Atrophic Gastritis Workup

Updated: Dec 20, 2018
  • Author: Nafea Zayouna, MD; Chief Editor: BS Anand, MD  more...
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Workup

Approach Considerations

2018 ASGE guidelines

Guidelines for sedation and anesthesia in gastrointestinal endoscopy were released in January 2018 by the American Society for Gastrointestinal Endoscopy (ASGE). [18]

It is recommended that all patients undergoing endoscopic procedures be evaluated to assess their risk of sedation related to preexisting medical conditions.

The combination of an opioid and benzodiazepine is recommended to be a safe and effective regimen for achieving minimal to moderate sedation for upper endoscopy and colonoscopy in patients without risk factors for sedation-related adverse events.

It is suggested to use an appropriate adjunctive agent (eg, diphenhydramine, promethazine, or droperidol) in combination with conventional sedative drugs in select clinical circumstances.

Providers should undergo specific training in the administration of endoscopic sedation and possess the skills necessary for the diagnosis and management of sedation-related adverse events, including rescue from a level of sedation deeper than that intended.

Recommend the routine monitoring of blood pressure, oxygen saturation, and heart rate in addition to clinical observation for changes in cardiopulmonary status during all endoscopic procedures using sedation. Supplemental oxygen administration should be considered for moderate sedation and should be administered during deep sedation. Supplemental oxygen should be administered if hypoxemia is anticipated or develops.

Suggest that capnography monitoring be considered for patients undergoing endoscopy targeting deep sedation.

Anesthesia provider–administered sedation should be considered for complex endoscopic procedures or patients with multiple medical comorbidities or at risk for airway compromise.

It is suggested that endoscopists use propofol-based sedation (endoscopist-directed or anesthesia-provider administered) when it is expected to improve patient safety, comfort, procedural efficiency, and/or successful procedure completion.

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Laboratory Studies

The diagnosis of atrophic gastritis can only be ascertained histologically. The endoscopic findings are not helpful for diagnosis, but endoscopy is essential to perform multiple gastric biopsy sampling. Obtain at least 2 biopsy samples from the gastric antrum, 2 from the corpus and 1 from the incisura, and submit to pathology in separate vials.

Decreased serum pepsinogen I levels and the ratio of pepsinogen I to pepsinogen II in the serum can be used to assess gastric atrophy. The finding of low pepsinogen I levels (< 20 ng/mL) has a sensitivity of approximately 96.2% and a specificity of 97% for detection of fundus atrophy. The reported best cut-off pepsinogen I value for patients with atrophic gastritis appears to be 40 mcg/L, with a 90% sensitivity, 67% specificity, 69% accuracy, and 92% negative predictive value, whereas the reported best cut-off value for the ratio of pepsinogen I to pepsinogen II appears to be 8, with a 71% sensitivity, specificity, and accuracy each, and an 86% negative predictive value. [19]

The combination of pepsinogen, gastrin-17 and anti- H pylori antibodies serological assays appears to be a reliable tool for the diagnosis of atrophic gastritis. [20] In a systematic review and meta-analysis of data from 20 studies (1995-2016) comprising 4241 subjects, investigators found a 27% prevalence of atrophic gastritis, a 74.7% summary sensitivity, a 95.6% sensitivity, and a 91% negative predictive value. [20]

Other laboratory findings may include the following [8] :

  • Elevated serum gastrin levels
  • Microcytic, hypochromic anemia (which may precede the development of megaloblastic, vitamin B12-associated anemia)
  • Vitamin B12 deficiency (which may elevated homocysteine levels)

Identifying the underlying cause of atrophic gastritis and assessing specific complications can require several laboratory tests.

Diagnosis of H pylori–associated atrophic gastritis is made as follows:

  • Histologic examination of gastric biopsy with H pylori special stains: Histologic identification of H pylori is the standard method to assess if the organism is the underlying cause of atrophic gastritis. Histologic examination also helps evaluate the degree and distribution of atrophy, which helps identify the type of atrophic gastritis. Although histologic identification of H pylori is the standard approach to identify the infection, at late stages of extensive atrophic gastritis, the number of H pylori organisms is decreased markedly because intestinal metaplasia creates an unfavorable environment for H pylori. In these cases, other tests, such as the urea breath test (ie, with nonradioactive isotope 13C or with radioactive isotope 14C), and serologic evidence of infection may provide evidence for H pylori infection.

