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Inoue I, Yoshimura N, Iidaka T, Horii C, Muraki S, Oka H, Kawaguchi H, Akune T, Maekita T, Mure K, Nakamura K, Tanaka S, Ichinose M. Trends in the prevalence of atrophic gastritis and Helicobacter pylori infection over a 10‑year period in Japan: The ROAD study 2005‑2015. Mol Clin Oncol 2023; 19:53. [PMID: 37323249 PMCID: PMC10265571 DOI: 10.3892/mco.2023.2649] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/05/2022] [Accepted: 04/27/2023] [Indexed: 06/17/2023] Open
Abstract
Few large population-based studies have examined the prevalence of atrophic gastritis (AG) and Helicobacter pylori infection in Japan. The purpose of the present study was to estimate the prevalence of AG and H. pylori infection by age, in addition to investigating their change rates from 2005 to 2016 in Japan using data from a large population-based cohort. A total of 3,596 participants [1,690 in the baseline survey (2005-2006) and 1,906 at the fourth survey (2015-2016)] aged 18 to 97 years were included in the cohort. The prevalence of AG and H. pylori infection were examined at baseline and in the fourth survey based on serological tests for the H. pylori antibody titer and pepsinogen levels. The prevalence of AG and H. pylori infection were 40.1% (men, 44.1%; women, 38.0%) and 52.2% (men, 54.8%; women, 50.8%), respectively, at baseline. AG seropositivity rates showed a significant decrease from 40.1 to 25.8% in 10 years. H. pylori seropositivity rates decreased significantly from 52.2 to 35.5% in 10 years. Stratified for age, the prevalence of AG showed an increasing trend with age, whereas the prevalence of H. pylori infection increased with aging, except for in the elderly group, showing an inverted U-shaped association. In this population-based, cross-sectional study with a 10-year interval survey, the prevalence of AG and H. pylori infection decreased significantly. This change may influence the prevalence of H. pylori-related diseases, including extra-gastric disorders associated with H. pylori-induced systemic subclinical inflammation and hypochlorhydria, such as colorectal neoplasia and arteriosclerosis.
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Affiliation(s)
- Izumi Inoue
- Health Service Center, Tokyo University of Marine Science and Technology, Tokyo 108-8477, Japan
| | - Noriko Yoshimura
- Department of Prevention Medicine for Locomotive Organ Disorders, 22nd Century Medical and Research Center, Tokyo 113-8655, Japan
| | - Toshiko Iidaka
- Department of Prevention Medicine for Locomotive Organ Disorders, 22nd Century Medical and Research Center, Tokyo 113-8655, Japan
| | - Chiaki Horii
- Department of Orthopedic Surgery, Sensory and Motor System Medicine, Graduate School of Medicine, Tokyo 113-8655, Japan
| | - Shigeyuki Muraki
- Department of Prevention Medicine for Locomotive Organ Disorders, 22nd Century Medical and Research Center, Tokyo 113-8655, Japan
| | - Hiroyuki Oka
- Department of Medical Research and Management for Musculoskeletal Pain, 22nd Century Medical and Research Center, The University of Tokyo, Tokyo 113-8655, Japan
| | - Hiroshi Kawaguchi
- Department of Orthopedic Surgery, Tokyo Neurological Center, Tokyo 105-0001, Japan
| | - Toru Akune
- Department of Orthopedic Surgery, National Rehabilitation Center for Persons with Disabilities, Saitama 359-0042, Japan
| | - Takao Maekita
- Department of Gastroenterology, School of Medicine, Wakayama Medical University, Wakayama 641-0012, Japan
| | - Kanae Mure
- Department of Public Health, School of Medicine, Wakayama Medical University, Wakayama 641-0012, Japan
| | - Kozo Nakamura
- Department of Orthopedic Surgery, Towa Hospital, Tokyo 120-0003, Japan
| | - Sakae Tanaka
- Department of Orthopedic Surgery, Sensory and Motor System Medicine, Graduate School of Medicine, Tokyo 113-8655, Japan
| | - Masao Ichinose
- Department of Gastroenterology, School of Medicine, Wakayama Medical University, Wakayama 641-0012, Japan
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Watabe H, Mitsushima T, Derakhshan MH, Yamaji Y, Okamoto M, Kawabe T, Omata M, McColl KEL. Study of association between atrophic gastritis and body mass index: a cross-sectional study in 10,197 Japanese subjects. Dig Dis Sci 2009; 54:988-95. [PMID: 18787953 DOI: 10.1007/s10620-008-0468-7] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/30/2008] [Accepted: 07/16/2008] [Indexed: 12/25/2022]
Abstract
OBJECTIVES The aim of this study was to elucidate the association between body mass index (BMI) and both Helicobacter pylori and atrophic gastritis. METHODS The study involved 10,197 subjects participating in a Japanese mass endoscopic gastric cancer screening program. Atrophic gastritis was assessed by pepsinogen I to II ratio. RESULTS In logistic regression models, BMI had an inverse association with atrophic gastritis, with the odds ratios (OR) decreasing progressively to 0.67 (95% confidence interval [CI] 0.57-0.79, P<0.0001) in the highest BMI quintiles (BMI >or=25.66) group compared with the lowest BMI quintiles (BMI <20.97) group. In linear regression models, atrophic gastritis predicted BMI (regression coefficient -0.326, 95% CI -0.469, -0.184, P<0.0001), whereas H. pylori antibody was not a predictor (regression coefficient 0.072, 95% CI -0.053, 0.198, P=0.3). CONCLUSIONS A small, inverse association between BMI and atrophic gastritis was found in the general population. In contrast, no association was observed between H. pylori seropositivity and BMI.
