Stomach
Stomach is an important organ for pathologists. It is often inflamed and may be a site that cancer arises from. Gastroenterologists often biopsy the organ. Surgeon take-out the organ. It connects the esophagus to the duodenum. An introduction to gastrointestinal pathology is in the gastrointestinal pathology article.
Normal stomach
Gross anatomy
- Cardia - first part of the stomach; joins with esophagus.
- Fundus - superior portion - not attached directly to the esophagus.
- Body - contains parietal cells.
- Pylorus - distal (think pyloric stenosis); it joins with the duodenum.
- AKA antrum.
Image: Stomach anatomy (WP).
Microscopic
Foveolar cells versus intestinal goblet cells
- Intestinal goblet cells - clear mucin.
- Foveolar cells - eosinophilic contents.
Stomach vs. intestine
A tabular comparison:[1]
| Intestine | Stomach | |
| Spacing | Goblets cell - spaced | Foveolar cells - beside one another |
| Morphology of epithelial cells | columnar | tall columnar (Champagne flute) |
| Vesicle at luminal surface | touching/small opening | wide open |
| PAS-D | -ve (???) | +ve (???) |
| Villin stain[2] | +ve | -ve |
| Images | Tubular adenoma - goblet cells on right of image (WC) |
Gastric biopsy (microscopy-uk.org.uk) |
Notes:
- Intraepithelial lymphocytes in the gastric mucosa have a clear halo around 'em.[3]
- Memory device: Folveolar cells have friends, i.e. they are close to other foveolar cells.
Ref.
- PMID 11984877.
Gastric antrum vs. gastric body
| Cell | Body | Antrum | Histology | Image |
|---|---|---|---|---|
| Parietal cell | abundant | few or none | parietal cells: intensely eosinophilic cytoplasm |
[1], [2] |
| Chief cell | present | absent | chief cells: basophilic cytoplasm, IHC: +ve for pepsinogen I |
[3] |
| G cell | absent | present | fried egg appearance (clear cytoplasm, round nucleus); look at high power - usu. middle 1/3 of gland,[4] IHC: +ve for gastrin. |
[4] |
| Surface | flat | blunted villi | antrum is somewhat duodenum-like |
body - flat |
| Gastric glands / mucosa |
thick | thin | not so useful for discrimination |
body - thick, body & antrum |
![[1]](http://commons.wikimedia.org/wiki/File:Parietal_cells.jpg){kind=link}
![[2]](http://commons.wikimedia.org/wiki/File:Normal_gastric_mucosa_intermed_mag.jpg){kind=link}
![[3]](http://commons.wikimedia.org/wiki/File:Chief_cells.JPG){kind=link}
![[4]](http://commons.wikimedia.org/wiki/File:G_cell_hyperplasia_-_very_high_mag.jpg){kind=link}
Notes:
- G cells may superficially resemble intraepithelial lymphocytes.
- G cell nucleus is usu. perfectly round and slightly larger (diameter of 12 micrometers?) than a lymphocyte nucleus (diameter ~ 9-10 micrometers?).
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Short version
STOMACH, BIOPSY: - BODY AND ANTRAL-TYPE GASTRIC MUCOSA WITHIN NORMAL LIMITS.
STOMACH, BIOPSY: - ANTRAL-TYPE GASTRIC MUCOSA WITHIN NORMAL LIMITS. - NEGATIVE FOR HELICOBACTER-LIKE ORGANISMS.
Long version
STOMACH, BIOPSY: - BODY/ANTRAL-TYPE GASTRIC MUCOSA. - INFLAMMATION: ABSENT. - ATROPHY: ABSENT. - INTESTINAL METAPLASIA: ABSENT. - HELICOBACTER-LIKE ORGANISMS: NOT IDENTIFIED WITH ROUTINE STAINS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
Sleeve gastrectomy
- Indication: morbid obesity.
STOMACH, GREATER CURVE, SLEEVE GASTRECTOMY: - STOMACH WALL WITHIN NORMAL LIMITS.
Introduction
Useful stains for stomach
- Cresyl violet stain[5] - used to find H. pylori.[6]
- Alcian blue - used to find mucin[7] which is present in intestinal metaplasia
- Other mucins stains:[8] mucicarmine, PAS, PASD (doesn't stain glycogen)
Things to look for...
- Parietal cells (indicate you're in the body of the stomach) - pink (eosinophilic) cytoplasm.
- Lack of parietal cells -- DDx: Bx of antrum (pylorus), Bx of cardia, pernicious anemia.
- Goblet cells = intestinal metaplasia.
- Architectural distortion of gastric glands - suspect cancer.
- Signet ring cells = (usually) gastric carcinoma.
- Can be very easy to miss in some biopsies.
- Inflammation + small bacteria = suspect H. pylori gastritis.
Non-neoplastic disease
Peptic ulcer disease
- Abbreviated PUD.
- For duodenal manifestations see Peptic duodenitis.
General
- Benign.
Complications:
- Hemorrhage.
- Obstruction.
- Perforation - can be fatal.
Etiology - typically:[9]
Gross
Features:
- Typically in the duodenum; duodenum:stomach = ~4:1.
