Increase in the Prevalence of Atrophic Gastritis Among Adults Age 35 to 44 Years Old in Northern Sweden Between 1990 and 2009

doi:10.1016/j.cgh.2015.04.001

Clinical Gastroenterology and Hepatology

Volume 13, Issue 9, September 2015, Pages 1592-1600.e1

https://doi.org/10.1016/j.cgh.2015.04.001 Get rights and content

Background & Aims

Atrophic corpus gastritis (ACG) is believed to be an early precursor of gastric adenocarcinoma. We aimed to investigate trends of ACG in Northern Sweden, from 1990 through 2009, and to identify possible risk factors.

Methods

We randomly selected serum samples collected from 5284 participants in 1990, 1994, 1999, 2004, and 2009, as part of the population-based, cross-sectional Northern Sweden Multinational Monitoring of Trends and Determinants in Cardiovascular Disease study (ages, 35–64 y). Information was collected on sociodemographic, anthropometric, lifestyle, and medical factors using questionnaires. Serum samples were analyzed for levels of pepsinogen I to identify participants with functional ACG; data from participants with ACG were compared with those from frequency-matched individuals without ACG (controls). Blood samples were analyzed for antibodies against Helicobacter pylori and Cag pathogenicity island protein A. Associations were estimated with unconditional logistic regression models.

Results

Overall, 305 subjects tested positive for functional ACG, based on their level of pepsinogen I. The prevalence of ACG in participants age 55 to 64 years old decreased from 124 per 1000 to 49 per 1000 individuals between 1990 and 2009. However, the prevalence of ACG increased from 22 per 1000 to 64 per 1000 individuals among participants age 35 to 44 years old during this time period. Cag pathogenicity island protein A seropositivity was associated with risk for ACG (odds ratio, 2.29; 95% confidence interval, 1.69–3.12). Other risk factors included diabetes, low level of education, and high body mass index. The association between body mass index and ACG was confined to individuals age 35 to 44 years old; in this group, overweight and obesity were associated with a 2.8-fold and a 4.7-fold increased risk of ACG, respectively.

Conclusions

Among residents of Northern Sweden, the prevalence of ACG increased from 1990 through 2009, specifically among adults age 35 to 44 years old. The stabilizing seroprevalence of H pylori and the increasing prevalence of overweight and obesity might contribute to this unexpected trend. Studies are needed to determine whether these changes have affected the incidence of gastric cancer.

Section snippets

Study Population

Age-stratified random samples of all residents aged 35 to 64 years in Norrbotten and Västerbotten, 2 counties located in Northern Sweden, were drawn in 1990, 1994, 1999, 2004, and 2009 as part of the Multinational MONitoring of Trends and Determinants in CArdiovascular Disease (MONICA) study. Details about this project have been described elsewhere.⁸ Each survey year, random samples (n = 250) were drawn from each sex/10-year age stratum, taking advantage of the complete and continuously updated

Pilot Study of Consistency of Results From the Two Pepsinogen Test Kits

In the pilot study, 894 sera from 900 randomly selected participants in the first 3 survey rounds, already analyzed with the old PG-I kit, were retested using the new kit (there was no more sera available from 6 participants). A strong correlation between paired measures of PG-I concentrations was noted (Pearson correlation coefficient, 0.85; intraclass correlation coefficient, 0.77), and plots of Bland–Altman analysis (Supplementary Figure 1) showed that the new kit could be of practical use,

Discussion

This analysis, based on population-based, quinquennial, cross-sectional surveys during 1990 to 2009 in 2 Northern counties in Sweden,¹⁴ showed a surprising monotonic and statistically significant upward trend in the prevalence of PG-I–defined functional ACG in the youngest investigated age bracket, age 35 to 44 years. In the oldest investigated age band, there was a clear and expected decrease. Because ACG in the long term is correlated tightly with the occurrence of gastric cancer, this change

