Ignite Creation Date:
2024-05-06 @ 8:09 PM
Last Modification Date:
2024-10-26 @ 3:21 PM
Study NCT ID:
NCT06272500
Status:
RECRUITING
Last Update Posted:
2024-05-30
First Post:
2024-02-15
Brief Title:
Exploring Methods for Treating Hypergastrinemia in Patients With Autoimmune Gastritis
Sponsor:
Jianning Yao
Organization:
The First Affiliated Hospital of Zhengzhou University
Study Overview
Official Title:
Exploring Methods for Treating Hypergastrinemia in Patients With Autoimmune Gastritis A Prospective Study
Status:
RECRUITING
Status Verified Date:
2024-08
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Autoimmune atrophic gastritis AAG is an organ-specific autoimmune disease that primarily affects the gastric body and fundus while sparing the antrum Its characteristics include destruction of gastric wall cells loss of intrinsic factors and atrophy of the gastric mucosa Endoscopic examination reveals features of reverse atrophy with significant atrophy in the gastric body and fundus appearing as a mosaic of red and white patches Currently AAG is believed to result from a pathological CD4 T-cell-mediated autoimmune response against the gastric HK-ATPase CD4 T lymphocytes target the parietal cells HK-ATPase stimulating plasma cells to secrete autoantibodies including parietal cell antibodies PCA and intrinsic factor antibodies IFA The former plays a key role in parietal cell destruction and glandular atrophy AAG is considered a premalignant condition with the potential development of gastric dysplasia cancer and type 1 gastric neuroendocrine tumours type 1 g-NET
Gastric neuroendocrine tumors g-NETs also known as gastric carcinoids account for approximately 23 of gastrointestinal and pancreatic neuroendocrine tumors Clinically g-NETs are mainly classified into three types Type III is typically sporadic tumors associated with normal gastrin levels and poor prognosis Although type 1 g-NETs caused by AAG are usually well-differentiated studies have reported that 8-23 of type 1 g-NETs extending into the deep submucosal layer may metastasize to regional lymph nodes or even to the liver Furthermore 3 of patients may develop neuroendocrine carcinoma highlighting the need for appropriate attention
Due to the destruction of gastric glands including parietal and chief cells in AAG patients there is a deficiency in intrinsic factor gastric acid and a decrease in pepsinogen I PG-I levels Insufficient gastric acid secretion leads to a compensatory increase in gastrin secretion by G cells in the gastric antrum which acts on receptors present in enterochromaffin-like cells ECL in the gastric body and fundus promoting ECL cell proliferation Prolonged stimulation by hypergastrinemia can result in the development of ECL cell tumors namely type 1 g-NETs Considering the close association between type 1 g-NETs and AAG primarily related to hypergastrinemia resulting from reduced gastric acid secretion it is hypothesized that supplementation with gastric acid could provide negative feedback regulation of gastrin reducing the risk of type 1 g-NET development in AAG patients This study aims to investigate the impact of Betaine hydrochlorideBHCL on gastrin levels in AAG patients thus exploring a simple and cost-effective method to reduce the risk of type 1 g-NETs in AAG patients
Gastric neuroendocrine tumors g-NETs also known as gastric carcinoids account for approximately 23 of gastrointestinal and pancreatic neuroendocrine tumors Clinically g-NETs are mainly classified into three types Type III is typically sporadic tumors associated with normal gastrin levels and poor prognosis Although type 1 g-NETs caused by AAG are usually well-differentiated studies have reported that 8-23 of type 1 g-NETs extending into the deep submucosal layer may metastasize to regional lymph nodes or even to the liver Furthermore 3 of patients may develop neuroendocrine carcinoma highlighting the need for appropriate attention
Due to the destruction of gastric glands including parietal and chief cells in AAG patients there is a deficiency in intrinsic factor gastric acid and a decrease in pepsinogen I PG-I levels Insufficient gastric acid secretion leads to a compensatory increase in gastrin secretion by G cells in the gastric antrum which acts on receptors present in enterochromaffin-like cells ECL in the gastric body and fundus promoting ECL cell proliferation Prolonged stimulation by hypergastrinemia can result in the development of ECL cell tumors namely type 1 g-NETs Considering the close association between type 1 g-NETs and AAG primarily related to hypergastrinemia resulting from reduced gastric acid secretion it is hypothesized that supplementation with gastric acid could provide negative feedback regulation of gastrin reducing the risk of type 1 g-NET development in AAG patients This study aims to investigate the impact of Betaine hydrochlorideBHCL on gastrin levels in AAG patients thus exploring a simple and cost-effective method to reduce the risk of type 1 g-NETs in AAG patients