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Affiliation(s)
- Hirotsugu Watabe
- Medical Sciences, Gardiner Institute, Western Infirmary, University of Glasgow, Glasgow G11 6NT, UK
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Ning PF, Liu HJ, Yuan Y. Dynamic expression of pepsinogen C in gastric cancer, precancerous lesions and Helicobacter pylori associated gastric diseases. World J Gastroenterol 2005; 11:2545-8. [PMID: 15849808 PMCID: PMC4305740 DOI: 10.3748/wjg.v11.i17.2545] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/19/2004] [Revised: 03/20/2004] [Accepted: 04/13/2004] [Indexed: 02/06/2023] Open
Abstract
AIM To investigate the relationship between the expression of pepsinogen C (PGC) and gastric cancer, precancerous diseases, and Helicobacter pylori (H pylori) infection. METHODS The expression of PGC was determined by immunohistochemistry method in 430 cases of gastric mucosa. H pylori infection was determined by HE staining, PCR and ELISA in 318 specimens. RESULTS The positive rate of PGC expression in 54 cases of normal gastric mucosa was 100%. The positive rates of PGC expression in superficial gastritis or gastric ulcer or erosion, atrophic gastritis or gastric dysplasia and gastric cancer decreased significantly in sequence (P<0.05; 100%/89.2% vs 14.3%/15.2% vs 2.4%). The over-expression rate of PGC in group of superficial gastritis with H pylori infection was higher than that in group without H pylori infection (P<0.05; chi2= 0.032 28/33 vs 15/25). The positive rate of PGC expression in group of atrophic gastritis with H pylori infection was lower than that in group without H pylori infection (P<0.01; chi2= 0.003 4/61 vs 9/30), and in dysplasia and gastric cancer. CONCLUSION The level of PGC expression has a close relationship with the degree of malignancy of gastric mucosa and development of gastric lesions. There is a relationship between H pylori infection and expression of antigen PGC in gastric mucosa, the positive rate of PGC expression increases in early stage of gastric lesions with H pylori infection such as gastric inflammation and decreases during the late stage such as precancerous diseases and gastric cancer. PGC-negative cases with H pylori-positive gastric lesions should be given special attention.
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Affiliation(s)
- Pei-Fang Ning
- Cancer Institute of the First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China
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Karita M, Teramukai S, Matsumoto S, Shibuta H. Intracellular VacA is a valuable marker to predict whether Helicobacter pylori induces progressive atrophic gastritis that is associated with the development of gastric cancer. Dig Dis Sci 2005; 50:56-64. [PMID: 15712638 DOI: 10.1007/s10620-005-1278-9] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
VacA was histochemically stained in biopsy specimen and was intracellularly and mainly located in fundic gland area. It is recognized gastric atrophy was observed in the H. pylori-positive patients with intracellular VacA compared with others. The aim of study is to understand the relationship between intracellular VacA and the progression of gastric atrophy that is associated with gastric cancer. Biopsy specimens and sera were obtained from 364 people in their 50s and 60s without gastric cancer diagnosed at first endoscopy undergoing diagnostic endoscopy, for H. pylori infection, histology, and the histochemical status of intracellular VacA using anti-VacA Ab during the follow-up period (mean, 7.3 years). Three hundred eleven of 364 enrolled patients were H. pylori positive and 53 patients were H. pylori negative at first endoscopy. VacA was intracellularly stained with vacuolation and cell destruction in the fundic gland in 98 of 311 H. pylori-positive patients and not stained in another 213 H. pylori-positive patients plus 53 H. pylori-negative patients at first endoscopy. Gastric atrophy has significantly progressed in the H. pylori-positive patints with intracellular VacA with gastric ulcers compared with the others and six gastric cancers have developed in this group during the follow-up period (mean, 7.3 years). Intracellular VacA is a valuable marker to predict whether Helicobacter pylori induces progressive atrophic gastritis that is associated with the development of gastric cancer.
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Affiliation(s)
- Mikio Karita
- Internal Medicine, Hofu-Onsen Hospital, 1640, Daidou, Houfu-shi, Yamaguchi-ken, Japan.
