Difference between revisions of "Stomach"
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*Helicobacter pylori IHC stain +ve. | *Helicobacter pylori IHC stain +ve. | ||
==Intestinal metaplasia== | ==Intestinal metaplasia of the stomach== | ||
*[[AKA]] ''gastric intestinal metaplasia''. | |||
*Abbreviated ''IM''. | |||
===General=== | ===General=== | ||
*Often part of surgical pathology report, e.g. "negative for intestinal metaplasia" or "intestinal metaplasia present". | *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 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.<ref name=pmid12477745>{{Cite journal | last1 = Walker | first1 = MM. | title = Is intestinal metaplasia of the stomach reversible? | journal = Gut | volume = 52 | issue = 1 | pages = 1-4 | month = Jan | year = 2003 | doi = | PMID = 12477745 | PMC = 1773527 | |||
}}</ref> | |||
Significance: | |||
*Moderate risk increase for carcinoma; risk less than for Barrett's esophagus.<ref name=pmid20203636>{{cite journal |author=Correa P, Piazuelo MB, Wilson KT |title=Pathology of gastric intestinal metaplasia: clinical implications |journal=Am. J. Gastroenterol. |volume=105 |issue=3 |pages=493–8 |year=2010 |month=March |pmid=20203636 |pmc=2895407 |doi=10.1038/ajg.2009.728 |url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895407/?tool=pubmed}}</ref> | *Moderate risk increase for carcinoma; risk less than for Barrett's esophagus.<ref name=pmid20203636>{{cite journal |author=Correa P, Piazuelo MB, Wilson KT |title=Pathology of gastric intestinal metaplasia: clinical implications |journal=Am. J. Gastroenterol. |volume=105 |issue=3 |pages=493–8 |year=2010 |month=March |pmid=20203636 |pmc=2895407 |doi=10.1038/ajg.2009.728 |url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895407/?tool=pubmed}}</ref> | ||
**Odds ratio for corpus (~5.8x) higher than antrum (2.3x) when compared to individuals without IM.<ref name=pmid21575058>{{Cite journal | last1 = Sakitani | first1 = K. | last2 = Hirata | first2 = Y. | last3 = Watabe | first3 = H. | last4 = Yamada | first4 = A. | last5 = Sugimoto | first5 = T. | last6 = Yamaji | first6 = Y. | last7 = Yoshida | first7 = H. | last8 = Maeda | first8 = S. | last9 = Omata | first9 = M. | title = Gastric cancer risk according to the distribution of intestinal metaplasia and neutrophil infiltration. | journal = J Gastroenterol Hepatol | volume = 26 | issue = 10 | pages = 1570-5 | month = Oct | year = 2011 | doi = 10.1111/j.1440-1746.2011.06767.x | PMID = 21575058 }}</ref> | |||
===Microscopic=== | ===Microscopic=== | ||
Features: | Features: | ||
*Goblet cells are present in the stomach.<ref>URL: [http://esynopsis.uchc.edu/eAtlas/GI/1280.htm http://esynopsis.uchc.edu/eAtlas/GI/1280.htm]. Accessed on: 16 August 2010.</ref> | *Goblet cells are present in the stomach.<ref>URL: [http://esynopsis.uchc.edu/eAtlas/GI/1280.htm http://esynopsis.uchc.edu/eAtlas/GI/1280.htm]. Accessed on: 16 August 2010.</ref> | ||
**With H&E vacuole may stain greyish. | **With H&E vacuole may stain greyish. | ||
Revision as of 14:32, 11 March 2012
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.
- AKA antrum.
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-specific disease
Gastric ulcer
General
- May be benign (e.g. peptic ulcer disease) or malignant (gastric carcinoma).
Complications:
- Hemorrhage.
- Obstruction.
- Perforation.
Gross
- Epithelial defect:
- Heaped edges - suggestive of cancer.
- Punched-out edges - suggestive of a benign process.
Microscopic
Features:
- Depends on the etiology.
Non-neoplastic disease
Gastritis
Etiology
A specific cause is uncommonly identified histologically.
Gastritis causes:[9]
- Infectious:
- H. pylori infection.
- Tuberculosis.
- Salmonellosis.
- CMV.
- Endocrine-related:
- Pernicious anemia.
- Diabetes - 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:
- Drugs,[10] esp. NSAIDs.
- Infectious.
- Inflammatory bowel disease.
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:
Lymphocytic gastritis
The DDx is limited:
- Helicobacter gastritis.
- Celiac disease.
- NSAIDs.
- Idiopathic.
Sydney criteria for gastritis
A bunch of pathologists in Sydney came-up with criteria... and these were revised in Houston.[11]
Classification
Updated Sydney classification:[11]
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.[12]
Severity
The Sydney group suggests grading severity with the following language:[11]
- 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.[11]):
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:
- Helicobacter pylori - most common.
- Helicobacter heilmannii.
Epidemiologic associations - Helicobacter infections are associated with:[13]
- Gastritis.
- Peptic ulcers.
- Cancer.
- Carcinoma.
- MALT lymphoma.
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.[14]
- 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).[15]
Stains
- Cresyl violet stain - background and organisms blue.
- Warthin-Starry stain - background yellow, organisms black.
IHC
- Helicobacter pylori IHC stain +ve.
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.[16]
Significance:
- Moderate risk increase for carcinoma; risk less than for Barrett's esophagus.[17]
- Odds ratio for corpus (~5.8x) higher than antrum (2.3x) when compared to individuals without IM.[18]
Microscopic
Features:
- Goblet cells are present in the stomach.[19]
- With H&E vacuole may stain greyish.
Image:
Inflammatory bowel disease & the stomach
- Histopathologic findings are usually non-specific.