- Epithelial defect with punched-out edges (suggestive of a benign process).
Note:
- Heaped edges - suggestive of cancer.
Image:
Microscopic
Features:
- Loss of epithelium.
- Inflammation.
- +/-Helicobacter organisms - see Helicobacter gastritis.
Gastritis
Etiology
A specific cause is uncommonly identified histologically.
Gastritis causes:[10]
- Infectious:
- H. pylori infection.
- Tuberculosis.
- Salmonellosis.
- CMV.
- Endocrine-related:
- Pernicious anemia.
- Diabetes mellitus - gastric atony.
- Trauma, e.g. NG tube.
- Vascular, ischemia.
- Autoimmune:
- Toxins:
- Radiation.
Endoscopic appearance
- Erythematous.
Microscopic
- Inflammatory cells - see below.
Acute gastritis
- AKA active gastritis.
Features:
- Neutrophils - especially when intraepithelial.
Focal active gastritis
DDx:
Chronic gastritis
Features:
- Plasma cells (in lamina propria).
- Various criteria:
- Two plasma cells kissing, i.e. two plasma cells touching/overlapping.
- Three is a crowd, i.e. three plasma cells in close proximity.
- Various criteria:
Note:
- Approximately 20% of cases with an inflamed cardia will have intestinal metaplasia.[12]
Lymphocytic gastritis
General
The DDx is limited:
- Helicobacter gastritis.
- Celiac disease.
- NSAIDs.[citation needed]
- Idiopathic.
- HIV/AIDS.
Microscopic
Features:[13]
- 25 lymphocytes / 100 epithelial cells.
Sydney criteria for gastritis
A bunch of pathologists in Sydney came-up with criteria... and these were revised in Houston.[14]
Classification
Updated Sydney classification:[14]
| Non-atrophic Helicobacter | Atrophic Helicobacter | Autoimmune | |
| Inflammation pattern | antral or diffuse | antrum & corpus, mild inflammation | corpus only |
| Atrophy & metaplasia | nil | atrophy present, metaplasia at incisura | corpus only |
Notes:
- Corpus = gastric body.
- Incisura = angular incisure, incisura angularis (Latin) - notched transition point on lesser curvature of the stomach between pylorus and body.[15]
Severity
The Sydney group suggests grading severity with the following language:[14]
- Mild.
- Moderate.
- Marked.
These terms are applied to the parameters described in a biopsy. The Sydney criteria lists H. pylori, neutrophils, mononuclear cells, antrum (atrophy), corpus (atrophy) and intestinal metaplasia. The paper that discusses this also give a visual analogue scale.
Parameters & Severity (adapted from Dixon et al.[14]):
| Feature | Mild | Moderate | Marked |
|---|---|---|---|
| H. pylori | few touching | many touching | piles |
| Neutrophils | few | bunches | crowded |
| Mononuclear cells | not touching | kissing | partying |
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Mild chronic
STOMACH, BIOPSY: - BODY AND ANTRAL-TYPE GASTRIC MUCOSA WITH MILD CHRONIC INFLAMMATION. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR HELICOBACTOR-LIKE ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
Moderate chronic active
STOMACH, BIOPSY: - BODY AND ANTRAL-TYPE GASTRIC MUCOSA WITH MODERATE CHRONIC ACTIVE INFLAMMATION. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR HELICOBACTOR-LIKE ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
Micro
The sections show gastric body type mucosa with small clusters of plasma cells. There are no intraepithelial neutrophils. Goblet cells are not identified. The epithelium matures normally to the surface. No Helicobacter organisms are seen.
Helicobacter gastritis
- Often abbreviated HP.
General
- Several Helicobacter species can cause gastritis:
- Helicobacter pylori - most common.
- Helicobacter heilmannii.
Epidemiologic associations - Helicobacter infections are associated with:[16]
- Gastritis.
- Peptic ulcers.
- Cancer.
- Carcinoma.
- MALT lymphoma.
Gross
- Thickened gastric folds.
- Erythema.
Microscopic
Features:
- Small - smaller than the nucleus of the gastric foveolar cell.
- On 400x they are still possible to miss.
- Look close to the opening of the gastric glands.
- Are often are found in groups.
- Location - can be antrum and/or body.[17]
- Helicobacter don't like the intestinal mucosa or mucosa that has undergone intestinal metaplasia -- you're unlikely to find 'em there.
- Helicobacter pylori:
- Typically have a "v" shape or a comma-like shape.
- Helicobacter heilmannii:
- Corkscrew appearance.
Images:
- H. pylori - IHC (WC).
- Helicobacter gastritis:
- Set of images - HP gastritis (WC).
- Helicobacter heilmannii (bmj.com).[18]
Stains
- Cresyl violet stain - background and organisms blue.
- Warthin-Starry stain - background yellow, organisms black.
IHC
- Helicobacter pylori IHC stain +ve.
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STOMACH, BIOPSY: - BODY-TYPE MUCOSA WITH MODERATE CHRONIC ACTIVE GASTRITIS. - ABUNDANT HELICOBACTER-LIKE ORGANISMS PRESENT. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
Intestinal metaplasia of the stomach
- AKA gastric intestinal metaplasia.
