P
.
Classification and grading of gastritis. The updated Sydney system
.
Am J Surg Pathol
.
1996 Oct
;
20
(
10
):
1161
81
.
10.
Andrew
A
,
Wyatt
JI
,
Dixon
MF
.
Observer variation in the assessment of chronic gastritis according to the Sydney system
.
Histopathology
.
1994 Oct
;
25
(
4
):
317
22
.
11.
Aydin
O
,
Egilmez
R
,
Karabacak
T
,
Kanik
A
.
Interobserver variation in histopathological assessment of Helicobacter pylori gastritis
.
World J Gastroenterol
.
2003 Oct
;
9
(
10
):
2232
5
.
12.
Kinoshita
Y
,
Ishihara
S
.
Eosinophilic gastroenteritis: epidemiology, diagnosis, and treatment
.
Curr Opin Allergy Clin Immunol
.
2020 Jun
;
20
(
3
):
311
5
.
13.
Talley
NJ
,
Shorter
RG
,
Phillips
SF
,
Zinsmeister
AR
.
Eosinophilic gastroenteritis: a clinicopathological study of patients with disease of the mucosa, muscle layer, and subserosal tissues
.
Gut
.
1990 Jan
;
31
(
1
):
54
8
.
14.
Haruma
K
,
Kato
M
,
Inoue
K
,
Murakami
K
,
Kamata
T
, editors.
Kyoto classification of gastritis
. 2nd ed.
Tokyo
:
Nihon Medical Center
;
2018
. p.
10
31
.
15.
Kimura
K
,
Takemoto
T
.
An endoscopic recognition of the atrophic border and its significance in chronic gastritis
.
Endoscopy
.
1969 Sep
;
1
(
3
):
87
97
.
16.
Toukan
AU
,
Kamal
MF
,
Amr
SS
,
Arnaout
MA
,
Abu-Romiyeh
AS
.
Gastroduodenal inflammation in patients with nonulcer dyspepsia: a controlled endoscopic and morphometric study
.
Dig Dis Sci
.
1985 Apr
;
30
(
4
):
313
20
.
17.
Kanda
Y
.
Investigation of the freely available easy-to-use software “EZR” for medical statistics
.
Bone Marrow Transplant
.
2013 Mar
;
48
(
3
):
452
8
.
18.
Suehiro
M
,
Kamada
T
,
Haruma
K
,
Nakamura
J
,
Manabe
N
,
Monobe
Y
,
.
The role of Kyoto classification in the diagnosis of Helicobacter pylori infection and histologic gastritis among young subjects in Japan
.
Kawasaki Med J
.
2019 Aug
;
45
:
43
52
.
19.
Nomura
S
,
Ida
K
,
Terao
S
,
Adachi
K
,
Kato
T
,
Watanabe
H
,
.
Endoscopic diagnosis of gastric mucosal atrophy: multicenter prospective study
.
Dig Endosc
.
2014 Nov
;
26
(
6
):
709
19
.
20.
Guarner
J
,
Herrera-Goepfert
R
,
Mohar
A
,
Sanchez
L
,
Halperin
D
,
Ley
C
,
.
Interobserver variability in application of the revised Sydney classification for gastritis
.
Hum Pathol
.
1999 Dec
;
30
(
12
):
1431
4
.
21.
Nakamura
M
,
Haruma
K
,
Kamada
T
,
Mihara
M
,
Yoshihara
M
,
Imagawa
M
,
.
Duodenogastric reflux is associated with antral metaplastic gastritis
.
Gastrointest Endosc
.
2001 Jan
;
53
(
1
):
53
9
.
22.
Matsuhisa
T
,
Arakawa
T
,
Watanabe
T
,
Tokutomi
T
,
Sakurai
K
,
Okamura
S
,
.
Relation between bile acid reflux into the stomach and the risk of atrophic gastritis and intestinal metaplasia: a multicenter study of 2283 cases
.
Dig Endosc
.
2013 Sep
;
25
(
5
):
519
25
.
23.
Frezza
M
,
Gorji
N
,
Melato
M
.
The histopathology of non-steroidal anti-inflammatory drug induced gastroduodenal damage: correlation with Helicobacter pylori, ulcers, and haemorrhagic events
.
J Clin Pathol
.
2001 Jul
;
54
(
7
):
521
5
.
24.
Adalı
Y
,
Binnetoğlu
K
,
Eroğlu
HA
,
Kaya
N
,
Güvendi
GF
.
The relationship between histopathologic findings and body mass index in sleeve gastrectomy materials
.
Obes Surg
.
2019 Jan
;
29
(
1
):
277
80
.
25.
Turan
G
,
Kocaöz
S
.
Helicobacter Pylori infection prevalence and histopathologic findings in laparoscopic sleeve gastrectomy
.
Obes Surg
.
2019 Nov
;
29
(
11
):
3674
9
.
26.
Chakhachiro
Z
,
Saroufim
M
,
Safadi
B
,
Attieh
M
,
Assaf
N
,
Shamseddine
G
,
.
Plasma cells and lymphoid aggregates in sleeve gastrectomy specimens: normal or gastritis
.
Medicine
.
2020 Feb
;
99
(
6
):
e18926
.
27.
Powell
N
,
Walker
MM
,
Talley
NJ
.
Gastrointestinal eosinophils in health, disease and functional disorders
.
Nat Rev Gastroenterol Hepatol
.
2010 Mar
;
7
(
3
):
146
56
.
28.
Oh
HE
,
Chetty
R
.
Eosinophilic gastroenteritis: a review
.
J Gastroenterol
.
2008 Oct
;
43
(
10
):
741
50
.
29.
Rothenberg
ME
.
Eosinophilic gastrointestinal disorders (EGID)
.
J Allergy Clin Immunol
.
2004 Jan
;
113
(
1
):
11
29
.
30.
Spergel
JM
,
Book
WM
,
Mays
E
,
Song
L
,
Shah
SS
,
Talley
NJ
,
.
Variation in prevalence, diagnostic criteria, and initial management options for eosinophilic gastrointestinal diseases in the United States
.
J Pediatr Gastroenterol Nutr
.
2011 Mar
;
52
(
3
):
300
6
.
31.
Kinoshita
Y
,
Furuta
K
,
Ishimaura
N
,
Ishihara
S
,
Sato
S
,
Maruyama
R
,
.
Clinical characteristics of Japanese patients with eosinophilic esophagitis and eosinophilic gastroenteritis
.
J Gastroenterol
.
2013 Mar
;
48
(
3
):
333
9
.
32.
Matsushita
T
,
Maruyama
R
,
Ishikawa
N
,
Harada
Y
,
Araki
A
,
Chen
D
,
.
The number and distribution of eosinophils in the adult human gastrointestinal tract: a study and comparison of racial and environmental factors
.
Am J Surg Pathol
.
2015 Apr
;
39
(
4
):
521
7
.
33.
Laine
L
,
Lewin
DN
,
Naritoku
W
,
Cohen
H
.
Prospective comparison of H&E, Giemsa, and Genta stains for the diagnosis of Helicobacter pylori
.
Gastrointest Endosc
.
1997 Jun
;
45
(
6
):
463
7
.
34.
Thijs
JC
,
van Zwet
AA
,
Thijs
WJ
,
Oey
HB
,
Karrenbeld
A
,
Stellaard
F
,
.
Diagnostic tests for Helicobacter pylori: a prospective evaluation of their accuracy, without selecting a single test as the gold standard
.
Am J Gastroenterol
.
1996 Oct
;
91
(
10
):
2125
9
.