- Conventional thinking was upper GI involvement = Crohn's disease; this is changing.[20]
Microscopic
Features:[21]
- 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
- Abbreviated GAVE.
- Antrum lesion - due dilated capillaries.
- AKA watermelon stomach - due to characteristic endoscopic appearance.[22]
Gross/endoscopic appearance
- Linear red streaks in antrum - oriented toward the pyloric valve... vaguely resembles a watermelon.
Endoscopic images:
Microscopic
Features:[23]
- Fibrin thrombi - characteristic feature.
- Dilated capillaries in lamina propria.
Images:
Reactive gastropathy
General
- AKA chemical gastropathy,[24] 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:[25]
- Excess acid.
- EtOH.
- Bile.
- H. pylori.
- Drugs:[24]
- Iron (brown pigment on histology).
- NSAIDs - synergistic effect with corticosteroids.
Drugs that cause erosions and/or ulcers -- adapted from Genta:[24]
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
- 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:
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.
Lymphocytic gastritis
General
DDx:
- Celiac disease.
- Check duodenum.
- H. pylori.
- HIV/AIDS.
Microscopic
Features:[27]
- 25 lymphocytes / 100 epithelial cells.
Pernicious anemia
General
- Gastric atrophy.
- Loss of parietal cells.
- Intrinsic factor antibodies present in serum.
- Intrinsic factor -- absorbs vitamin B12.
- Macrocytic anemia.
Microscopic
Features:
- Corpus predominant inflammation.
- Increased G cells in the antrum.
- Increased gastrin level to try and stimulate (missing) parietal cells.
- See gastric atrophy section.
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
General
- AKA Gastritic cystica profunda. (???)
- May be assoc. with glandular proliferation as well.[28] (???)
- 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.[29]
Clinical:[30]
- Classic: nausea, emesis, abdominal pain and peripheral edema.
Other:
- Gastric mass (may mimic cancer).
- Hypochlorhydria.
- Protein loss - leads to peripheral edema.
Microscopic
Features:[29]
- Foveolar cell hyperplasia - key feature.
DDx:
Images:
Gastric xanthoma
General
- Uncommon.
- Benign.
Gross/endoscopic
Microscopic
Features:[32]
- Collections of gastric lamina propria with lipid-laden macrophages.
DDx:
- Signet ring cell carcinoma.[33]
- Whipple disease.
- MAC infection.
Images:
IHC
- CD68 +ve.
- Panker (AE1/AE3) -ve.
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.
- Adenomatous polyp.
Inflammatory fibroid polyp
General
- Benign.
- Through-out GI tract.
- Can be thought of as granulation tissue-like.[34]
Microscopic
Features:[35]
- Proliferating spindle cells (fibroid) - key feature.
- Inflammation:
- Eosinophils - often prominent.
- +/-Leiomyoma/schwannoma-like areas - with nuclear palisading.[34]
- +/-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.[37]
Images:
IHC
Features:[35]
- CD34 +ve.
- There is a CD34 -ve variant.
- Vimentin +ve -- diffuse.[38]
Others:
- CD117 -ve.[39]
- S100 -ve.
Molecular
- A subset have mutations in PDGFRA.[35]
Hyperplastic polyp of the stomach
- AKA gastric hyperplastic polyp.
General
- Benign.
- Most common gastric polyp.[40]
Microscopic
Features:[41]
- 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:
- Ménétrier's disease[42] (hyperplastic hypersecretory gastropathy).
- Juvenile polyp.[40]
- Peutz-Jeghers polyp.
Images:
- www:
- WC:
Adenomatous polyps
General
- Divided into "gastric" and "intestinal type". (???)
- Can be grouped various ways.[42] (???)
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
Clinical significance
- Weak association with FAP (familial adenomatous polyposis).[43][44]
- Associated with chronic proton pump inhibitors (PPI) use -- approximately 4x risk.[45]
Notes:
- Animal studies suggested PPIs cause neuroendocrine tumours -- but this has not been found in humans.[46]
Microscopic
Features:[47]
- 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:[48]
- Benign.
- Indefinite for gastric epithelial dysplasia.
- Low-grade gastric epithelial dysplasia.
- High-grade gastric epithelial dysplasia.
- 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:
- High grade gastric dysplasia - low mag. (WC).
- High grade gastric dysplasia - very high mag. (WC).
- Gastric adenoma (WC).
Neoplastic rare
Gastric calcifying fibrous tumour
Gastric cancer
Gastric lymphoma
General
- Associated with helicobacter infection.[49]
- 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.[50]
- 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;[51] 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)).[54]
- Surgery - if triple therapy fails.
Review paper: PMID 16950858.
Familial gastric carcinoma
Gastric adenocarcinoma
General
Epidemiology:
- Associated with helicobacter infections, i.e. helicobacter gastritis.
- 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.
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).
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.
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
- ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/CorePages/GIT/git.htm. Accessed on: 3 December 2010.
- ↑ 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.
- ↑ http://www.histology-world.com/stains/stains.htm
- ↑ http://www.histology-world.com/stains/stains.htm
- ↑ 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.
- ↑ 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.
- ↑ 11.0 11.1 11.2 11.3 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.
- ↑ http://en.wikipedia.org/wiki/Angular_incisure
- ↑ 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.
- ↑ 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.
- ↑ 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/.
- ↑ 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.
- ↑ 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.
- ↑ URL: http://esynopsis.uchc.edu/eAtlas/GI/1280.htm. Accessed on: 16 August 2010.
- ↑ 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.
- ↑ RK. 13 December 2010.
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- ↑ ALS. 5 February 2009.
- ↑ El-Zimaity. 18 October 2010.
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- ↑ 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.