- Abbreviated IM.
General
- Often part of surgical pathology report, e.g. "negative for intestinal metaplasia" or "intestinal metaplasia present".
- May be associated with Helicobacter spp. infection -- though Helicobacter don't like intestinal type mucosa, i.e. H. pylori are not typically found in regions with intestinal metaplasia.
- May be reversible - some epidemiological evidence.[19]
Significance:
- Moderate risk increase for carcinoma; risk less than for Barrett's esophagus.[20]
- Odds ratio for corpus (~5.8x) higher than antrum (2.3x) when compared to individuals without IM.[21]
Microscopic
Features:
- Goblet cells are present in the stomach - key feature.[22]
- In H&E sections the vacuole often stains light grey.
- Foveolar epithelium should be present in the same fragment.
- +/-Paneth cells - deep in the glands.[23]
- Very rarely present.
- Very uncommon in isolation.
Note:
- Intestinal metaplasia (IM) is occasionally subdivided:[24]
- Complete IM = goblet cells and (intestinal) brush border.
- Incomplete IM = mucus vacuoles of various sizes, no (intestinal) brush border.
DDx:
- Normal small bowel mucosa - no foveolar epithelium present.
Image:
Stains
- Alcian blue (pH 2.5)/PAS +ve.[25]
- Alican blue stain +ve.[citation needed]
Image:
IHC
- CDX2 +ve (-ve in normal stomach).[19]
- Strong assoc. with Helicobacter gastritis as well as IM.[28]
Others:
- Lysozyme +ve - marks paneth cells.[23]
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STOMACH, BIOPSY: - BODY-TYPE MUCOSA WITH INTESTINAL METAPLASIA, FOCAL. - MINIMAL CHRONIC GASTRITIS (BODY OF STOMACH). - NEGATIVE FOR HELICOBACTER-LIKE ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
STOMACH, BIOPSY: - ANTRAL-TYPE MUCOSA WITH INTESTINAL METAPLASIA, EXTENSIVE. - MILD CHRONIC (ANTRAL) GASTRITIS. - NEGATIVE FOR HELICOBACTER-LIKE ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
Inflammatory bowel disease & the stomach
- Histopathologic findings are usually non-specific.
- Conventional thinking was upper GI involvement = Crohn's disease; this is changing.[29]
Microscopic
Features:[30]
- Focal inflammation.
- Common finding - non-specific.
- +/-Granulomas.
Miscellaneous
This is a grab bag of stuff seen in the stomach. Some of it is quite rare.
Gastric antral vascular ectasia
General
- Lesion of the antrum - due to dilated capillaries.
Gross/endoscopic appearance
- Linear red streaks in antrum - oriented toward the pyloric valve... vaguely resembles a watermelon.
Endoscopic images:
Microscopic
Features:[32]
- Fibrin thrombi - characteristic feature.
- Dilated capillaries in lamina propria.
- +/-Foveollar hyperplasia.[33]
DDx:
- Portal hypertensive gastropathy - predominantly in the gastric body, usu. associated with cirrhosis, do not have fibrin thrombi.[34]
Images:
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STOMACH, BIOPSY: - GASTRIC ANTRAL VASCULAR ECTASIA WITH FOVEOLAR HYPERPLASIA. - MILD CHRONIC ACTIVE ANTRAL GASTRITIS. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR DYSPLASIA. - NEGATIVE FOR HELICOBACTER ORGANISMS.
Micro
The sections show antral-type gastric mucosa with dilated lamina propria blood vessels and intravascular fibrin thrombi. There is mild foveolar hyperplasia. Numerous neutrophils are present between the foveollar cells and within the lamina propria. Several large clusters of plasma cells are present in the lamina propria.
Reactive gastropathy
General
- May be seen in the context of a previous resection/surgical reconstruction, e.g. Billroth II.
Epidemiology
General assocations:
- Increases with age.[36]
Etologic factors - associated with:[37]
- Excess acid.
- EtOH.
- Bile.
- H. pylori.
- Drugs:[35]
- Iron (brown pigment on histology).
- NSAIDs - synergistic effect with corticosteroids.
Drugs that cause erosions and/or ulcers -- adapted from Genta:[35]
| Drug | Comment | Indication for Rx |
|---|---|---|
| NSAIDs | common cause | pain, reduce cardiovascular risk |
| Corticosteroids | synergistic effect with NSAIDs | rheumatologic diseases + others |
| Potassium (KCl) | common cause | renal failure |
| Bisphophonates | uncommon cause | osteoporosis |
| Ferrous sulfate | very common if symptomatic | iron deficiency anemia |
| Chloroquine | uncommon | only in the context of malaria |
| Sodium polystyrene sulfonate (Kayexalate) | rare | renal failure patients |
Relation to gastritis
- May mimic a (true) gastritis symptomatically and visually in an endoscopic examination.
- "Chemical gastritis" is misnomer. Etymologically, the -itis in gastritis, implies an inflammatory process. Chemical gastropathy is not (predominantly) an inflammatory process.
