Difference between revisions of "Esophagus"
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====Classification==== | ====Classification==== | ||
#Indefinite for dysplasia. | |||
* | #*[[Diagnosis]] used in the context of uncertainty (like ''[[gynecologic cytopathology|ASCUS]]'' and ''[[prostate gland|ASAP]]''); the classic reason for its use is: the surface (epithelium) cannot be seen (which precludes assessment of maturation); may be used in the context of inflammation. | ||
#Low grade dysplasia. | |||
#High grade dysplasia. | |||
====Management==== | ====Management==== | ||
Revision as of 11:27, 10 October 2012
Esophagus connects the pharynx to the stomach. It is afflicted by tumours on occasion. For some reason or another, it seems everyone at SMH gets a esophageal biopsy... yet patients at SB don't have esophagi.
Normal
General:
- Stratified squamous non-keratinized epithelium.
Normal (esophageal) squamous epithelium:
- Should "mature" to the surface like good stratified squamous epithelium does.
- No nuclei at luminal surface.
- Cells should become less hyperchromatic as you go toward the lumen.
- Mitoses should be rare and should NOT be above the basal layer.
- Inflammatory cells should be very rare.
Diagnoses
Common
- Normal.
- Metaplasia (Barrett's esophagus).
- Dysplasia.
- Adenocarcinoma.
Less common
- Squamous cell carcinoma.
- Eosinophilic esophagitis.
- Candidiasis.
- CMV esophagitis.
Tabular summary
Simplified overview
| Entity | Key feature | Other features | IHC/Special | Clinical | Image |
| Normal | squamous epi. matures to surface | no inflammation, no atypia | - | - | [1] |
| GERD | inflammation (eosinophils, lymphocytes) | elongated (epithelial) papillae, basal cell hyperplasia | incr. risk of Barrett's | ||
| Eosinophilic esophagitis | abundant eosinophils | elongated (epithelial) papillae, basal cell hyperplasia, lymphocytes | unresponsive to PPIs | microscopic, endoscopic | |
| Barrett's type change | goblet cells | no dysplasia | Alcian blue +ve | incr. risk of adenocarcinoma | [2] |
| Dysplasia, low grade | nuclear crowding at surface | hyperchromasia, mild arch. complexity, no necrosis | incr. risk of carcinoma | ||
| Dysplasia, high grade | cribriforming and/or necrosis | nuclei often round & large, hyperchromasia | marked incr. risk of carcinoma |
![[1]](http://commons.wikimedia.org/wiki/File:Tinci%C3%B3n_hematoxilina-eosina.jpg){kind=link}
![[2]](http://commons.wikimedia.org/wiki/File:Barretts_alcian_blue.jpg){kind=link}
Columnar dysplasia
| Entity | Surface maturation | Architecture | Cytology | Other | Clinical | Image |
| Normal | matures | round glands | no nuclear atypia | - | - | Image |
| Barrett's eosphagus | matures | round glands, normal gland density | +/-scant nuclear atypia | goblet cells | clinical diagnosis | Image |
| Indefinite for columnar dysplasia | minimal maturation or cannot see surface | round glands, normal gland density | mild nuclear atypia, nuclear pseudostratification, no necrosis | - | follow-up | Image |
| Low-grade columnar dysplasia | minimal-to-scant maturation | round glands, +/-rare budding, increased gland density | mild-to-moderate nuclear atypia, nuclear pseudostratification, no necrosis | - | follow-up | Image |
| High-grade columnar dysplasia | no maturation | incr. density of irregular glands with budding and/or rare cribriforming and/or gland dilation | moderate-to-marked nuclear atypia (usu. plump round nuclei), hyperchromasia, +/-necrosis | - | EMR, surgery | Image |
| Intramucosal adenocarcinoma | no maturation | single cells or back-to-back irregular glands with budding and/or cribriforming and/or gland dilation or glands with long axis along muscularis mucosae | moderate-to-marked nuclear atypia - usu. round large nuclei, hyperchromasia, +/-necrosis | - | EMR, surgery | Image |
Columnar dysplasia - another table
| Feature | Indefinite for columnar dysplasia | Low-grade columnar dysplasia | High-grade columnar dysplasia | Intramucosal carcinoma (IMCa) | Utility |
|---|---|---|---|---|---|
| Depth of glands | superficial only | superficial only | superficial/deep | deep | low vs. high |
| Gland density | normal | near normal | increased | back-to-back | low vs. high vs. IMCa |
| Gland morphology | round | round | irregular/rare cribriforming | irregular/cribriform/sheeting | low vs. high vs. IMCa |
| Necrosis | none | none | may be present | may be present | low vs. high & IMCa |
| Hyperchromasia | +/- | present | present | present | indef. vs. low |
| Palisaded/crowded nuclei | present | present | absent/present | uncommon | low vs. high |
| Round nuclei + enlargement | absent | absent | present/absent | present | low vs. high |
| Desmoplasia | absent | absent | absent | +/- (uncommon) | high vs. IMCa |
| Surface involvement | present (required) | present (required) | +/- | +/- | low vs. high |
Indications
- Pyrosis = heartburn.[1]
Infectious esophagitis
Main article: Microorganisms
Is a relatively common problem, especially in those that live at the margins (EtOH abusers) and immunosuppressed individuals (HIV/AIDS).