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Systemic immune-inflammation index and prognostic nutritional index are independent risk factors for the prognosis of patients with gastric cancer. The decrease in systemic immune-inflammation index and the increase in prognostic nutritional index suggest a better prognosis, and the combination of systemic immune-inflammation index and prognostic nutritional index can improve the prediction efficiency.
AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review
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The estimated prevalence of AG is up to 15% in US populations, and may be greater in specific populations with a higher baseline prevalence of H pylori or incidence of gastric adenocarcinoma, such as non-White racial/ethnic minority groups and early-generation immigrants from high-risk countries.6–12
The purpose of this Clinical Practice Update Expert Review is to provide clinicians with guidance on the diagnosis and management of atrophic gastritis, a common preneoplastic condition of the stomach, with a primary focus on atrophic gastritis due to chronic Helicobacter pylori infection—the most common etiology—or due to autoimmunity. To date, clinical guidance for best practices related to the diagnosis and management of atrophic gastritis remains very limited in the United States, which leads to poor recognition of this preneoplastic condition and suboptimal risk stratification. In addition, there is heterogeneity in the definitions of atrophic gastritis, autoimmune gastritis, pernicious anemia, and gastric neoplasia in the literature, which has led to confusion in clinical practice and research. Accordingly, the primary objective of this Clinical Practice Update is to provide clinicians with a framework for the diagnosis and management of atrophic gastritis. By focusing on atrophic gastritis, this Clinical Practice Update is intended to complement the 2020 American Gastroenterological Association Institute guidelines on the management of gastric intestinal metaplasia. These recent guidelines did not specifically discuss the diagnosis and management of atrophic gastritis. Providers should recognize, however, that a diagnosis of intestinal metaplasia on gastric histopathology implies the diagnosis of atrophic gastritis because intestinal metaplasia occurs in underlying atrophic mucosa, although this is often not distinctly noted on histopathologic reports. Nevertheless, atrophic gastritis represents an important stage with distinct histopathologic alterations in the multistep cascade of gastric cancer pathogenesis.
The Best Practice Advice statements presented herein were developed from a combination of available evidence from published literature and consensus-based expert opinion. No formal rating of the strength or quality of the evidence was carried out. These statements are meant to provide practical advice to clinicians practicing in the United States.
Best Practice Advice Statements
Atrophic gastritis is defined as the loss of gastric glands, with or without metaplasia, in the setting of chronic inflammation mainly due to Helicobacter pylori infection or autoimmunity. Regardless of the etiology, the diagnosis of atrophic gastritis should be confirmed by histopathology.
Providers should be aware that the presence of intestinal metaplasia on gastric histology almost invariably implies the diagnosis of atrophic gastritis. There should be a coordinated effort between gastroenterologists and pathologists to improve the consistency of documenting the extent and severity of atrophic gastritis, particularly if marked atrophy is present.
Providers should recognize typical endoscopic features of atrophic gastritis, which include pale appearance of gastric mucosa, increased visibility of vasculature due to thinning of the gastric mucosa, and loss of gastric folds, and, if with concomitant intestinal metaplasia, light blue crests and white opaque fields. Because these mucosal changes are often subtle, techniques to optimize evaluation of the gastric mucosa should be performed.
When endoscopic features of atrophic gastritis are present, providers should assess the extent endoscopically. Providers should obtain biopsies from the suspected atrophic/metaplastic areas for histopathological confirmation and risk stratification; at a minimum, biopsies from the body and antrum/incisura should be obtained and placed in separately labeled jars. Targeted biopsies should additionally be obtained from any other mucosal abnormalities.
In patients with histology compatible with autoimmune gastritis, providers should consider checking antiparietal cell antibodies and anti-intrinsic factor antibodies to assist with the diagnosis. Providers should also evaluate for anemia due to vitamin B-12 and iron deficiencies.
All individuals with atrophic gastritis should be assessed for H pylori infection. If positive, treatment of H pylori should be administered and successful eradication should be confirmed using nonserological testing modalities.
The optimal endoscopic surveillance interval for patients with atrophic gastritis is not well-defined and should be decided based on individual risk assessment and shared decision making. A surveillance endoscopy every 3 years should be considered in individuals with advanced atrophic gastritis, defined based on anatomic extent and histologic grade.
The optimal surveillance interval for individuals with autoimmune gastritis is unclear. Interval endoscopic surveillance should be considered based on individualized assessment and shared decision making.
Providers should recognize pernicious anemia as a late-stage manifestation of autoimmune gastritis that is characterized by vitamin B-12 deficiency and macrocytic anemia. Patients with a new diagnosis of pernicious anemia who have not had a recent endoscopy should undergo endoscopy with topographical biopsies to confirm corpus-predominant atrophic gastritis for risk stratification and to rule out prevalent gastric neoplasia, including neuroendocrine tumors.
Individuals with autoimmune gastritis should be screened for type 1 gastric neuroendocrine tumors with upper endoscopy. Small neuroendocrine tumors should be removed endoscopically, followed by surveillance endoscopy every 1–2 years, depending on the burden of neuroendocrine tumors.
Providers should evaluate for iron and vitamin B-12 deficiencies in patients with atrophic gastritis irrespective of etiology, especially if corpus-predominant. Likewise, in patients with unexplained iron or vitamin B-12 deficiency, atrophic gastritis should be considered in the differential diagnosis and appropriate diagnostic evaluation pursued.
In patients with autoimmune gastritis, providers should recognize that concomitant autoimmune disorders, particularly autoimmune thyroid disease, are common. Screening for autoimmune thyroid disease should be performed.
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Chronic atrophic gastritis: Natural history, diagnosis and therapeutic management. A position paper by the Italian Society of Hospital Gastroenterologists and Digestive Endoscopists [AIGO], the Italian Society of Digestive Endoscopy [SIED], the Italian Society of Gastroenterology [SIGE], and the Italian Society of Internal Medicine [SIMI]
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When comparing individuals under and over 40 years of age, a two times higher prevalence in CAG [biopsy- or serology-based] for the older group was shown [36]. In contrast, a Swedish cross-sectional study [37] based on serological diagnosis of CAG reported an unexpected age-trend with an increase in the prevalence of CAG among adults aged 35–44 years from 22 to 64/1000 between 1990 and 2009, but a decreased prevalence of CAG in participants aged 55–64 years from 124 to 49/1000 in the same observation period. With regard to the incidence of CAG, a systematic review [31] based on studies published between 1988 and 2008 showed a wide range (0%–10.9%) of incidence rates per year, probably explained by the different clinical settings in which the diagnoses were made.
Chronic atrophic gastritis (CAG) is an underdiagnosed condition characterised by translational features going beyond the strict field of gastroenterology as it may manifest itself by a variable spectrum of gastric and extra-gastric symptoms and signs. It is relatively common among older adults in different parts of the world, but large variations exist. Helicobacter pylori-related CAG [multifocal] and autoimmune CAG (corpus-restricted) are apparently two different diseases, but they display overlapping features. Patients with cobalamin and/or iron deficiency anaemia or autoimmune disorders, including autoimmune thyroiditis and type 1 diabetes mellitus, should be offered screening for CAG. Pepsinogens, gastrin-17, and anti-H. pylori antibodies serum assays seem to be reliable non-invasive screening tools for the presence of CAG, helpful to identify individuals to refer to gastroscopy with five standard gastric biopsies in order to obtain histological confirmation of diagnosis. Patients with CAG are at increased risk of developing gastric cancer, and they should be estimated with histological staging systems (OLGA or OLGIM). H. pylori eradication may be beneficial by modifying the natural history of atrophy, but not that of intestinal metaplasia. Patients with advanced stages of CAG (Stage III/IV OLGA or OLGIM) should undergo endoscopic surveillance every three years, those with autoimmune CAG every three-five years. In patients with CAG, a screening for autoimmune thyroid disease and micronutrient deficiencies, including iron and vitamin B₁₂, should be performed. The optimal treatment for dyspeptic symptoms in patients with CAG remains to be defined. Proton pump inhibitors are not indicated in hypochlorhydric CAG patients.
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: Conflicts of interest The authors disclose no conflicts.