- This type of confusion is not uncommon. Steatohepatitis is another example of this; it is not a process with significant inflammation yet, confusingly, carries the -itis ending.
Gross/endoscopic
Features:[38]
- Antral erythema +/- erosions.
- +/-Bile.
Microscopic
- Foveolar hyperplasia.
- Tortuosity of glands in the "neck" region of the gastric glands.
- Associated with "mucin depletion" - cytoplasm not clear -- as is usual.
- Smooth muscle fibre hyperplasia.
- Abundant eosinophilic lamina propria.
- Scant acute & chronic inflammatory cells.
Additional features.
- +/-Edema.
- +/-Erosions.
Notes:
- Triad rarely present; mild inflammation common.
DDx:
Images:
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STOMACH, BIOPSY: - ANTRAL-TYPE GASTRIC MUCOSA WITH REACTIVE GASTROPATHY, SEE COMMENT. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR HELICOBACTER ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY. COMMENT: This nonspecific finding may be due to a number of causes, including medications (especially NSAIDs), alcohol and bile reflux.
Not well-developed
STOMACH, BIOPSY: - BODY-TYPE GASTRIC MUCOSA WITHIN NORMAL LIMITS. - ANTRAL-TYPE GASTRIC MUCOSA WITH SMOOTH MUSCLE HYPERPLASIA AND FOCAL GASTRIC GLAND TORTUOSITY, SEE COMMENT. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR HELICOBACTER ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY. COMMENT: These findings are suggestive of a reactive gastropathy; however, gland corkscrewing is not evident.
STOMACH, BIOPSY: - ANTRAL-TYPE GASTRIC MUCOSA WITH PROMINENT SMOOTH MUSCLE, OTHERWISE WITHIN NORMAL LIMITS. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR HELICOBACTER ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
Gastric atrophy
General
- Has a wide differential diagnosis.
Microscopic
Can take three general forms:
- Intestinal metaplasia - see intestinal metaplasia section.
- Pseudopyloric metaplasia; gastric body looks like gastric antrum.
- Characterized by foveolar hyperplasia.
- Cell loss without replacement.
- Clue is deep inflammation in the body.
Pernicious anemia
General
- Pathology: loss of parietal cells, gastric atrophy, macrocytic anemia.
- Etiology: autoimmune.
Diagnosis based on serology for antibodies to:[41]
- Parietal cells.
- Intrinsic factor.
Others:
Note:
- Parietal cells produce intrinsic factor (important for vitamin B12 absorption) and hydrogen chloride, i.e. stomach acid.
Microscopic
Features:
- Corpus predominant inflammation - usu. moderate or severe - key feature.
- Loss of parietal cells.
- Increased G cells in the antrum.
- Produce gastrin to stimulate the (missing) parietal cells.
DDx:
Notes:
- Compare with other types of gastric atrophy.
IHC
Features:[44]
- Chromogranin A +ve (demonstrates nodular enterochromaffin-like cell hyperplasia).
- Gastrin -ve (body of stomach).
- +ve in antrum.
Collagenous gastritis
General
- Very rare.
- Associated with collagenous colitis.
Microscopic
Features:
- Eosinophilic material (collagen) expands lamina propria.
- Band of collagen must be ~thick as RBC diameter.
- Proven by trichrome stain that highlights collagen.
- Band of collagen must be ~thick as RBC diameter.
Granulomatous gastritis
- Usual DDx of granulomatous disease (see Basics article):
- DNF AAII:
- Drugs, Neoplasms, Foreign body, Autoimmune, Allergic, Infectious, Idiopathic.
- DNF AAII:
Important ones:
- Autoimmune - Crohn's disease.
- Infectious - Tuberculosis.
- Idiopathic - Sarcoidosis.
Plasma cells in the stomach
DDx of plasmacytosis:
- Plasma cell neoplasm.
- Syphilis.
- Chronic gastritis.
Gastritis cystitis profunda
- AKA Gastritic cystica profunda.[citation needed]
General
- May be associated with glandular proliferation as well.[45] (???)
- Super rare.
- Similar to cystitis cystica.
Microscopic
Features:
- Cystic spaces lined by foveolar epithelium.
Ménétrier's disease
General
- Super rare.
- Increased risk of gastric adenocarcinoma.[46]
Clinical:[47]
- Classical: nausea, emesis, abdominal pain and peripheral edema.
- Emesis (intractable) - most important.
Other:
- Gastric mass (may mimic cancer).
- Hypochlorhydria.
- Protein loss (hypoalbuminemia) - leads to peripheral edema.
Epidemiology:
- Men > women.
- Adults usually 50s.
- Associated with ulcerative colitis.
Treatment:
- EGFR inhibitors.[48]
- Gastrectomy.
Gross
- "Bag of worms" appearance - very thick gastric folds.
Microscopic
Features:[46]
- Foveolar cell hyperplasia - key feature.
- Decreased parietal cells.
- +/-Inflammation.
DDx:
Images:
Gastric xanthoma
General
- Uncommon.
- Benign.
