Chronic Gastritis: Background, Pathophysiology, Etiology. The pathophysiology of chronic gastritis complicating a systemic disease, such as hepatic cirrhosis, uremia, or an infection, is described in the articles specifically dealing with these diseases. The pathogenesis of the most common forms of gastritis is described below. H pylori–associated chronic gastritis.
Helicobacter pylori is the leading cause of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and primary gastric lymphoma. First described by Marshall and Warren in 1. H pylori is a spiral gram- negative rod that has the ability to colonize and infect the stomach. The bacteria survive within the mucous layer that covers the gastric surface epithelium and the upper portions of the gastric foveolae. The infection is usually acquired during childhood. Once present in the stomach, the bacteria passes through the mucous layer and becomes established at the luminal surface of the stomach causing an intense inflammatory response in the underlying tissue. The host response to H pylori and bacterial products is composed of T and B lymphocytes, denoting chronic gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes (PMNs) that eventually phagocytize the bacteria.
Peptic ulcer (stomach, duodenum) are sores in the lining of the stomach or duodenum. Peptic ulcer formation is related to H.
An ulcer is a lesion that develops on the skin or mucus membranes of the body. The symptoms are acute for. Learn all about H. This article looks at the treatment and symptoms of H. Lyme disease is transmitted through the bite of infected ticks. Here we cover symptoms through to treatments and answer some frequently asked questions. Stomach cancer symptoms. Some common stomach cancer symptoms may include: Unexplained weight loss: Lack of appetite or unexplained weight loss is a common sign of cancer.
The presence of PMNs in the gastric mucosa is diagnostic of active gastritis. Gastric epithelial cells express class II molecules, which may increase the inflammatory response by presenting H pylori antigens, leading to the activation of numerous transcription factors, including NF- k. B, AP- 1 and CREB- 1.
This in turn leads to further cytokine release and more inflammation. High levels of cytokines, particularly tumor necrosis factor- . When inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid secretion. Continued inflammation results in loss of parietal cells, and the reduction in acid secretion becomes permanent.
![H Pylori Diet Symptoms Of Lyme H Pylori Diet Symptoms Of Lyme](https://upload.wikimedia.org/wikipedia/commons/9/9d/Lyme_Disease_Risk_Map.gif)
Antral inflammation alters the interplay between gastrin and somatostatin secretion, affecting G cells (gastrin- secreting cells) and D cells (somatostatin- secreting cells), respectively. Specifically, gastrin secretion is abnormal in individuals who are infected with H pylori, with an exaggerated meal- stimulated release of gastrin being the most prominent abnormality. Paralleling the slow resolution of the monocytic infiltrates, meal- stimulated gastrin secretion returns to normal.
Chest pain Chest pain may occur if the lymphoma affects the thymus Unexplained weight loss Sudden and unexpected weight loss of 10% or more of total body weight could. This is a personal account of how I cured myself of H. Pylori with natural remedies and treated gastritis with some meds prescribed by my doctor.
Biofilm Busting Protocol for H. Go Way Beyond Digestive Issues. Symptoms of H Pylori Bacteria are often tricky to detect. The “classic” symptoms are gastrointestinal symptoms such as abdominal.
People infected with H pylori strains that secrete the vacuolating toxin A (vac. A) are more likely to develop peptic ulcers than people infected with strains that do not secrete this toxin. The PAI contains the sequence for several genes and encodes the CAGA gene.
Strains that produce Cag. A protein (Cag. A+) are associated with a greater risk of development of gastric carcinoma and peptic ulcers. However, infection with Cag. A- strains also predisposes the person to these diseases. The overwhelming majority of those infected do not develop significant clinical complications and remain carriers with asymptomatic chronic gastritis. Some individuals who carry additional risk factors may develop peptic ulcers, gastric mucosa–associated lymphoid tissue (MALT) lymphomas, or gastric adenocarcinomas. An increased duodenal acid load may precipitate and wash out bile salts, which normally inhibit the growth of H pylori.
![H Pylori Diet Symptoms Of Lyme H Pylori Diet Symptoms Of Lyme](https://s-media-cache-ak0.pinimg.com/originals/a6/61/15/a66115c86e65570f0fba92afde580a93.jpg)
Progressive damage to the duodenum promotes gastric foveolar metaplasia, resulting in sites for H pylori growth and more inflammation. This cycle renders the duodenal bulb increasingly unable to neutralize acid entering from the stomach until changes in the bulb structure and function are sufficient for an ulcer to develop. H pylori can survive in areas of gastric metaplasia in the duodenum, contributing to the development of peptic ulcers. The stomach usually lacks organized lymphoid tissue, but after infection with H pylori, lymphoid tissue is universally present.
Acquisition of gastric lymphoid tissue is thought to be due to persistent antigen stimulation from byproducts of chronic infection with H pylori. MALT lymphomas are monoclonal proliferations of neoplastic B cells that have the ability to infiltrate gastric glands. Gastric MALT lymphomas typically are low- grade T- cell–dependent B- cell lymphomas, and the antigenic stimulus of gastric MALT lymphomas is thought to be H pylori.
