The acid-free stomach is ultimately colonized with a microbe flora from the mouth [ 58 ]. The microbes and the acid-free stomach are capable to produce class 1 carcinogens, like acetaldehyde and nitrosoamines [ 39 , 59 ]. Gastric cancer and peptic ulcer diseases excluding NSAID ulcers are the most serious diseases linked with the chronic H. A successful eradication of the H.
In spite of the associations of peptic ulcers and cancer with H. Peptic duodenal ulcers DU occur typically in people with non-atrophic H. Gastric ulcers associate often, on the other hand, with the phenotypes of gastritis in which a marked atrophy and IM occur in antrum and incisura, and in which cases, the corpus mucosa may even be slightly atrophic but is never severely atrophic and stomach is never achlorhydric [ 62 ].
The stomach cancer, the intestinal type in particular, is seen in patients with a hypochlorhydric or achlorhydric stomach and may particularly occur in subjects with advanced stages of atrophy and IM in both antrum and corpus [ 39 , 69 ]. Relative risk of peptic ulcer disease duodenal or gastric ulcer or gastric cancer in various phenotypes of chronic atrophic Helicobacter pylori gastritis.
The risks are extrapolated and estimated from a case-control study done in Finland in the 80s [ 69 ]. Note that the risks of peptic ulcer diseases and gastric cancer are associated with very dissimilar phenotypes of chronic gastritis. Gastric carcinogenesis is heterogeneous and extremely varied at the molecular level [ 53 , 54 ].
Even though the gene errors are plentiful, no specific or comprehensive molecular markers, gene errors or mutations have been found in cancer or in precancer lesions so far. Although the two main histological types of stomach cancer, intestinal and diffuse one, are meaningful entities in clinical and morphological perspectives, and both being bound to a preceding or co-existing H.
In diffuse type, the background morphology is often a non-atrophic H. In intestinal cancer type, on the other hand, the overt tumors or the precancer lesions associate often with a hypochlorhydric stomach, and with a marked atrophic gastritis, and with extensive IM in the underlying mucosa [ 37 , 38 , 70 , 71 ].
Therefore, the carcinogenetic processes in this cancer type may be linked with mechanisms that arise in atrophic gastritis or are triggered on by a hypochlorhydric or acid-free stomach. Atrophic gastritis and acid-free stomach are the most important independent risk conditions for stomach cancer known so far. Statistically, the atrophic gastritis is a higher risk condition for cancer than the pure H. The likelihood of gastric cancer in gastritis rises exponentially with the progression of the H.
The risk may rise even to fold in patients with severe atrophic gastritis in both antrum and corpus severe panatrophy; multifocal atrophic gastritis MAG compared to the cancer risk in subjects with a normal and healthy stomach mucosa Figure 7 [ 69 ].
The cancer risk is remarkably low in people without the H. The risk rises approximately to two-fold in patients with a pure H. Thus, in DU patients, who typically have the non-atrophic H. Paradoxically, the load of the stomach mucosa with helicobacteria is typically high in subjects with a relatively low cancer risk, as the case is in the ordinary DU patients. Paradoxically again, the load tends to diminish when the cancer risk rises, as the case is in the patients with advanced atrophic gastritis [ 69 ].
The cancer risk may be, for example, high in subjects with a severe atrophic gastritis and acid-free stomach in whom there may even be no objective signs of an on-going H. The acceptance that H. This sorting requires examination of the subjects with endoscopy and endoscopy biopsy, or can be done with non-invasive blood tests applying the stomach-specific biomarkers [ 72 , 73 , 74 , 75 , 76 , 77 ].
The Sydney System and its updating are the guidelines for interpretation of the microscopical appearances in biopsy specimens in endoscopy practice [ 5 , 6 ]. A proper biopsy protocol and correct microscopical reading of the biopsies are fundamental requirements for a correct and successful delineation of patients into the clinically meaningful risk groups [ 78 , 79 ]. Such classifications or lineations are not possibly with endoscopy alone, or cannot be done with testing of the H.
This classification delineates the patients into five subgroups 0—IV with markedly dissimilar likelihood to have or get a gastric cancer Figure 8. The classification and sorting may objectively advice which one of the patients would need and benefit most of endoscopic surveillances and follow-ups [ 79 , 80 ].
OLGA staging for risk of stomach cancer. Modified from a paper of Rugge et al [ 79 ]. The staging is a practical tool for the delineation of patients to high stages III—IV and low stages 0—II risk groups for cancer, for gastric cancer of the intestinal type in particular.
The delineation of the subjects into OLGA subcategories can be performed also non-endoscopically and noninvasively by applying simple blood tests, based on assessment of the levels of the stomach-specific biomarkers pepsinogens I and II, gastrin and H. This cannot be done with the H. Purification of stomach pepsinogens in the 70s, understanding of natural course of H. At present, these blood tests can be performed reliably in any laboratory and they do not need special arrangements.
Several detailed and comprehensive reviews, consensus reports and guidelines on practical usage of the biomarker tests in the diagnosis of atrophic gastritis have been published previously in this and other medical journals see references [ 72 , 80 , 84 ].