Gross/endoscopic
Microscopic
Features:[50]
- Collections of gastric lamina propria with lipid-laden macrophages.
DDx:
- Signet ring cell carcinoma.[51]
- Whipple disease.
- MAC infection.
Images:
IHC
- CD68 +ve.
- Panker (AE1/AE3) -ve.
Gastric ischemia
- Gastric necrosis redirects here.
General
Microscopic
Features:
Image:
Gastric polyps
Similar to colonic polyps - see intestinal polyps.
DDx polyp (similar to colon & rectum):
- Hyperplastic - most common, characterised by abundant elongated foveola + glands.
- Hamartomatous - weriod stuff.
- Inflammatory fibroid polyp - inflammation, myxoid stroma.
- Fundic gland polyp - cystic dilation, flat epithelium.
- Gastric adenoma - polypoid gastric dysplasia.
Inflammatory fibroid polyp
General
- Benign.
- Through-out GI tract.
- Can be thought of as granulation tissue-like.[55]
Microscopic
Features:[56]
- Proliferating spindle cells (fibroid) - key feature.
- Inflammation:
- Eosinophils - often prominent.
- +/-Leiomyoma/schwannoma-like areas - with nuclear palisading.[55]
- +/-Vascular for fibrous tissue.
- Poorly circumscribed/infiltrates into the lamina propria.
DDx:
- Inflammatory myofibroblastic tumour.
- GIST - usually sharply demarcated border.
Notes:
- Concentric = share the same centre.[58]
Images:
IHC
Features:[56]
- CD34 +ve.
- There is a CD34 -ve variant.
- Vimentin +ve -- diffuse.[59]
Others:
- CD117 -ve.[60]
- S100 -ve.
Molecular
- A subset have mutations in PDGFRA.[56]
Hyperplastic polyp of the stomach
Main article: Hyperplastic polyp
- AKA gastric hyperplastic polyp.
General
- Benign.
- Most common gastric polyp.[61]
Microscopic
Features:[62]
- Abundant foveolar cells and elongated glands - key feature.
- +/-Gland dilation.
Negatives:
- No atypical nuclei.
- No hyperchromasia.
- No loss of pseudostratification.
Notes:
- No serrations - as in the colon.
DDx:
- Ménétrier's disease[63] (hyperplastic hypersecretory gastropathy).
- Juvenile polyp[61] - abundant lamina propria, dilated glands may have neutrophils.[64]
- Peutz-Jeghers polyp - thick superficial muscle.
- Fundic gland polyp - doesn't have foveolar hyperplasia.
Images:
- www:
- WC:
Fundic gland polyp
- Abbreviated FGP.
General
Clinical significance
- Weak association with FAP (familial adenomatous polyposis).[65][66]
- Associated with chronic proton pump inhibitors (PPI) use -- approximately 4x risk.[67]
Notes:
- Animal studies suggested PPIs cause neuroendocrine tumours -- but this has not been found in humans.[68]
Microscopic
Features:[69]
- Polypoid shape (may not be appreciated on microscopy).
- Dilated gastric glands.
- Flatted epithelial lining (consisting of normal foveolar epithelium) - key feature.
Notes:
- The presence of dysplastic changes should prompt consideration of FAP.
DDx:
- Hyperplastic polyp of the stomach - has foveolar hyperplasia, gland dilation may be present.
Image:
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POLYP, STOMACH, BIOPSY: - FUNDIC GLAND POLYP. - NEGATIVE FOR INTESTINAL METAPLASIA. - NEGATIVE FOR HELICOBACTER-LIKE ORGANISMS. - NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.
Neoplastic
The spectrum from benign to malignant is divided into five:[24]
- Benign.
- Indefinite for gastric epithelial dysplasia.
- Low-grade gastric epithelial dysplasia.
- High-grade gastric epithelial dysplasia.
- Gastric carcinoma.
Gastric dysplasia
- Gastric adenoma directs here.
- AKA gastric columnar dysplasia.
General
- Lesions that protrude into the lumen and are macroscopically apparent are known as: adenomas.[24]
- Polypoid forms are grouped various ways.[63]
Grading
Like in the colon - they are divided into:
- Low grade.
- High grade.
Subclassification
One subclassification:[70]
- Intestinal: goblet cells or Paneth cells.
- Not associated with FAP.
- Gastric: foveolar epithelium.
- Associated with familial adenomatous polyposis (FAP).
Microscopic
- Histologic criteria similar to columnar dysplasia in the esophagus.
- The threshold is much lower than in the colon and rectum.
Foveolar type
Features:
- Hyperchromasia at the surface - key feature.
- Cytoplasm with (shortened) champagne flute-like luminal aspect (apical mucin caps).
- Nuclear changes:
- Hyperchromasia.
- Enlargement.
- No intestinal metaplasia.
DDx:
Intestinal type
Features - intestinal:
- Intestinal metaplasia.
- Hyperchromasia of cytoplasm.
- Nuclear changes:
- Loss of nuclear polarity.
- Increased NC ratio.
- Elongation of nucleus and pseudostratification.
