– Mild chronic gastritis

– Chronic active gastritis

– Helicobacter organisms identified

– Reactive (chemical) gastropathy

 

Comment for when you suspect Helicobacter, but the stain is negative.

COMMENT: The histologic sections show a chronic active gastritis with a superficial lymphoplasmacytosis, which is suspicious for Helicobacter infection. Although the immunohistochemical stain is negative, if clinical concern persists, additional studies (such as serology or stool antigen testing) could be considered. Clinical correlation is recommended.

 

Pediatric “Focally enhanced gastritis” (focally injured gastric glands surrounded by a cuff of inflammation)

  – Focally enhanced gastritis (see comment)

COMMENT: The histologic sections show a focally enhanced gastritis. Although not entirely specific, in the pediatric setting studies have found this to be associated with inflammatory bowel disease (particularly Crohn’s disease) (see reference below). Clinical and endoscopic correlation is recommended

REFERENCE: McHugh JB, Gopal P, Greenson JK. The clinical significance of focally enhanced gastritis in children. Am J Surg Pathol. 2013 Feb;37(2):295-9.

 

If there is intestinal metaplasia, add:

– Intestinal metaplasia, negative for dysplasia

 

 

Autoimmune gastritis  

 – Chronic gastritis, with findings suggestive of autoimmune gastritis (see comment)

– Intestinal metaplasia, negative for dysplasia 

– Linear and/or micronodular neuroendocrine cell hyperplasia 

COMMENT: Histologic sections of the stomach body biopsies show antral/pyloric-type mucosa with an absence of oxyntic glands.  There is an associated basal lymphoplasmacytic infiltrate and extensive intestinal metaplasia. Together, these findings are suggestive of autoimmune gastritis (sometimes also referred to as autoimmune metaplastic atrophic gastritis). An immunohistochemical stain for Helicobacter organisms is negative. A synaptophysin stain demonstrates linear and/or micronodular neuroendocrine cell hyperplasia. Correlation with clinical and laboratory findings is recommended.

 

Lymphocytic gastritis 

   – Lymphocytic gastritis (see comment)

COMMENT: Histologic sections of the stomach biopsy show a lymphocytic gastritis with numerous intraepithelial lymphocytes. This finding is nonspecific and can be seen in association with a variety of other conditions including celiac disease and Helicobacter infection. The differential diagnosis also includes lymphocytic colitis, Crohn’s disease, CVID, and medication-effect (particularly ticlopidine and Olmesartan). An immunohistochemical stain for Helicobacter organisms is negative. Clinical correlation is recommended.

Collagenous gastritis 

   – Collagenous gastritis (see comment)

COMMENT: The biopsies from the stomach body demonstrate a marked deposition of subepithelial collagen, which is highlighted by a trichrome stain. There is also a chronic gastritis. Together, these findings are consistent with a collagenous gastritis pattern of inflammation. This pattern of inflammation is non-specific and can be seen in a variety of settings including immune-mediated conditions (such as Celiac Disease, Hashimoto’s Thyroiditis, etc…), in association with collagenous colitis/enteritis, with Helicobacter infection, and with certain medications (such as Olmesartan). In this case, an immunohistochemical stain for Helicobacter is negative. Clinical and endoscopic correlation is recommended.

Eosinophilic gastritis 

   – Eosinophil-rich gastritis (with up to *** Eosinophils per single high power field) (see comment)

COMMENT: Histologic sections of the stomach biopsy show an eosinophilic gastritis with up to *** eosinophils per single high-power field. There is also eosinophil degranulation and microabscess formation. This finding is nonspecific and can be seen in association with a variety of other conditions including a food allergy, medication-effect, Helicobacter infection, parasitic infection, Crohn’s disease, and systemic connective tissue diseases. The differential diagnosis also includes eosinophilic gastroenteritis, which is a diagnosis of exclusion. An immunohistochemical stain for Helicobacter organisms is negative. Clinical correlation is recommended.

