Autoimmune atrophic gastritis (AAG) is an immune-mediated disorder characterized by the loss of oxyntic glands and mucosal atrophy1.Specific autoantibodies directed to gastric parietal cells (PCA) and/or to intrinsic factors are inconstantly present1.Despite its morbidity, data on the epidemiology are scant. Its global prevalence has been estimated to be 0.5-4.5%.Hypo-achlorhydria and lack of intrinsic factor lead to malabsorption of many nutrients, as vit. B12, iron and calcium.A damage on elevated turnover cells may develop, affecting hemopoiesis, nervous system, gut, and myocardium, depicting a systemic disease.Moreover, one of the primary function of gastric acidity as a bactericidal defensive barrier is impaired resulting in both gastric and intestinal microbiota modification. It was recently shown that conditions causing hypo-achlorhydria modify the composition of microbiota from stomach to colon. In particular, at colonic level a decrease in the abundance of commensal bacteria associated to a reduction in microbial diversity and an increase of oral bacteria in the stool were shown.The clinical spectrum is unspecific, especially in early stages, leading to substantial diagnostic delay.Patients may be asymptomatic or complain of gastrointestinal manifestations such as atrophic glossitis, malabsorption, diarrhea, and dyspepsia.These symptoms are insufficient for the diagnosis.Neurological and psychiatric symptoms are often overlooked; myocardial infarction due to demand imbalance may occur.Most of AAG manifestations and complications are due to cyanocobalamin deficiency that may be clinically silent for years.Vit. B12 deficiency has also been associated with infertility, very early recurrent miscarriage, failure of assisted reproductive technologies, and neural tube defects.Furthermore, AAG is a preneoplastic condition as may predispose to the development of type I carcinoids and gastric adenocarcinoma.A previous publication of our group on the NH of AAG,showed that all patients evolved into a higher degree of gastric atrophy and/or metaplasia; additionally,6.3%of these patients developed a neoplastic complication (median time of 3 yo).These data underlined the need to feel the gap of knowledge in the identification and characterization of the factors promoting neoplastic development or associated with carcinogenesis.Moreover, strategies for prevention and management of non-neoplastic complications and extra-gastrointestinal manifestation have to be better determined Hence, a larger, prospective study looking at this issue is warranted.
Age range
18 Years
Sex
ALL
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Generated to help you prepare — always confirm anything about your own eligibility and care with the study team and your doctor.
The trial coordinator is the person who runs the study day to day. These cover the practical side — logistics, costs, and what taking part would actually mean for your life. The study team confirms whether you meet the criteria; these are questions to ask, not a sign you qualify.
A starting point for the conversation — always confirm anything about your own eligibility, costs, and care with the study team and your doctor.
Clarify the natural history and the epidemiology of AAG in order to early diagnose patients, and to prevent irreversible complications
Timeframe: Baseline visit: all patients will be evaluated and all laboratory test required for protocol will be performed. 6 months, patients will be evaluated, for symptoms associated to AAG with VAS scale. 12 months a last evaluation will be performed.