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Karita M, Noriyasu A, Teramukai S, Matsumoto S. Atrophic progression induced by H. pylori infection is correlated with a changing pepsinogen I value and associated with the development of gastric cancer. Dig Dis Sci 2004; 49:1615-20. [PMID: 15573915 DOI: 10.1023/b:ddas.0000043374.80528.ee] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
It is well known that H. pylori infection induces gastric mucosal atrophy, and patients with gastric cancer, which is often complicated by H. pylori infection, possess gastric mucosal atrophy including intestinal metaplasia as a background. One hundred forty-seven patients with dyspeptic symptom and without gastric cancer diagnosed at first endoscopy have been prospectively studied to detect early gastric cancer every year by endoscopy for approximately 6 years. The status of H. pylori infection was detected by histology and ELISA, the value of pepsinogen I (PGI) determined by ELISA, and atrophic pattern determined by the histology of multiple specimens. After the follow-up period (mean, 6.1 years), 6 early gastric cancers had developed in the 49 H. pylori-positive patients with transformation of the atrophic pattern, and no cancer had developed in either the 48 H. pylori-positive patients without transformation of the atrophic pattern or the 50 H. pylori-negative patients. There is a significant relationship between the incidence of transformation of the atrophic pattern and that of the development of gastric cancer in the H. pylori-positive patients. PGI per year in the H. pylori-positive group with transformation of the atrophic pattern was significantly decreased compared with that in the other two groups. Gastric cancers have a background of progressive atrophy, and PGI per year can be a good marker to detect gastric cancer at early stages which is developing or has developed on the background of atrophic progression.
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Affiliation(s)
- Mikio Karita
- Internal Medicine, Hofu-Onsen Hospital, 1640 Daidou, Houfu-shi, Yamaguchi, Japan.
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Sun LP, Gong YH, Yuan Y. Serum pepsinogen concentration as an index for Helicobacter pylori eradication. Shijie Huaren Xiaohua Zazhi 2004; 12:1827-1830. [DOI: 10.11569/wcjd.v12.i8.1827] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the utilization of serum pepsinogen (PG) as an index for Helicobacter eradication.
METHODS: Serum PGI and PGⅡ concentrations were detected with immunoradiometric assay (IRMA) in 359 patients with H. pylori infection, who were treated for eradication by routine triple therapy, before and 1, 5 and 18 mos after treatment. Three methods were used to determine the result of eradication: HE staining, Hp-DNA PCR and ELISA analysis.
RESULTS: Compared to serum level before treatment, serum PGI and PGⅡ concentrations decreased significantly in the eradication group (64.52±31.74 vs 48.02±25.69 μg/L, P < 0.01; 11.22±6.12 vs 7.58±5.41 μg/L, P < 0.01), and PGI/II ratio also increased significantly (6.54±3.57 vs 7.96±4.39, P < 0.01). Serum PGI and PGⅡ levels decreased after eradication in different disease groups. 1 and 5 mos after treatment, serum PGI and PGⅡconcentrations in the eradication group were significantly lower than those before treatment (PGI: 66.83±28.04 vs 52.54±27.96 μg/L, P < 0.01; 11.85±4.91 vs 6.55±3.59 μg/L, P < 0.01; PGII: 60.19±29.30 vs 43.94±26.27 μg/L; 10.93±6.12 vs 6.66±5.30 μg/L, P < 0.01), and PGI/Ⅱratio were significantly higher than the latter (5.84±2.38 vs 8.95±4.61, P < 0.01; 6.60±4.21 vs 8.35±4.82, P < 0.01); The marked drop was found with PGI/Ⅱratio 18 mos after treatment (68.12±36.05 vs 50.11±23.50 μg/L, P < 0.01). There were no remarkable changes with serum PG concentrations in uneradication group.
CONCLUSION: Serum pepsinogen levels are suitable for determining the effect of H. pylori eradication. PGI/Ⅱ ratio can be used as a good marker for determination in the early eradication.
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Ning PF, Liu HJ, Yuan Y. Expression of pepsinogen C in Helicobacter pylori-associated gastric lesions. Shijie Huaren Xiaohua Zazhi 2004; 12:1089-1091. [DOI: 10.11569/wcjd.v12.i5.1089] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the expression of pepsinogen C and its relation with H. pylori infection in gastric cancer and precancerous lesions.
METHODS: The method of immunohistochemistry was used to examine the expression of pepsinogen C in 318 cases of stomach mucosa; the H. pylori infection was determined by H-E stain, PCR and ELISA.
RESULTS: The rate of PGC over-expression in group of superficial gastritis of H. pylori infection was higher than that of non-infection (P < 0.05, 28/33 vs 15/25). The positive rate of PGC in group of atrophic gastritis of H. pylori infection was lower than that of non-infection (P < 0.01, 4/61 vs 9/30) and so were in dysplasia and gastric cancer.
CONCLUSION: There is a relationship between the H. pylori infection and the expression of PGC in gastric mucosa. The expression of PGC increases in superficial gastritis and decreases in atrophic gastritis, dysplasia and gastric cancer with H. pylori infection.
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