Useful stains
- PAS.
- Gram stain.
Overview
Candida esophagitis
Main article: Candidiasis
- AKA esophageal candidiasis.
Gross (endoscopic)
Features:
- White patches.
DDx (endoscopic):[2]
Microscopic
Features:
- Worm-like micro-organisms.
- Pseudohyphae (single cells).
- Thickness ~ 1/3-1/2 of squamous cell nucleus.
- Should be within (squamous) epithelium.
- On top of epithelium does not count,[3] i.e. it is likely an artifact.
Image: Esophageal candidiasis (WC).
_PAS_stain.jpg){kind=link}
Cytomegalovirus esophagitis
Microscopic
Features:
- Classically at the base of the ulcer; within endothelial cells - key point.
Note:
- Biopsying the the base of an ulcer usually just yields (non-diagnostic) necrotic debris; so, clinicians are told to biopsy the edge of the lesion. A suspected CMV infection is the exception to this rule!
Herpes esophagitis
General
Etiology:
Gross/endoscopic
Features:
- Ulcers with a "punched-out" appearance with a brown/red edge.
Images:
- Herpes esophagitis - gross (utah.edu).
- Herpes esophagitis - endoscopy (gastrohep.com).
- Herpes eosphagitis - endoscopy (WC).
Microscopic
Features (3 Ms):
- Moulding.
- Multinucleation.
- Margination of chromatin.
Images:
Human papillomavirus esophagitis
General:
Microscopic
Features:
- Koilocytes:
- Perinuclear clearing.
- Nuclear changes.
- Size similar (or larger) to those in the basal layer of the epithelium.
- Nuclear enlargement should be evident on low power, i.e. 25x. [7]
- Central location - nucleus should be smack in the middle of the cell.
Images:
Other
Gastroesophageal reflux disease
General
- Abbreviated GERD and GORD (gastro-oesophageal reflux disease).
Clinical:
- Treated with proton pump inhibitors (PPIs).
Microscopic
Features:
- Basal cell hyperplasia;[4] > 3 cells thick or >15% of epithelial thickness.
- Papillae elongated; papillae reach into the top 1/3 of the epithelial layer.[5]
- Inflammation, esp. eosinophils, lymphocytes with convoluted nuclei ("squiggle cells").
- +/-Spongiosis.
- +/-Apoptotic cells.[6]
Notes:
- Intraepithelial cells with irregular nuclear contours, "squiggle cells" (T lymphocytes[7]), may mimic neutrophils.
DDx:
- Eosinophilic esophagitis - characterized by similar histomorphologic features. The key difference is: more eosinophils.
Images:
Eosinophilic esophagitis
- Abbreviated EE.
General
- The current thinking is that it is a clinico-pathologic diagnosis.[8]
Clinical:
Treatment:
- Avoid exacerbating antigens.
- Topical corticosteroids, e.g. fluticasone.
Biopsies:
- Should be taken from: upper, mid, lower and submitted in separate containers (eosinophilia present through-out-- to differentiate from GERD).
Associations:
- Atopy.[11]
- Celiac disease.[12]
- Oral antigens, i.e. particular foods.[9]
- Familial association.[9]
Gross/endoscopic
DDx (endoscopic):
Image:
Microscopic
Features:[11]
- Mucosa with "abundant eosinophils".