DDx:
Images:
- Gastric polyps - several images (sciencedirect.com).
- Gastric polyps - several images (achivesofpathology.org).
Grading
Low-grade gastric dysplasia
Features:
- Nuclear changes:
- Nuclear crowding/pseudostratification with hyperchromasia.
- Elongation of nuclei (cigar-shaped nuclei).
- Nuclear stratification intact; nuclei close to the basement membrane.
- Architecture:
- Focal irregularities in the glandular contours.
Negatives:
- No desmoplasia.
- No necrosis.
- No surface maturation.
DDx:
- Indefinite for dysplasia.
- High-grade gastric columnar dysplasia - see below.
- The threshold is much lower than in the colon and rectum!
Images:
High-grade gastric dysplasia
Features:
- Nuclear changes:
- Round hyperchromatic nuclei.
- Loss of normal nuclear stratification.
- Architecture:
- Irregularities in the glandular contours.
- Back-to-back glands.
- Cribriforming of the glands.
- +/-Necrosis.
Negatives:
- No desmoplasia.
DDx:
- Low-grade gastric columnar dysplasia.
- Gastric adenocarcinoma.
Images:
- WC:
- www:
.jpg){kind=link}
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Foveolar type
STOMACH POLYP, BIOPSY: - ADENOMATOUS POLYP, FOVEOLAR TYPE. - NEGATIVE FOR HIGH-GRADE DYSPLASIA. - NEGATIVE FOR HELICOBACTER-LIKE ORGANISMS.
Gastric neuroendocrine tumour
- AKA neuroendocrine tumour of the stomach.
General
- Behaviour dependent on the subtype.
- Uncommon.
Overview of subtypes
Divided into four types:[72]
| Tumour type | Relative prevalence | Multifocality | Tumour size | Typical location | Clinical | Other | Histology |
|---|---|---|---|---|---|---|---|
| Type 1 | ~75% | yes | small (5-10 mm) | body | benign typically, female:male ~ 4:1, 50-60 years | chronic atrophic gastritis - usu. autoimmune | WDNET, WDNEC |
| Type 2 | rare | yes | small ~15 mm | body | aggressive, ~50 years old | assoc. MEN I, hyperchlorhydia | WDNEC, WDNET |
| Type 3 | 10-15% | no | small and large | variable location | aggressive if >2.0 cm, males > females | normal gastrin levels | WDNET |
| Type 4 | extremely rare | no | large | variable location | aggressive (mets usu. at time of Dx), males > females | elevated gastrin d/t parietal cell dysfunction | PDNEC |
Notes:
- WDNET = well-differentiated neuroendocrine tumour.
- WDNEC = well-differentiated neuroendocrine carcinoma.
- PDNEC = poorly-differentiated neuroendocrine carinoma.
Microscopic
Neoplastic rare
Gastric calcifying fibrous tumour
Main article: Calcifying fibrous tumour
Gastric cancer
Gastric lymphoma
Main article: MALT lymphoma
General
- Associated with helicobacter infection.[73]
- Usually MALT lymphoma (mucosa-associated lymphoid tissue lymphoma).
Microscopic
Features:
- Sheets of lymphoid cells.
- "Lymphoepithelial lesion" - gastric crypts invaded by a monomorphous population of lymphocytes.[74]
- Features:
- Cluster of lymphocytes - three cells or more - key feature.
- Single lymphocytes don't count.
- Clearing around the lymphocyte cluster.
- Cluster of lymphocytes - three cells or more - key feature.
- Associated with MALT lymphoma;[75] however, not specific.
- Features:
DDx:
IHC
- Panker -- most useful.
Others:
- CD3 (T cells) - scatter positivity.
- CD20 (B cells) +ve.
- CD138 (plasma cells).
- kappa, lambda -- often one is predominant, suggesting clonality.
- BCL2 +ve.
Treatment
- Triple therapy (two antibiotics, proton pump inhibitor (PPI)).[78]
- Surgery - if triple therapy fails.
Review paper: PMID 16950858.
Hereditary gastric cancer
Several syndromes are associated with gastric cancer:[79]
| Disease | Gene | Histology | Other |
|---|---|---|---|
| Hereditary diffuse gastric cancer (HDGC) syndrome | CDH1 (E-cadherin)[80] | diffuse - more specifically signet ring cell carcinoma | most important; assoc. invasive lobular carcinoma[81] |
| Lynch syndrome | MSH2, MLH1, others | ? | colorectal carcinoma, endometrial carcinoma |
| Familial adenomatous polyposis | APC | ? | adenomatous polyps |
| Peutz-Jeghers syndrome | STK11 | ? | stomach hamartomas - not precursor |
| Li-Fraumeni syndrome | TP53 (p53) | ? | AKA SBLA syndrome = sarcomas, breast, brain, leukemia, laryngeal, lung, adrenocortical carcinoma |
| Familial breast and ovarian cancer 2[82] | BRCA2 | ? | ? |
Gastric adenocarcinoma
General
Epidemiology:
- Prognosis is often poor as it is discovered at a late stage.
- Higher prevalence in countries in the far east (e.g. Japan) - thought to be environmental, e.g. diet.