Several commercial radioimmunoassays and ELISA tests have been available for pepsinogen 1 and 2 for a quite long time. These tests have, however, limitations because they can be used in the diagnosis of atrophic corpus gastritis only [ 74 ]. The serum levels of pepsinogens 1 and 2 do not give any hints of possible atrophic gastritis in gastric antrum where the atrophic and metaplastic alterations appear, however, first.
This test panel enables assessments of atrophy also in the gastric antrum and gives hints of intragastric acidity in addition to the information of possible corpus atrophy, and makes, therefore, the comprehensive OLGA classification possible [ 72 , 73 , 77 , 78 , 80 ]. Antral atrophic gastritis loss of antral glands is accompanied with a loss of antral G cell, which cell loss results in low plasma levels of both fasting and stimulated gastrin after a drink with protein powder, stimulation with bombesin gastrin releasing peptide or stimulation with proton pump inhibitor PPI.
Both options are indications for upper gi-endoscopy because of the cancer risk due to possible antral atrophy and because of the peptic ulcer risk due to hyperchlorhydria high-acid output see Figure 7.
The absence of H. The atrophic gastritis is advanced and extensive in these cases, occupies the whole stomach mucosa OLGA class IV , and the stomach is concomitantly acid free. Even though the H. Due to the microbial origin and infectious background, and by the knowledges of epidemiology and natural course of chronic H.
With these improvements, the risk to acquire H. As the case is with tuberculosis, chronic gastritis may move in the future decades to periphery of the medical practice and significance, in developed countries at least.
Consequently, peptic ulcers will be rare and gastric cancer will become an infrequent malignancy. Declaration of interest : Dr. Pentti Sipponen is a share holder and member of the scientific committee of Biohit Oyj. The company develops and markets laboratory tests mainly for gastrointestinal diseases.
National Center for Biotechnology Information , U. Scandinavian Journal of Gastroenterology. Scand J Gastroenterol. Published online Apr Author information Article notes Copyright and License information Disclaimer.
This article has been cited by other articles in PMC. Abstract Prevalence of chronic gastritis has markedly declined in developed populations during the past decades.
Key Words: gastric cancer, gastritis, Helicobacter pylori , peptic ulcer. Introduction Chronic gastritis is one of the most common life-long, serious and insidious illnesses in human beings. Natural course Chronic gastritis is a multistep, progressive and life-long inflammation [ 3 , 16 , 20 , 21 , 22 , 23 , 24 ]. Open in a separate window. Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Epidemiology and the birth cohort phenomenon The observations from population studies on chronic gastritis may empower some fundamental conclusions concerning the epidemiology of chronic gastritis and its sequelae.
Figure 6. Autoimmune chronic gastritis Although H. Influences on stomach physiology A long-lasting life-long chronic and active inflammation cannot be harmless and will result in destruction of stomach mucosa via several mechanisms which may interact with renewal, growth, integrity, differentiation and function of the gastric epithelium [ 1 , 24 , 39 , 53 , 54 ].
Cancer and peptic ulcer Gastric cancer and peptic ulcer diseases excluding NSAID ulcers are the most serious diseases linked with the chronic H. Figure 7. Cancer risk Atrophic gastritis and acid-free stomach are the most important independent risk conditions for stomach cancer known so far. The Sydney system and operative link on gastritis classifications The acceptance that H. Figure 8. Plasma biomarkers in diagnosis and screening of atrophic gastritis Purification of stomach pepsinogens in the 70s, understanding of natural course of H.
Future trends and the healthy stomach initiative Even though the H. Acknowledgments Declaration of interest : Dr. Lyon, June Chronic gastritis. Klin Wochenschr. The story of gastritis. Scand J Gastroenterol Suppl. Prevalence of undiagnosed advanced atrophic corpus gastritis in Finland: an observational study among 4, volunteers without specific complaints. The Sydney System: histological division. J Gastroenterol Hepatol. Classification and grading of gastritis.
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Cancer Res. Fall in the prevalence of chronic gastritis over 15 years: analysis of outpatient series in Finland from , , and Helicobacter pylori gastritis—epidemiology. J Gastroenterol. Han preservado las identidades de los pacientes. Autoimmune atrophic gastritis, is a chronic disease that affects the body and fundus of the stomach, is more common in women ratio , person over 60 years of age, and Scandinavian descent.
This disease is characterized by a progressive loss of acid-secreting parietal cells that leads to hypo-achlorhydria. Most patients will remain asymptomatic for years, with a late presentation of nonspecific manifestations, mainly hematological, gastroenterological, and neuropsychiatric. Diagnosis generally requires the combination of clinical, serologic, and histopathologic data. The treatment is therapy with vitamin supplements that cover deficiencies and surveillance of precancerous lesions.
Pylori 1,6. Esta atrofia de la mucosa es promovida por citocinas pro inflamatorias, incluidas IL e IL Sin embargo, aun queda por determinar si el H.
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