Another complication of H pylori gastritis is the development of gastric carcinomas, especially in individuals who develop extensive atrophy and intestinal metaplasia of the gastric mucosa. It is well accepted that a multistep process initiated by H pylori related chronic inflammation of the gastric mucosa progresses to chronic atrophic gastritis, intestinal metaplasia, dysplasia, and finally leading to the development adenocarcinoma. Although the relationship between H pylori and gastritis is constant, only a small proportion of individuals infected with H pylori develop gastric cancer. The incidence of gastric cancer usually parallels the incidence of H pylori infection in countries with a high incidence of gastric cancer and is consistent with H pylori being the cause of the precursor lesion, chronic atrophic gastritis. Studies have provided evidence of the accumulation of mutations in the gastric epithelium secondary to oxidative DNA damage associated with chronic inflammatory byproducts and secondary to deficiency of DNA repair induced by chronic bacterial infection. Although the role of H pylori in peptic ulcer disease is well established, the role of the infection in non- ulcer or functional dyspepsia remains highly controversial. A recent meta- analysis demonstrates that H pylori eradication therapy is associated with improvement of dyspeptic symptoms in patients with functional dyspepsia in Asian, European, and American populations.
Therefore, H pylori eradication strategies in patients with nonulcer dyspepsia must be considered on a patient- by- patient basis. Infectious granulomatous gastritis. Granulomatous gastritis (see the image below) is a rare entity. Tuberculosis may affect the stomach and cause caseating granulomas.
Fungi, including cryptococcus, can also cause caseating granulomas and necrosis, a finding that is usually observed in patients who are immunosuppressed. Granulomatous gastritis has also been associated with H pylori infection. Histologically, a patchy, mild inflammatory infiltrate is observed in the lamina propria. Typical intranuclear eosinophilic inclusions and, occasionally, smaller intracytoplasmic inclusions are present in the gastric epithelial cells and in the endothelial or mesenchymal cells in the lamina propria. Severe necrosis may result in ulceration. Other infectious causes of chronic gastritis in immunosuppressed patients, include the Herpes simplex virus (HSV), which causes basophilic intranuclear inclusions in epithelial cells.
Mycobacterial infections involving Mycobacterium avium- intracellulare are characterized by diffuse infiltration of the lamina propria by histiocytes, which rarely form granulomas. Autoimmune atrophic gastritis. Autoimmune atrophic gastritis is associated with serum anti- parietal and anti–intrinsic factor (IF) antibodies. The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia.
In addition to hypochlorhydria, autoimmune gastritis is associated with serum anti- parietal and anti- IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin, eventually leading to pernicious anemia in some patients. Hypochlorhydria induces G- Cell (Gastrin producing) hyperplasia, leading to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin- like (ECL) cells and is hypothesized to be one of the mechanisms leading to the development of gastric carcinoid tumors (ECL tumors).
There are two types of IF antibodies, types I and II. Type 1 antibody prevents the attachment of B1. IF and Type II antibody prevents attachment of the vitamin B1. T- cell lymphocytes infiltrate the gastric mucosa and contribute to the epithelial cell destruction and resulting gastric atrophy. Chronic reactive chemical gastropathy. Chronic reactive chemical gastritis is associated with long- term intake of aspirin or NSAIDs.
It also develops when bile- containing intestinal contents reflux into the stomach. Although bile reflux may occur in the intact stomach, most of the features associated with bile reflux are typically found in patients with partial gastrectomy, in whom the lesions develop near the surgical stoma. The mechanisms through which bile alters the gastric epithelium involve the effects of several bile constituents. Both lysolecithin and bile acids can disrupt the gastric mucous barrier, allowing the back diffusion of positive hydrogen ions and resulting in cellular injury. Pancreatic juice enhances epithelial injury in addition to bile acids.
In contrast to other chronic gastropathies, minimal inflammation of the gastric mucosa typically occurs in chemical gastropathy. Chronic noninfectious granulomatous gastritis. Noninfectious diseases are the usual cause of gastric granulomas; these include Crohn disease, sarcoidosis, and isolated granulomatous gastritis. Crohn disease demonstrates gastric involvement in approximately 3. Granulomas have also been described in association with gastric malignancies, including carcinoma and malignant lymphoma. Sarcoidlike granulomas may be observed in people who use cocaine, and foreign material is occasionally observed in the granuloma.
An underlying cause of chronic granulomatous gastritis cannot be identified in up to 2. These patients are considered to have idiopathic granulomatous gastritis (IGG). Because its histopathology is similar to that of celiac disease, lymphocytic gastritis has been proposed to result from intraluminal antigens. A number of cases may develop secondary to intolerance to gluten and drugs such as ticlopidine.