Risk factors:
- Associated with helicobacter infections, i.e. Helicobacter gastritis.
- Alcohol - heavy use.[83]
- Genetic syndromes - see hereditary gastric cancer.
Note:
- Possible association with tobacco use - dependent on the study.[84]
Treatment:
- Surgical excision.
- Proximal tumours may require a complete gastrectomy as the stomach is innervated from its proximal part.
Classification
- Two different classification schemes.
Lame memory device STOMACH:
- Signet ring, Tubular, Oh papillary, Mucinous, Adenosquamouas, Crappy High grade (Undifferentiated).
Gross
Location:
- Large carcinomas preferentially involve the lesser curvature.[87]
- Ulceration with heaped (raised) edges.
- Appearance of the typical intestinal type tumour.
- Diffuse wall thickening with loss of the rugae - called linitis plastica.
- Typically due to diffuse carcinoma.
Main DDx of ulcer:
- Peptic ulcer disease - have a "punched-out" appearance: sharp edge, no granularity of surrounding mucosa.
Images:
- Linitis plastica - endoscopic image (WC).
- Ulcerating gastric carcinoma (WC).
- Ulcerating gastric carcinoma (WC).
Microscopic
Features - variable, either of the two following:
- "Typical adenocarcinoma":
- Gland-forming lesion that infiltrates into the lamina propria or beyond.
- Nuclear pleomorphism - common.
- +/-Signet ring carcinoma.
- Scattered single cells in the lamina propria or beyond with:
- Abundant cytoplasm containing one large (mucin-filled) vacuole.
- A peripheral nucleus (displaced by the vacuole).
- Scattered single cells in the lamina propria or beyond with:
DDx:
- Gastric xanthoma - may mimic signet ring cell carcinoma.
Images:
- WC:
- www:
IHC
- CK7 +ve.
- CK20 -ve, occasionally +ve.
Molecular
- May have HER2 over expression - more common in intestinal-type tumours.[88]
- Poor prognosis - like in breast cancer.
- Scoring system different than in breast cancer - complete membrane staining is not required.
See also
References
- ↑ ALS. 4 Feb 2009.
- ↑ Osborn M, Mazzoleni G, Santini D, Marrano D, Martinelli G, Weber K (1988). "Villin, intestinal brush border hydrolases and keratin polypeptides in intestinal metaplasia and gastric cancer; an immunohistologic study emphasizing the different degrees of intestinal and gastric differentiation in signet ring cell carcinomas". Virchows Arch A Pathol Anat Histopathol 413 (4): 303–12. PMID 2459839.
- ↑ Sternberg H4P 2nd Ed., P.484
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- ↑ http://www.histology-world.com/stains/stains.htm
- ↑ Goggin N, Rowland M, Imrie C, Walsh D, Clyne M, Drumm B (December 1998). "Effect of Helicobacter pylori eradication on the natural history of duodenal ulcer disease". Arch. Dis. Child. 79 (6): 502-5. PMC 1717771. PMID 10210995. http://adc.bmj.com/cgi/pmidlookup?view=long&pmid=10210995.
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- ↑ http://www.histology-world.com/stains/stains.htm
- ↑ Malfertheiner, P.; Chan, FK.; McColl, KE. (Oct 2009). "Peptic ulcer disease.". Lancet 374 (9699): 1449-61. doi:10.1016/S0140-6736(09)60938-7. PMID 19683340.
- ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 812-3. ISBN 0-7216-0187-1.
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- ↑ Maaroos HI, Kekki M, Villako K, Sipponen P, Tamm A, Sadeniemi L (October 1990). "The occurrence and extent of Helicobacter pylori colonization and antral and body gastritis profiles in an Estonian population sample". Scand. J. Gastroenterol. 25 (10): 1010-7. PMID 2263873.
- ↑ URL: http://gut.bmj.com/content/58/12/1669.extract. Accessed on: 2 March 2012.
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- ↑ Rivera-Hueto, F.; Lag-Asturiano, E.; Utrilla-Alcolea, JC.; Herrerías-Gutiérrez, JM. (Feb 2004). "Advanced gastric carcinoma with a complete intestinal metaplasia phenotype associated with early intestinal-type carcinoma.". Arch Pathol Lab Med 128 (2): 218-21. doi:10.1043/1543-2165(2004)128218:AGCWAC2.0.CO;2. PMID 14736279.
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- ↑ Iacobuzio-Donahue, Christine A.; Montgomery, Elizabeth A. (2005). Gastrointestinal and Liver Pathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Churchill Livingstone. pp. 119. ISBN 978-0443066573.
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- ↑ Rich, A.; Toro, TZ.; Tanksley, J.; Fiske, WH.; Lind, CD.; Ayers, GD.; Piessevaux, H.; Washington, MK. et al. (Dec 2010). "Distinguishing Ménétrier's disease from its mimics.". Gut 59 (12): 1617-24. doi:10.1136/gut.2010.220061. PMID 20926644.
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- ↑ Iacobuzio-Donahue, Christine A.; Montgomery, Elizabeth A. (2005). Gastrointestinal and Liver Pathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Churchill Livingstone. pp. 102. ISBN 978-0443066573.