- Basal cell hyperplasia.
- Three cells thick or >15% of epithelial thickness.
- Papillae elongated.
- Papillae that reach into the top 1/3 of the epithelial layer - definition for GERD.[5]
Notes "abundant eosinophils":
- Criteria for number of eosinophils/area is highly variable; there is a 23X fold variation in published values and only 11% of studies actually define an area (most studies, embarassing for pathologists that understand this issue, only give the number of eosinophils per "HPF")![15]
- The group that published the article cited above did another one... [16]
- The most commonly reported cut points are 15, 20 and 24 eosinophils/HPF, without defining HPF.[15]
- The Foundation Series book[11] says: "> 20/HPF"; VL sees this definition as garbage, as "HPF" is not defined (see HPFitis).
- There is a consensus paper[17] that makes note of HPFitis... and then goes on to ignore to whole issue by defining EE as 15/HPF. It blows my mind that the people could be so will fully blind and that the idiotic reviewers didn't understand this.
- Most resident microscopes at the Toronto teaching hospitals have 22 mm eye pieces and have for their highest magnification objective a 40X. De facto, this means most people in Toronto are using the Liacouras et al. definition.[18]
DDx:[2]
- Gastroesophageal reflux disease - no mid and proximal involvement.
- Infectious esophagitis.
- Eosinophilic gastroenteritis.
- Hypereosinophilic syndrome.
Images:
- Eosinophilic esophagitis - very high mag. (WC).
- Eosinophilic esophagitis - high mag. (WC).
- Eosinophilic esophagitis (nih.gov).
- EE versus GERD (archivesofpathology.org).[8]
Erosive esophagitis
DDx
- Infections.
- Crohn's disease.
- Pill esophagitis.
Work-up
Pill esophagitis
Classic causes:
- Alendronate (Fosamax) - for osteoporosis.
- Iron (can be demonstrated with Prussian blue stain).
- Doxycycline.
Preneoplastic
Barrett esophagus
- Intestinal metaplasia of the esophagus redirects here.
- Abbreviated BE.
General
- Diagnosis is made by clinicans not pathologists.
- A common histologic correlate is metaplastic transformation of stratified squamous epithelium to simple columnar epithelium with goblet cells.
- Associated with chronic reflux - see: gastroesophageal reflux disease.
Significance of Barrett's esophagus:
- Increased risk of adenocarcinoma of the esophagus.
- Need on-going surveillance, i.e. long term follow-up/repeat esophagogastroduodenoscopy.
Gross
- Red/light brown esophageal mucosa.
- Normal mucosa = light pink.
Image:
Microscopic
Features:
- Columnar epithelium.
- Goblets cells - key feature.
- +/-Mild hyperchromasia.
- +/-Reactive squamous epithelium suggestive of reflux.
Images:
Stains
- Alcian blue (pH 2.5)[21] - goblet cells +ve.
Sign-out
ESOPHAGUS, DISTAL, BIOPSY:
- COLUMNAR EPITHELIUM WITH MODERATE CHRONIC INFLAMMATION AND INTESTINAL METAPLASIA, SEE COMMENT.
- SQUAMOUS EPITHELIUM WITHIN NORMAL LIMITS.
- NEGATIVE FOR DYSPLASIA AND MALIGNANCY.
Comment:
The findings are consistent with Barrett's esophagus in the appropriate endoscopic setting.
Neoplastic
Columnar dysplasia of the esophagus
- AKA esophageal columnar dysplasia, abbreviated ECD.[22]
- AKA dysplasia in the columnar-lined esophagus.[23]
- AKA columnar epithelial dysplasia.[24]
General
- Arises in the setting of Barrett esophagus.
Classification
- Indefinite for dysplasia.
- Low grade dysplasia.
- High grade dysplasia.
Management
Low grade dysplasia.
- Follow-up.
High grade dysplasia.
- Endoscopic mucosal resection.[25]
- Surgical resection.
Microscopic
Features to assess:[26]
- Lack of surface maturation.
- Lack of lighter staining at surface.
- Nuclear crowding at surface.
- Nuclei at the surface not smaller.
- Architecture - esp. at low power.
