Stomach

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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

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.

Image: Stomach anatomy (WP).

Microscopic

Foveolar cells vs. intestinal goblet cells

  • Intestinal goblet cells - clear mucin.
  • Foveolar cells - eosinophilic contents.

Stomach vs. intestine[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

Body Antrum Histology Image
Parietal cells abundant few or none parietal cells: intensely
eosinophilic cytoplasm 		[1], [2]
Chief cells present absent chief cells: basophilic cytoplasm,
IHC: +ve for pepsinogen I 		[3]
G cells 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

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?).

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:

Gastritis

Etiology

A specific cause is uncommonly identified histologically.

Gastritis causes:[10]

Endoscopic appearance

  • Erythematous.

Microscopic

  • Inflammatory cells - see below.

Acute gastritis

  • AKA active gastritis.

Features:

  • Neutrophils - especially when intraepithelial.
Focal active gastritis

DDx:

  1. Drugs,[11] esp. NSAIDs.
  2. Infectious.
  3. Inflammatory bowel disease.

Chronic gastritis

Features:

  • Plasma cells (in lamina propria).
    • Various criteria:
      1. Two plasma cells kissing, i.e. two plasma cells touching/overlapping.
      2. Three is a crowd, i.e. three plasma cells in close proximity.
Lymphocytic gastritis

The DDx is limited:

  1. Helicobacter gastritis.
  2. Celiac disease.
  3. NSAIDs.
  4. Idiopathic.

Sydney criteria for gastritis

A bunch of pathologists in Sydney came-up with criteria... and these were revised in Houston.[12]

Classification

Updated Sydney classification:[12]

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.[13]

Severity

The Sydney group suggests grading severity with the following language:[12]

  • 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.[12]):

Mild Moderate Marked
H. pylori few touching many touching piles
Neutrophils few bunches crowded
Mononuclear cells not touching kissing partying

Helicobacter gastritis

General

  • Several Helicobacter species can cause gastritis:

Epidemiologic associations - Helicobacter infections are associated with:[14]

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.[15]
  • 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:

Stains

IHC

  • Helicobacter pylori IHC stain +ve.

Intestinal metaplasia of the stomach

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.[17]

Significance:

  • Moderate risk increase for carcinoma; risk less than for Barrett's esophagus.[18]
    • Odds ratio for corpus (~5.8x) higher than antrum (2.3x) when compared to individuals without IM.[19]

Microscopic

Features:

  • Goblet cells are present in the stomach.[20]
    • In H&E the vacuole often stains light grey.

Image:

Stains

  • Alcian blue (pH 2.5)/PAS +ve.[21]
    • May be used to divide into complete and incomplete.[22]

Image:

IHC

Inflammatory bowel disease & the stomach

See inflammatory bowel disease.
  • Histopathologic findings are usually non-specific.
  • Conventional thinking was upper GI involvement = Crohn's disease; this is changing.[24]

Microscopic

Features:[25]

  • 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

  • Abbreviated GAVE.
  • AKA watermelon stomach - due to characteristic endoscopic appearance.[26]

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:[27]

  • Fibrin thrombi - characteristic feature.
  • Dilated capillaries in lamina propria.

Images:

Reactive gastropathy

General

  • AKA chemical gastropathy,[28] incorrectly referred to as chemical gastritis (see below).
  • May be seen in the context of a previous resection/surgical reconstruction, e.g. Billroth II.

Epidemiology

Associated with:[29]

  • Excess acid.
  • EtOH.
  • Bile.
  • H. pylori.
  • Drugs:[28]
    • Iron (brown pigment on histology).
    • NSAIDs - synergistic effect with corticosteroids.

Drugs that cause erosions and/or ulcers -- adapted from Genta:[28]

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.

Microscopic

Features - triad:[30][28]

  1. Foveolar hyperplasia.
    • Tortuosity of glands in the "neck" region of the gastric glands.
    • Associated with "mucin depletion" - cytoplasm not clear -- as is usual.
  2. Smooth muscle fibre hyperplasia.
    • Abundant eosinophilic lamina propria.
  3. Scant acute & chronic inflammatory cells.

Additional features.

  • +/-Edema.
  • +/-Erosions.

Notes:

  • Triad rarely present; mild inflammation common.

DDx:

Images:

Gastric atrophy

General

  • Has a wide differential diagnosis.

Microscopic

Can take three general forms:

  1. Intestinal metaplasia - see intestinal metaplasia section.
  2. Pseudopyloric metaplasia; gastric body looks like gastric antrum.
    • Characterized by foveolar hyperplasia.
  3. Cell loss without replacement.
    • Clue is deep inflammation in the body.

