World J Gastroenterol 2023 June 21; 29(23): 3733-3747, DOI: 10.3748/wjg.v29.i23.3733
[ARTICLE HIGHLIGHTS]
Research background
Gastrointestinal symptoms such as dyspepsia and early satiety are very common in autoimmune gastritis (AIG), being second in terms of frequency only to anemia, which is the most typical feature of AIG. Understanding the pathophysiology of each condition can also guide the choice of appropriate treatments, including lifestyle modifications, dietary changes, and medication management.
Research motivation
The management of dyspepsia in patients with AIG, a chronic, immune-mediated disease, remains a challenge, as it can overlap with functional dyspepsia and gastroesophageal reflux disease. Currently, there are no specific therapies. A tailored treatment approach based on a better understanding of putative pathogenic mechanisms underlying symptoms is needed.
Research objectives
In this review, we will discuss the putative pathogenic mechanisms underlying symptom generation in AIG, their clinical implications, and the current management strategies for this complex and multifaceted disease.
Research methods
An extensive bibliographical search was performed in PubMed to identify guidelines and primary literature (retrospective and prospective studies, systematic reviews, case series) published in the last 10 years, using both medical subject heading terms and free-language keywords: Dyspepsia; dyspeptic symptoms; gastro-intestinal symptoms; chronic autoimmune atrophic gastritis; diagnosis; treatment.
Research results
A total of 125 records were reviewed and 80 were defined as fulfilling the criteria. Research conclusions AIG can cause a range of clinical manifestations, including dyspepsia. The pathophysiology of dyspepsia in AIG is complex and involves changes in acid secretion, gastric motility, hormone signaling, and gut microbiota, among other factors. Managing dyspeptic symptoms of AIG is challenging and currently, there are no specific therapies. A tailored treatment approach based on a better understanding of putative pathogenic mechanisms underlying symptoms is needed. While proton pump inhibitors are commonly used to treat dyspepsia and GERD, they may not be appropriate for AIG. Prokinetic agents, antidepressant drugs, and non-pharmacological treatments may be of help, even if not adequately evidence-based supported. A multidisciplinary approach for the management of dyspepsia in AIG is recommended, and further research is needed to develop and validate more effective therapies for dyspepsia.
Research perspectives
As a future perspective, targeting dyspepsia in AIG based on changes in the microbiota and advanced endoscopic techniques to treat severe dyspeptic symptoms might be an area of ongoing research.
Figure 1. Flow chart showing the process of study selection.

* More than half of the patients affected by AIG (56.7%, 215 out of 397) reported GI symptoms with a prevalence of upper GI symptoms (69.8%) including dyspepsia (71.2%), described as postprandial fullness, early satiety and/or epigastric pain, GERD related symptoms (7.2%) such as heartburn and/or regurgitation, overlap dyspepsia-GERD symptoms (17.2%) and nausea and vomiting (3.8%). 15.8% of the patients enrolled in this study also reported lower irritable bowel syndrome (IBS) -like GI symptoms with overlapping of upper and lower GI symptoms in 14.4% of the patients (Figure 2).
Figure 2. More common gastrointestinal symptoms seen in patients with autoimmune gastritis. GERD: Gastroesophageal reflux disease; GI: Gastrointestinal.

Table 1. Reported upper gastrointestinal symptoms and the underlying pathophysiological mechanisms in patients with autoimmune atrophic gastritis

Figure 3. Possible diagnostic algorithm for dyspepsia or gastroesophageal reflux disease-like symptoms in autoimmune atrophic gastritis. A: Dyspeptic symptoms; B: Gastroesophageal reflux disease symptoms. AIG: Autoimmune gastritis; EGDs: Esophagogastroduodenoscopy; GERD: Gastroesophageal reflux disease; GI: Gastrointestinal; H. pylori: Helicobacter pylori; PPIs: Proton pump inhibitors.

Figure 4. Therapeutic approaches for dyspeptic or with gastroesophageal reflux disease-like symptoms in patients with autoimmune gastritis. AIG: Autoimmune gastritis; G POEM: Gastric per-oral endoscopic myotomy; GERD: Gastroesophageal reflux disease.

<Abstract>
BACKGROUND
Autoimmune gastritis (AIG) is a progressive, chronic, immune-mediated inflammatory disease characterized by the destruction of gastric parietal cells leading to hypo/anacidity and loss of intrinsic factor. Gastrointestinal symptoms such as dyspepsia and early satiety are very common, being second in terms of frequency only to anemia, which is the most typical feature of AIG.
AIM
To address both well-established and more innovative information and knowledge about this challenging disorder.
METHODS
An extensive bibliographical search was performed in PubMed to identify guidelines and primary literature (retrospective and prospective studies, systematic reviews, case series) published in the last 10 years.
RESULTS
A total of 125 records were reviewed and 80 were defined as fulfilling the criteria.
CONCLUSION
AIG can cause a range of clinical manifestations, including dyspepsia. The pathophysiology of dyspepsia in AIG is complex and involves changes in acid secretion, gastric motility, hormone signaling, and gut microbiota, among other factors. Managing dyspeptic symptoms of AIG is challenging and there are no specific therapies targeting dyspepsia in AIG. While proton pump inhibitors are commonly used to treat dyspepsia and gastroesophageal reflux disease, they may not be appropriate for AIG. Prokinetic agents, antidepressant drugs, and non-pharmacological treatments may be of help, even if not adequately evidence-based supported. A multidisciplinary approach for the management of dyspepsia in AIG is recommended, and further research is needed to develop and validate more effective therapies for dyspepsia.
Key Words: Dyspepsia; Dyspeptic symptoms; Gastro-intestinal symptoms; Autoimmune gastritis; Chronic autoimmune atrophic gastritis; Treatment