- Glands not round.
- Low-grade feature: gland budding.
- High-grade features: cribriforming, cystic dilation, necrotic debris.
- Gland density:
- Increased & round - think low-grade dysplasia.
- Increased & irregular - think high-grade dysplasia.
- Glands not round.
- Cytology, esp. at high magnification.
- Nuclear abnormalities in: size, staining, shape.
- Loss of "nuclear polarity" = high-grade feature
- Loss of palisaded appearance, rounding-up of nuclei.
- Inflammation, erosions & ulceration.
- Marked inflammation should prompt consideration of knocking down the diagnosis one step, i.e. low-grade becomes indefinite or high-grade becomes low-grade.
Negatives:
- No desmoplasia.
- Stromal fibrotic reaction to the tumour.
- Desmoplasia is rare in the superficial esophagus.[27]
- Stromal fibrotic reaction to the tumour.
- No single cells.
- No extensive back-to-back glands.
Notes:
- Changes similar to those see in colorectal tubular adenomas; however, what would be low-grade dysplasia in the rectum is high-grade dysplasia in the esophagus.
- Presence of goblet cells suggests it is not dysplasia.[28]
- Desmoplasia present = invasive adenocarcinoma.[29]
- Some literature suggests community pathologists should not make this call, i.e. it should be diagnosed by an expert.[30]
Image:
Sign out
ESOPHAGUS, DISTAL, BIOPSY: - LOW-GRADE COLUMNAR EPITHELIAL DYSPLASIA, SEE COMMENT. - COLUMNAR EPITHELIUM WITH GOBLET CELL METAPLASIA. - REACTIVE SQUAMOUS EPITHELIUM. COMMENT: This was reviewed with Dr. X and they agree with the diagnosis.
Leiomyoma of the esophagus
Main article: Leiomyoma
General
- Benign.
- Uncommon.
- Before the time of GISTs - this was a relatively common diagnosis.
- Like leiomyomas elswhere.
Microscopic
- See: Leiomyoma.
DDx:
Gastrointestinal stromal tumour
Main article: Gastrointestinal stromal tumour
Cancer
General
- Proximal esophagus: squamous cell carcinoma.
- Distal esophagus: adenocarcinoma arising from Barrett's esophagus.
Risks:
Squamous cell carcinoma of the esophagus
- AKA esophageal squamous cell carcinoma, abbreviated esophageal SCC.
Main article: Squamous carcinoma
General
- Like squamous cell carcinoma elsewhere.
Risk factors:[32]
- Alcohol consumption.
- Tobacco use.
- Food with nitrosamines.
- Burning-hot beverages.
Note:
- Reflux is not a risk factor for esophageal SCC.
Microscopic
- See Squamous carcinoma.
Note:
- Just to make things confusing, the Staging of early SCC differs from that of early adenocarcinoma!
Esophageal adenocarcinoma
- AKA adenocarcinoma of the esophagus.
General
- Often a prognosis poor - as diagnosed in a late stage.
- May be difficult to distinguish from adenocarcinoma of the stomach.
- By convention (in the CAP checklist) gastroesophageal junction carcinomas are staged as esophageal carcinomas.[33]
Tx
- Adenocarcinoma in situ (AIS) - may be treated with endoscopic mucosal resection & follow-up.[25]
- Surgery - esophagectomy.
Esophagus vs. stomach
The convention is it's esophageal if both of the following are true:[34]
- Epicenter of tumour is in the esophagus.
- Barrett's mucosa is present.
Microscopic
Features:
- Adenocarcinoma:
- Cell clusters that form glands.
- Nuclear atypia of malignancy:
- Size variation.
- Shape variation.
- Staining variation.
- Mitoses common.
Images:
Grading
Graded like other adenocarcinoma:[34]
- >95 % of tumour in glandular arrangement = well-differentiated.
- 95-50% of tumour in glandular arrangement= moderately-differentiated.
- <50% of tumour in glandular arrangment = poorly-differentiated.
Staging
Early esophageal adenocarcinoma has its own staging system:[35][36]
- M1 = lamina propria.
- M2 = superficial muscularis mucosae.
- M3 = submucosa.
- M4 = muscularis propria.
IHC
- CK7 +ve.
- CK20 +ve.
To rule-out SCC:
- p63 -ve.