 

 

Polyps & Tumors 

Non-neoplastic

– Fundic gland polyp

– Hyperplastic polyp

– Gastric xanthoma

   – Gastric polyp with features of a hamartomatous polyp (see comment)

COMMENT: Histologic sections of the stomach polyp show a spectrum of changes including epithelial hyperplasia, a prominent smooth muscle component, and cystically dilated glands.  These findings raise the possibility of a hamartomatous polyp. Unfortunately, there are no reliable histologic features to distinguish stomach hamartomatous polyps from reactive lesions such as hyperplastic polyps or inflammatory polyps. Syndromes involving gastrointestinal hamartomatous polyps (e.g., Peutz-Jeghers syndrome, Cowden syndrome, and Juvenile polyposis syndrome) should be ruled out clinically. Clinical and endoscopic correlation is recommended.

 

Neoplastic

– Low-grade dysplasia

– High-grade dysplasia

Note: Consider mentioning dysplasia type: 1)Intestinal (most common, like a colonic adenoma), 2)Foveolar, 3)Serrated

 Intestinal-type adenoma, with *** grade dysplasia

– Foveolar-type adenoma, with *** grade dysplasia

– Pyloric gland adenoma, with *** grade dysplasia

  – Oxyntic-gland adenoma, with *** grade dysplasia

 

  – Adenocarcinoma, at least intramucosal (see comment)

 

Subtypes/patterns of growth include: 1)Tubular (most common), 2)Papillary, 3)Poorly-cohesive carcinoma, including signet-ring cell carcinoma, 4)Mucinous adenocarcinoma, 6)Gastric adenocarcinoma with lymphoid stroma, 7) Hepatoid carcinoma, 8) Micropapillary adenocarcinoma, and 9) Fundic-gland type gastric adenocarcinoma. Some tumors also show “mixed” morphology.

Grading: Usually just Low or High, based on gland formation (most applicable to tubular and papillary subtypes).

Usual “Tubular” gastric adenocarcinoma

  – Invasive Adenocarcinoma (see comment)

COMMENT: Histologic sections of the stomach mass biopsy demonstrate an invasive adenocarcinoma with a predominantly tubular pattern of growth. There is *** gland formation, consistent with a provisional WHO grade of ***.  No signet ring cells are identified.

 

Poorly-cohesive/signet-ring cell adenocarcinoma

  – Invasive signet-ring cell carcinoma (see comment)

COMMENT: Histologic sections of the stomach mass biopsy demonstrate an invasive adenocarcinoma composed of primarily single, infiltrating signet-ring cells.

 

Adenocarcinoma with lymphoid stroma

  – Invasive adenocarcinoma with lymphoid stroma (see comment)

COMMENT: Histologic sections of the stomach mass biopsy demonstrate an invasive adenocarcinoma with abundant lymphoid stroma. An in situ hybridization for EBV is positive. Together, these findings are diagnostic of a gastric adenocarcinoma with abundant lymphoid stroma, a specific type of gastric cancer can be associated with a better prognosis.

 

 

  – Well-differentiated neuroendocrine tumor (WHO grade ***) (see comment)

COMMENT: Histologic sections of the stomach biopsy show a proliferation of nests of cells with round nuclei and stippled chromatin. These cells show strong, diffuse staining with synaptophysin and chromogranin immunohistochemical stains, consistent with neuroendocrine differentiation. No necrosis or mitotic figures are identified. Overall, these findings are diagnostic of a well-differentiated neuroendocrine tumor.  A Ki67 stain shows a proliferation index of ***% (***/500 cells counted), consistent with a WHO grade of ***.

Note: If it is a biopsy, you may opt to report a “provisional” WHO grade (and defer final classification to the anticipated resection specimen).

 

If WD-NET is associated with autoimmune gastritis (autoimmune metaplastic atrophic gastritis): Type 1

Neuroendocrine tumors arising in the setting of autoimmune gastritis (autoimmune metaplastic atrophic gastritis), Type 1 gastric well-differentiated neuroendocrine tumors, are usually benign with indolent behavior and only very rare metastases. As such, they are often treated conservatively. Clinical and endoscopic correlation is recommended.

 

Last updated: November 1, 2019