Lymphocytic gastritis

General

DDx:

  • Celiac disease.
  • H. pylori.
  • HIV/AIDS.

Microscopic

Features:[32]

  • 25 lymphocytes / 100 epithelial cells.

Pernicious anemia

General

  • Pathology: loss of parietal cells, gastric atrophy, macrocytic anemia.
  • Etiology: autoimmune.

Diagnosis based on serology for antibodies to:[33]

  • Parietal cells.
  • Intrinsic factor.

Others:

  • Gastrin level (increased).[34]
    • Normal < 100 pg/mL.[35]

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:

IHC

Features:[36]

  • Chromogranin A +ve (demonstrates nodular enterochromaffin-like cell hyperplasia).
  • Gastrin -ve (body of stomach).

Collagenous gastritis

General

Microscopic

Features:

  • Eosinophilic material (collagen) expands lamina propria.
    • 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.

Important ones:

  • Autoimmune - Crohn's disease.
  • Infectious - Tuberculosis.
  • Idiopathic - Sarcoidosis.

Plasma cells in the stomach

DDx of plasmacytosis:

Gastritis cystitis profunda

General

  • May be associated with glandular proliferation as well.[37] (???)
  • Super rare.
  • Similar to cystitis cystica.

Microscopic

Features:

  • Cystic spaces lined by foveolar epithelium.

Ménétrier's disease

  • AKA diffuse foveolar cell hyperplasia.[38]

General

  • Super rare.
  • Increased risk of gastric adenocarcinoma.[38]

Clinical:[39]

  • Classic: nausea, emesis, abdominal pain and peripheral edema.

Other:

  • Gastric mass (may mimic cancer).
  • Hypochlorhydria.
  • Protein loss - leads to peripheral edema.

Microscopic

Features:[38]

  • Foveolar cell hyperplasia - key feature.

DDx:

Images:

Gastric xanthoma

  • Abbreviated GX.
  • AKA xanthelasma.
  • AKA stomach lipidosis.

General

  • Uncommon.
  • Benign.

Gross/endoscopic

  • Yellowish nodule or plaque.[41]
    • Classically lesser curvature and antrum.[42]

Microscopic

Features:[41]

  • Collections of gastric lamina propria with lipid-laden macrophages.

DDx:

Images:

IHC

  • CD68 +ve.
  • Panker (AE1/AE3) -ve.

Gastric polyps

Similar to colonic polyps - see intestinal polyps.

DDx polyp (similar to colon & rectum):

Inflammatory fibroid polyp

General

  • Benign.
  • Through-out GI tract.
  • Can be thought of as granulation tissue-like.[43]

Microscopic

Features:[44]

  • Proliferating spindle cells (fibroid) - key feature.
    • Loosely arranged, concentrically, around blood vessels.[45]
    • Perivascular hypocellular zones.[43]
  • Inflammation:
    • Eosinophils - often prominent.
  • +/-Leiomyoma/schwannoma-like areas - with nuclear palisading.[43]
  • +/-Vascular for fibrous tissue.
  • Poorly circumscribed/infiltrates into the lamina propria.

DDx:

Notes:

  • Concentric = share the same centre.[46]

Images:

IHC

Features:[44]

  • CD34 +ve.
    • There is a CD34 -ve variant.
  • Vimentin +ve -- diffuse.[47]

Others:

  • CD117 -ve.[48]
  • S100 -ve.

Molecular

  • A subset have mutations in PDGFRA.[44]

Hyperplastic polyp of the stomach

Main article: Hyperplastic polyp
  • AKA gastric hyperplastic polyp.

General

  • Benign.
  • Most common gastric polyp.[49]

Microscopic

Features:[50]

  • Abundant foveolar cells and elongated glands - key feature.

Negatives:

  • No atypical nuclei.
  • No hyperchromasia.
  • No loss of pseudostratification.

Notes:

  • No serrations - as in the colon.

DDx:

Images:

Adenomatous polyps

General

  • Divided into "gastric" and "intestinal type". (???)
  • Can be grouped various ways.[51] (???)

Microscopic

  • Type.
    • Intestinal: goblet cells or Paneth cells.
    • Gastric: foveolar epithelium. (???)
  • Architectural crowding of glands.
  • Hyperchromasia of cytoplasm.
  • Nuclear changes:
    • Loss of nuclear polarity.
    • Increased NC ratio.
    • Elongation of nucleus.