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- ↑ Freeman HJ (March 2008). "Proton pump inhibitors and an emerging epidemic of gastric fundic gland polyposis". World J. Gastroenterol. 14 (9): 1318-20. PMID 18322941. http://www.wjgnet.com/1007-9327/14/1318.asp.
- ↑ Jalving M, Koornstra JJ, Wesseling J, Boezen HM, DE Jong S, Kleibeuker JH (November 2006). "Increased risk of fundic gland polyps during long-term proton pump inhibitor therapy". Aliment. Pharmacol. Ther. 24 (9): 1341-8. doi:10.1111/j.1365-2036.2006.03127.x. PMID 17059515.
- ↑ Masaoka T, Suzuki H, Hibi T (May 2008). "Gastric epithelial cell modality and proton pump inhibitor". J Clin Biochem Nutr 42 (3): 191-6. doi:10.3164/jcbn.2008028. PMC 2386521. PMID 18545640. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2386521/.
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- ↑ URL: http://surgpathcriteria.stanford.edu/gitumors/gastric-adenoma/printable.html. Accessed on: 18 December 2012.
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- ↑ Mbulaiteye, SM.; Hisada, M.; El-Omar, EM. (2009). "Helicobacter Pylori associated global gastric cancer burden.". Front Biosci 14: 1490-504. PMID 19273142.
- ↑ Bailey, D. 6 August 2010.
- ↑ Papadaki, L.; Wotherspoon, AC.; Isaacson, PG. (Nov 1992). "The lymphoepithelial lesion of gastric low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT): an ultrastructural study.". Histopathology 21 (5): 415-21. PMID 1452124.
- ↑ Kim, K.; Kim, EJ.; Kim, MJ.; Song, HJ.; Lee, YS.; Jung, KW.; Yu, E. (Dec 2009). "Clinicopathological features of syphilitic gastritis in Korean patients.". Pathol Int 59 (12): 884-9. doi:10.1111/j.1440-1827.2009.02462.x. PMID 20021615.
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- ↑ Zullo, A.; Hassan, C.; Andriani, A.; Cristofari, F.; De Francesco, V.; Ierardi, E.; Tomao, S.; Morini, S. et al. (Aug 2009). "Eradication therapy for Helicobacter pylori in patients with gastric MALT lymphoma: a pooled data analysis.". Am J Gastroenterol 104 (8): 1932-7; quiz 1938. doi:10.1038/ajg.2009.314. PMID 19532131.
- ↑ Sereno, M.; Aguayo, C.; Guillén Ponce, C.; Gómez-Raposo, C.; Zambrana, F.; Gómez-López, M.; Casado, E. (Sep 2011). "Gastric tumours in hereditary cancer syndromes: clinical features, molecular biology and strategies for prevention.". Clin Transl Oncol 13 (9): 599-610. PMID 21865131.
- ↑ Online 'Mendelian Inheritance in Man' (OMIM) 192090
- ↑ Guilford, P.; Hopkins, J.; Harraway, J.; McLeod, M.; McLeod, N.; Harawira, P.; Taite, H.; Scoular, R. et al. (Mar 1998). "E-cadherin germline mutations in familial gastric cancer.". Nature 392 (6674): 402-5. doi:10.1038/32918. PMID 9537325.
- ↑ Online 'Mendelian Inheritance in Man' (OMIM) 600185
- ↑ Duell, EJ.; Travier, N.; Lujan-Barroso, L.; Clavel-Chapelon, F.; Boutron-Ruault, MC.; Morois, S.; Palli, D.; Krogh, V. et al. (Nov 2011). "Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.". Am J Clin Nutr 94 (5): 1266-75. doi:10.3945/ajcn.111.012351. PMID 21993435.
- ↑ Nomura, A.; Grove, JS.; Stemmermann, GN.; Severson, RK. (Nov 1990). "Cigarette smoking and stomach cancer.". Cancer Res 50 (21): 7084. PMID 2208177.
- ↑ LAUREN P (1965). "THE TWO HISTOLOGICAL MAIN TYPES OF GASTRIC CARCINOMA: DIFFUSE AND SO-CALLED INTESTINAL-TYPE CARCINOMA. AN ATTEMPT AT A HISTO-CLINICAL CLASSIFICATION". Acta Pathol Microbiol Scand 64: 31–49. PMID 14320675.
- ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 823. ISBN 0-7216-0187-1.
- ↑ Yamagawa, H.; Onishi, T. (Sep 1989). "[A clinicopathological study of early gastric cancers with a diameter larger than five centimeters].". Gan No Rinsho 35 (10): 1114-8. PMID 2550682.
- ↑ Romiti, A.; Di Rocco, R.; Milione, M.; Ruco, L.; Ziparo, V.; Zullo, A.; Duranti, E.; Sarcina, I. et al. (Jan 2012). "Somatostatin receptor subtype 2 A (SSTR2A) and HER2 expression in gastric adenocarcinoma.". Anticancer Res 32 (1): 115-9. PMID 22213295.