World J Gastroenterol 2023 June 21; 29(23): 3733-3747, DOI: 10.3748/wjg.v29.i23.3733
[ARTICLE HIGHLIGHTS]
Research background
Gastrointestinal symptoms such as dyspepsia and early satiety are very common in autoimmune gastritis (AIG), being second in terms of frequency only to anemia, which is the most typical feature of AIG. Understanding the pathophysiology of each condition can also guide the choice of appropriate treatments, including lifestyle modifications, dietary changes, and medication management.
Research motivation
The management of dyspepsia in patients with AIG, a chronic, immune-mediated disease, remains a challenge, as it can overlap with functional dyspepsia and gastroesophageal reflux disease. Currently, there are no specific therapies. A tailored treatment approach based on a better understanding of putative pathogenic mechanisms underlying symptoms is needed.
Research objectives
In this review, we will discuss the putative pathogenic mechanisms underlying symptom generation in AIG, their clinical implications, and the current management strategies for this complex and multifaceted disease.
Research methods
An extensive bibliographical search was performed in PubMed to identify guidelines and primary literature (retrospective and prospective studies, systematic reviews, case series) published in the last 10 years, using both medical subject heading terms and free-language keywords: Dyspepsia; dyspeptic symptoms; gastro-intestinal symptoms; chronic autoimmune atrophic gastritis; diagnosis; treatment.
Research results
A total of 125 records were reviewed and 80 were defined as fulfilling the criteria. Research conclusions AIG can cause a range of clinical manifestations, including dyspepsia. The pathophysiology of dyspepsia in AIG is complex and involves changes in acid secretion, gastric motility, hormone signaling, and gut microbiota, among other factors. Managing dyspeptic symptoms of AIG is challenging and currently, there are no specific therapies. A tailored treatment approach based on a better understanding of putative pathogenic mechanisms underlying symptoms is needed. While proton pump inhibitors are commonly used to treat dyspepsia and GERD, they may not be appropriate for AIG. Prokinetic agents, antidepressant drugs, and non-pharmacological treatments may be of help, even if not adequately evidence-based supported. A multidisciplinary approach for the management of dyspepsia in AIG is recommended, and further research is needed to develop and validate more effective therapies for dyspepsia.
Research perspectives
As a future perspective, targeting dyspepsia in AIG based on changes in the microbiota and advanced endoscopic techniques to treat severe dyspeptic symptoms might be an area of ongoing research.
Figure 1. Flow chart showing the process of study selection.
* More than half of the patients affected by AIG (56.7%, 215 out of 397) reported GI symptoms with a prevalence of upper GI symptoms (69.8%) including dyspepsia (71.2%), described as postprandial fullness, early satiety and/or epigastric pain, GERD related symptoms (7.2%) such as heartburn and/or regurgitation, overlap dyspepsia-GERD symptoms (17.2%) and nausea and vomiting (3.8%). 15.8% of the patients enrolled in this study also reported lower irritable bowel syndrome (IBS) -like GI symptoms with overlapping of upper and lower GI symptoms in 14.4% of the patients (Figure 2).
Figure 2. More common gastrointestinal symptoms seen in patients with autoimmune gastritis. GERD: Gastroesophageal reflux disease; GI: Gastrointestinal.
Table 1. Reported upper gastrointestinal symptoms and the underlying pathophysiological mechanisms in patients with autoimmune atrophic gastritis
Figure 3. Possible diagnostic algorithm for dyspepsia or gastroesophageal reflux disease-like symptoms in autoimmune atrophic gastritis. A: Dyspeptic symptoms; B: Gastroesophageal reflux disease symptoms. AIG: Autoimmune gastritis; EGDs: Esophagogastroduodenoscopy; GERD: Gastroesophageal reflux disease; GI: Gastrointestinal; H. pylori: Helicobacter pylori; PPIs: Proton pump inhibitors.
Figure 4. Therapeutic approaches for dyspeptic or with gastroesophageal reflux disease-like symptoms in patients with autoimmune gastritis. AIG: Autoimmune gastritis; G POEM: Gastric per-oral endoscopic myotomy; GERD: Gastroesophageal reflux disease.
<Abstract>
BACKGROUND
Autoimmune gastritis (AIG) is a progressive, chronic, immune-mediated inflammatory disease characterized by the destruction of gastric parietal cells leading to hypo/anacidity and loss of intrinsic factor. Gastrointestinal symptoms such as dyspepsia and early satiety are very common, being second in terms of frequency only to anemia, which is the most typical feature of AIG.
AIM
To address both well-established and more innovative information and knowledge about this challenging disorder.
METHODS
An extensive bibliographical search was performed in PubMed to identify guidelines and primary literature (retrospective and prospective studies, systematic reviews, case series) published in the last 10 years.
RESULTS
A total of 125 records were reviewed and 80 were defined as fulfilling the criteria.
CONCLUSION
AIG can cause a range of clinical manifestations, including dyspepsia. The pathophysiology of dyspepsia in AIG is complex and involves changes in acid secretion, gastric motility, hormone signaling, and gut microbiota, among other factors. Managing dyspeptic symptoms of AIG is challenging and there are no specific therapies targeting dyspepsia in AIG. While proton pump inhibitors are commonly used to treat dyspepsia and gastroesophageal reflux disease, they may not be appropriate for AIG. Prokinetic agents, antidepressant drugs, and non-pharmacological treatments may be of help, even if not adequately evidence-based supported. A multidisciplinary approach for the management of dyspepsia in AIG is recommended, and further research is needed to develop and validate more effective therapies for dyspepsia.
Key Words: Dyspepsia; Dyspeptic symptoms; Gastro-intestinal symptoms; Autoimmune gastritis; Chronic autoimmune atrophic gastritis; Treatment