Fundic gland polyp

General

  • Most common stomach polyp.[52]
  • Fundic location - duh!
    • May be in the body.[52]

Clinical significance

Notes:

Microscopic

Features:[56]

  • Polypoid shape (may not be appreciated on microscopy).
  • Dilated gastric glands.
    • Flatted epithelial lining (consisting of normal foveolar epithelium) - key feature.

Image:

Notes:

  • The presence of dysplastic changes should prompt consideration of FAP.

Neoplastic

The spectrum from benign to malignant is divided into five:[57]

  1. Benign.
  2. Indefinite for gastric epithelial dysplasia.
  3. Low-grade gastric epithelial dysplasia.
  4. High-grade gastric epithelial dysplasia.
  5. Gastric carcinoma.

Gastric columnar dysplasia

  • AKA gastric dysplasia.

General

  • Criteria similar to columnar dysplasia in the esophagus.

Divided into:

  • Low grade.
  • High grade.

Microscopic

Low-grade gastric columnar 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.

Images:

High-grade gastric columnar 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.

Images:

Gastric neuroendocrine tumour

  • AKA neuroendocrine tumour of the stomach.

General

  • Behaviour dependent on the subtype.
  • Uncommon.

Overview of subtypes

Divided into four types:[58]

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

See neuroendocrine tumours

Neoplastic rare

Gastric calcifying fibrous tumour

Main article: Calcifying fibrous tumour

Gastric cancer

Gastric lymphoma

Main article: MALT lymphoma

General

  • Associated with helicobacter infection.[59]
  • 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.[60]
    • Features:
      1. Cluster of lymphocytes - three cells or more - key feature.
        • Single lymphocytes don't count.
      2. Clearing around the lymphocyte cluster.
    • Associated with MALT lymphoma;[61] however, not specific.

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)).[64]
  • Surgery - if triple therapy fails.

Review paper: PMID 16950858.

Hereditary gastric cancer

Several syndromes are associated with gastric cancer:[65]

Disease Gene Histology Other
Hereditary diffuse gastric cancer (HDGC) syndrome CDH1 (E-cadherin)[66] diffuse - more specifically signet ring cell carcinoma most important; assoc. invasive lobular carcinoma[67]
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[68] 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:

Note:

  • Possible association with tobacco use - dependent on the study.[70]

Treatment:

  • Surgical excision.
    • Proximal tumours may require a complete gastrectomy as the stomach is innervated from its proximal part.

Classification

  • Two different classification schemes.
    • Lauren[71] - two types:
      • Intestinal type (mass forming).
      • Diffuse type (infiltrative).
    • WHO classification - 6 subtypes for adenocarcinoma:[72]
      1. Papillary carcinoma.
      2. Tubular carcinoma.
      3. Mucinous carcinoma.
      4. Signet-ring carcinoma.
      5. Undifferentiated carcinoma.
      6. Adenosquamous carcinoma.

Lame memory device STOMACH:

  • Signet ring, Tubular, Oh papillary, Mucinous, Adenosquamouas, Crappy High grade (Undifferentiated).

Gross

Location:

  • Large carcinomas preferentially involve the lesser curvature.[73]
  • 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:

Microscopic

Features - variable, either of the two following:

  1. "Typical adenocarcinoma":
    • Gland-forming lesion that infiltrates into the lamina propria or beyond.
    • Nuclear pleomorphism - common.
  2. +/-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).

DDx:

Images:

IHC

  • CK7 +ve.
  • CK20 -ve, occasionally +ve.

Molecular

  • May have HER2 over expression - more common in intestinal-type tumours.[74]
    • Poor prognosis - like in breast cancer.
    • Scoring system different than in breast cancer - complete membrane staining is not required.