  • Rapid urease test from gastric biopsy tissue

  • Bacterial culture of gastric biopsy specimens: This usually is performed in the research setting or to assess antibiotic susceptibility in patients in whom first-line eradication therapy fails.

  • Serologic detection of anti-H pylori antibodies

Diagnosis of autoimmune gastritis is made as follows:

  • Antiparietal and anti-IF antibodies in the serum

  • Achlorhydria, both basal and stimulated, and hypergastrinemia

  • Low serum cobalamin (B-12) levels (< 100 pg/mL)

  • Shilling test: Results may be abnormal and can be corrected by IF.

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Procedures

Upper GI endoscopy is essential to establish a diagnosis of atrophic gastritis. Areas of intestinal metaplasia may be recognized with endoscopy; perform sampling of multiple biopsy specimens.

Tissue sampling from both the gastric antrum and corpus is essential to establish the topography of gastritis and to identify atrophy and intestinal metaplasia, which may be patchy.

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Histologic Findings

H pylori–associated atrophic gastritis

H pylori–associated atrophic gastritis can display different levels of severity, as demonstrated in the following images.

Atrophic gastritis. Schematic representation of He Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric antrum, with progressive development of gastric atrophy as a result of the loss of gastric glands and partial replacement of gastric glands by intestinal-type epithelium, or intestinal metaplasia (represented by the blue areas in the diagram) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis. Inflammation mostly limited to the antrum characterizes antral-predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequent pattern in the Western countries.
Patterns of atrophic gastritis associated with chr Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.
Atrophic gastritis. Helicobacter pylori–associated Atrophic gastritis. Helicobacter pylori–associated chronic active gastritis (Genta stain, 20x). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.
Atrophic gastritis. Intestinal metaplasia of the g Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20x). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.

H pylori organisms are found within the gastric mucous layer and frequently accumulate in groups of bacteria at the apical side of gastric surface cells, occasionally in the lower portions of the gastric foveolae, and rarely within the deeper areas of the mucosa in association with glandular cells.

Patients with typical infection initially develop chronic active gastritis, in which H pylori organisms are observed in both the antrum and corpus (usually more numerous in the antrum). PMNs infiltrate the lamina propria, glands, surface, and foveolar epithelium, occasionally spilling into the lumen and forming small microabscesses. Lymphoid aggregates and occasional well-developed lymphoid follicles are observed expanding the lamina propria of the mucosa, and occasional lymphocytes permeate the epithelium.

In disease of longer duration, significant loss of gastric glands is observed, which is known as gastric atrophy. Gastric atrophy may result from the loss of gastric epithelial cells that were not replaced by appropriate cell proliferation or from replacement of the epithelium by intestinal-type epithelium (intestinal metaplasia). In advanced stages of atrophy associated with chronic H pylori infection, both the corpus and antrum display extensive replacement by intestinal metaplasia, which is associated with the development of hypochlorhydria. With the expansion of intestinal metaplasia, the numbers of H pylori detectable in the stomach decrease because H pylori are excluded from areas of metaplastic epithelium. This end stage is known as atrophic gastritis.

Autoimmune atrophic gastritis

The histologic changes vary in different phases of autoimmune atrophic gastritis (see the 2 images below).

Patterns of atrophic gastritis associated with chr Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.
Atrophic gastritis. Intestinal metaplasia of the g Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20x). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.

During the early phase, multifocal diffuse infiltration of the lamina propria by mononuclear cells and eosinophils occurs, as does focal T-cell infiltration of oxyntic glands with glandular destruction. Focal mucous neck cell hyperplasia (ie, pseudopyloric metaplasia) and hypertrophic changes of parietal cells also are observed.

During the florid phase of the disease, increased lymphocytic inflammation, oxyntic gland atrophy, and focal intestinal metaplasia occur. Diffuse involvement of the gastric corpus and fundus by chronic atrophic gastritis associated with intestinal metaplasia characterizes the end stage. Some patients present with gastric polyps, mostly nonneoplastic hyperplastic polyps and polypoid areas of preserved islands of relatively normal oxyntic mucosa that may appear polypoid endoscopically. The antrum is spared.

On routine gastric body biopsies, the histologic features of autoimmune metaplastic atrophic gastritis may be identifiable but subtle. In a subset of patients whose histologic findings consist of metaplasia, full-thickness chronic inflammation, and/or oxyntic destruction, it may be prudent to include a note in the medical record that suggests laboratory testing and/or close clinical followup. [21]

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