Detailed Description:
Autoimmune atrophic gastritis AAG is an organ-specific autoimmune disease that primarily affects the gastric body and fundus while sparing the antrum Its characteristics include destruction of gastric wall cells loss of intrinsic factors and atrophy of the gastric mucosa Endoscopic examination reveals features of reverse atrophy with significant atrophy in the gastric body and fundus appearing as a mosaic of red and white patches predominantly white with flattened and partially disappearing folds and visible blood vessels Currently AAG is believed to result from a pathological CD4 T-cell-mediated autoimmune response against the gastric HK-ATPase CD4 T lymphocytes target the parietal cells HK-ATPase stimulating plasma cells to secrete autoantibodies including parietal cell antibodies PCA and intrinsic factor antibodies IFA The former plays a key role in parietal cell destruction and glandular atrophy while the latter is the main mechanism underlying vitamin B12 deficiency and pernicious anaemia AAG is considered a premalignant condition with the potential development of gastric dysplasia cancer and type 1 gastric neuroendocrine tumours type 1 g-NET
Gastric neuroendocrine tumors g-NETs also known as gastric carcinoids account for approximately 23 of gastrointestinal and pancreatic neuroendocrine tumors Clinically g-NETs are mainly classified into three types Type I and type II are associated with chronic atrophic autoimmune gastritis9 and gastrinoma-related Zollinger-Ellison syndrome ZES leading to hypergastrinemia while type III is typically sporadic tumors associated with normal gastrin levels and poor prognosis Although type 1 g-NETs caused by AAG are usually well-differentiated studies have reported that 8-23 of type 1 g-NETs extending into the deep submucosal layer may metastasize to regional lymph nodes or even to the liver Furthermore 3 of patients may develop neuroendocrine carcinoma highlighting the need for appropriate attention
Due to the destruction of gastric glands including parietal and chief cells in AAG patients there is a deficiency in intrinsic factor gastric acid and a decrease in pepsinogen I PG-I levels Insufficient gastric acid secretion leads to a compensatory increase in gastrin secretion by G cells in the gastric antrum which acts on receptors present in enterochromaffin-like cells ECL in the gastric body and fundus promoting ECL cell proliferation Prolonged stimulation by hypergastrinemia can result in the development of ECL cell tumors namely type 1 g-NETs Considering the close association between type 1 g-NETs and AAG primarily related to hypergastrinemia resulting from reduced gastric acid secretion it is hypothesized that supplementation with gastric acid could provide negative feedback regulation of gastrin reducing the risk of type 1 g-NET development in AAG patients This study aims to investigate the impact of Betaine hydrochlorideBHCL on gastrin levels in AAG patients thus exploring a simple and cost-effective method to reduce the risk of type 1 g-NETs in AAG patients
Gastric neuroendocrine tumors g-NETs also known as gastric carcinoids account for approximately 23 of gastrointestinal and pancreatic neuroendocrine tumors Clinically g-NETs are mainly classified into three types Type I and type II are associated with chronic atrophic autoimmune gastritis9 and gastrinoma-related Zollinger-Ellison syndrome ZES leading to hypergastrinemia while type III is typically sporadic tumors associated with normal gastrin levels and poor prognosis Although type 1 g-NETs caused by AAG are usually well-differentiated studies have reported that 8-23 of type 1 g-NETs extending into the deep submucosal layer may metastasize to regional lymph nodes or even to the liver Furthermore 3 of patients may develop neuroendocrine carcinoma highlighting the need for appropriate attention
Due to the destruction of gastric glands including parietal and chief cells in AAG patients there is a deficiency in intrinsic factor gastric acid and a decrease in pepsinogen I PG-I levels Insufficient gastric acid secretion leads to a compensatory increase in gastrin secretion by G cells in the gastric antrum which acts on receptors present in enterochromaffin-like cells ECL in the gastric body and fundus promoting ECL cell proliferation Prolonged stimulation by hypergastrinemia can result in the development of ECL cell tumors namely type 1 g-NETs Considering the close association between type 1 g-NETs and AAG primarily related to hypergastrinemia resulting from reduced gastric acid secretion it is hypothesized that supplementation with gastric acid could provide negative feedback regulation of gastrin reducing the risk of type 1 g-NET development in AAG patients This study aims to investigate the impact of Betaine hydrochlorideBHCL on gastrin levels in AAG patients thus exploring a simple and cost-effective method to reduce the risk of type 1 g-NETs in AAG patients
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None