See also

References

  1. ↑ ALS. 4 Feb 2009.
  2. ↑ 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.
  3. ↑ Sternberg H4P 2nd Ed., P.484
  4. ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/CorePages/GIT/git.htm. Accessed on: 3 December 2010.
  5. ↑ http://www.histology-world.com/stains/stains.htm
  6. ↑ 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.
  7. ↑ http://www.histology-world.com/stains/stains.htm
  8. ↑ http://www.histology-world.com/stains/stains.htm
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ Parfitt, JR.; Driman, DK. (Apr 2007). "Pathological effects of drugs on the gastrointestinal tract: a review.". Hum Pathol 38 (4): 527-36. doi:10.1016/j.humpath.2007.01.014. PMID 17367604.
  12. ↑ 12.0 12.1 12.2 12.3 Dixon MF, Genta RM, Yardley JH, Correa P (October 1996). "Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994". Am. J. Surg. Pathol. 20 (10): 1161-81. PMID 8827022. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0147-5185&volume=20&issue=10&spage=1161.
  13. ↑ http://en.wikipedia.org/wiki/Angular_incisure
  14. ↑ 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. 814. ISBN 0-7216-0187-1.
  15. ↑ 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.
  16. ↑ URL: http://gut.bmj.com/content/58/12/1669.extract. Accessed on: 2 March 2012.
  17. ↑ 17.0 17.1 Walker, MM. (Jan 2003). "Is intestinal metaplasia of the stomach reversible?". Gut 52 (1): 1-4. PMC 1773527. PMID 12477745. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1773527/.
  18. ↑ Correa P, Piazuelo MB, Wilson KT (March 2010). "Pathology of gastric intestinal metaplasia: clinical implications". Am. J. Gastroenterol. 105 (3): 493–8. doi:10.1038/ajg.2009.728. PMC 2895407. PMID 20203636. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895407/?tool=pubmed.
  19. ↑ Sakitani, K.; Hirata, Y.; Watabe, H.; Yamada, A.; Sugimoto, T.; Yamaji, Y.; Yoshida, H.; Maeda, S. et al. (Oct 2011). "Gastric cancer risk according to the distribution of intestinal metaplasia and neutrophil infiltration.". J Gastroenterol Hepatol 26 (10): 1570-5. doi:10.1111/j.1440-1746.2011.06767.x. PMID 21575058.
  20. ↑ URL: http://esynopsis.uchc.edu/eAtlas/GI/1280.htm. Accessed on: 16 August 2010.
  21. ↑ 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.
  22. ↑ Iida, F.; Kusama, J. (Dec 1982). "Gastric carcinoma and intestinal metaplasia. Significance of types of intestinal metaplasia upon development of gastric carcinoma.". Cancer 50 (12): 2854-8. PMID 7139576.
  23. ↑ Satoh, K.; Mutoh, H.; Eda, A.; Yanaka, I.; Osawa, H.; Honda, S.; Kawata, H.; Kihira, K. et al. (Jun 2002). "Aberrant expression of CDX2 in the gastric mucosa with and without intestinal metaplasia: effect of eradication of Helicobacter pylori.". Helicobacter 7 (3): 192-8. PMID 12047325.
  24. ↑ Lin J, McKenna BJ, Appelman HD (November 2010). "Morphologic findings in upper gastrointestinal biopsies of patients with ulcerative colitis: a controlled study". Am. J. Surg. Pathol. 34 (11): 1672–7. doi:10.1097/PAS.0b013e3181f3de93. PMID 20962621.
  25. ↑ RK. 13 December 2010.
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  29. ↑ ALS. 5 February 2009.
  30. ↑ El-Zimaity. 18 October 2010.
  31. ↑ 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. 69. ISBN 978-0443066573.
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  33. ↑ Oh, R.; Brown, DL. (Mar 2003). "Vitamin B12 deficiency.". Am Fam Physician 67 (5): 979-86. PMID 12643357.
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  42. ↑ 42.0 42.1 Drude, RB.; Balart, LA.; Herrington, JP.; Beckman, EN.; Burns, TW. (Jun 1982). "Gastric xanthoma: histologic similarity to signet ring cell carcinoma.". J Clin Gastroenterol 4 (3): 217-21. PMID 6284833.
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  44. ↑ 44.0 44.1 44.2 Daum, O.; Hatlova, J.; Mandys, V.; Grossmann, P.; Mukensnabl, P.; Benes, Z.; Michal, M. (May 2010). "Comparison of morphological, immunohistochemical, and molecular genetic features of inflammatory fibroid polyps (Vanek's tumors).". Virchows Arch 456 (5): 491-7. doi:10.1007/s00428-010-0914-8. PMID 20393746.
  45. ↑ 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. 115. ISBN 978-0443066573.
  46. ↑ URL: http://dictionary.reference.com/browse/concentric. Accessed on: 29 November 2011.
  47. ↑ Kolodziejczyk, P.; Yao, T.; Tsuneyoshi, M. (Nov 1993). "Inflammatory fibroid polyp of the stomach. A special reference to an immunohistochemical profile of 42 cases.". Am J Surg Pathol 17 (11): 1159-68. PMID 8214261.
  48. ↑ Ozolek, JA.; Sasatomi, E.; Swalsky, PA.; Rao, U.; Krasinskas, A.; Finkelstein, SD. (Mar 2004). "Inflammatory fibroid polyps of the gastrointestinal tract: clinical, pathologic, and molecular characteristics.". Appl Immunohistochem Mol Morphol 12 (1): 59-66. PMID 15163021.
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  53. ↑ 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.
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