: Funding Supported by grants from the Swedish Cancer Society (3913-B97-01XAB and 2013-798) and the Swedish Research Council (2011-3182), and supported in part by a scholarship from the China Scholarship Council (H.S.). The Northern Sweden Multinational MONitoring of Trends and Determinants in CArdiovascular Disease study was supported by grants from the Norrbotten and Västerbotten County Councils.

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Original articleAlimentary tractIncrease in the Prevalence of Atrophic Gastritis Among Adults Age 35 to 44 Years Old in Northern Sweden Between 1990 and 2009

Background & Aims

Methods

Results

Conclusions

Section snippets

Study Population

Pilot Study of Consistency of Results From the Two Pepsinogen Test Kits

Discussion

Gastroenterology

Am J Gastroenterol

Clin Biochem

Cancer Incidence in Sweden 2011

Age-specific trends in incidence of noncardia gastric cancer in US adults

JAMA

Fall in the prevalence of chronic gastritis over 15 years: analysis of outpatient series in Finland from 1977, 1985, and 1992

Gut

Epidemiological trends of pre-malignant gastric lesions: a long-term nationwide study in the Netherlands

Gut

Rationale in diagnosis and screening of atrophic gastritis with stomach-specific plasma biomarkers

Scand J Gastroenterol

Incidence of chronic atrophic gastritis: systematic review and meta-analysis of follow-up studies

Eur J Epidemiol

The events registration and survey procedures in the Northern Sweden MONICA Project

Scand J Public Health Suppl

Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy

Gut

Serum biomarkers provide an accurate method for diagnosis of atrophic gastritis in a general population: the Kalixanda study

Scand J Gastroenterol

Original article
Alimentary tract
Increase in the Prevalence of Atrophic Gastritis Among Adults Age 35 to 44 Years Old in Northern Sweden Between 1990 and 2009