- HWMK -ve.
Weird stuff
- Inflammatory polyp - assoc. trauma/previous intervention.
- Giant fibrovascular polyp - loose connective tissue covered with squamous epithelium.
- Granular cell tumour.
- Squamous papilloma - koilocytes.
- Heterotopic gastric mucosa ("inlet patch") - benign appearing gastric mucosa.
Granular cell tumour
Main article: Granular cell tumour
Microscopic
Features:
- Abundant eosinophilic granular cytoplasm key feature.
- Granules:
- Size: 1-3 micrometers.
- Poorly demarcated.
- Granules:
- Usu. bland (cytologically non-malignant) nuclei.
Images:
_skin.jpg){kind=link}
_S-100.JPG){kind=link}
Esophagitis dissecans superficials
General
- Rare & benign condition that resolves without last pathology.[37]
- Case report - chronic with strictures.[38]
- Sloughing of large fragments of the esophageal mucosa - seen on endoscopy.
Microscopic
Features:[37]
- Flaking of superficial squamous epithelium.
- Focal bullous separation of the layers.
- Parakeratosis.
- Variable acute or chronic inflammation.
Glycogenic acanthosis of the esophagus
General
- Uncommon.
- Benign.
- Possible association with ingestion of hot liquids.[39]
Gross/endoscopic
- Distinctive endoscopic appearance - grey/white raised lesion.[39]
Microscopic
Features:[39]
- Squamous epithelium with:
- Superficial clearing of the cytoplasm.
- Thickening.
Images:
Achalasia
General
- Uncommon.
- Risk factor for squamous cell carcinoma (in men and women) and adenocarcinoma (in men).[40]
Microscopic
Features:
- Mucosa usually normal.[41]
See also
References
- ↑ URL: http://dictionary.reference.com/browse/pyrosis. Accessed on: 21 June 2010.
- ↑ 2.0 2.1 Odze, Robert D.; Goldblum, John R. (2009). Surgical pathology of the GI tract, liver, biliary tract and pancreas (2nd ed.). Saunders. pp. 244. ISBN 978-1416040590.
- ↑ ALS. 4 October 2010.
- ↑ Steiner, SJ.; Kernek, KM.; Fitzgerald, JF. (May 2006). "Severity of basal cell hyperplasia differs in reflux versus eosinophilic esophagitis.". J Pediatr Gastroenterol Nutr 42 (5): 506-9. doi:10.1097/01.mpg.0000221906.06899.1b. PMID 16707971.
- ↑ 5.0 5.1 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. 804. ISBN 0-7216-0187-1.
- ↑ Wetscher GJ, Schwelberger H, Unger A, et al. (December 1998). "Reflux-induced apoptosis of the esophageal mucosa is inhibited in Barrett's epithelium". Am. J. Surg. 176 (6): 569–73. PMID 9926792.
- ↑ Cucchiara, S.; D'Armiento, F.; Alfieri, E.; Insabato, L.; Minella, R.; De Magistris, TM.; Scoppa, A. (Nov 1995). "Intraepithelial cells with irregular nuclear contours as a marker of esophagitis in children with gastroesophageal reflux disease.". Dig Dis Sci 40 (11): 2305-11. PMID 7587806.
- ↑ 8.0 8.1 8.2 Genevay, M.; Rubbia-Brandt, L.; Rougemont, AL. (Jun 2010). "Do eosinophil numbers differentiate eosinophilic esophagitis from gastroesophageal reflux disease?". Arch Pathol Lab Med 134 (6): 815-25. doi:10.1043/1543-2165-134.6.815. PMID 20524860. http://www.archivesofpathology.org/doi/full/10.1043/1543-2165-134.6.815.
- ↑ 9.0 9.1 9.2 Rothenberg, ME. (Oct 2009). "Biology and treatment of eosinophilic esophagitis.". Gastroenterology 137 (4): 1238-49. doi:10.1053/j.gastro.2009.07.007. PMID 19596009.
- ↑ URL: http://www.medicinenet.com/eosinophilic_esophagitis/page2.htm#tocc. Accessed on: 1 December 2009.
- ↑ 11.0 11.1 11.2 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. 19. ISBN 978-0443066573.
- ↑ Leslie C, Mews C, Charles A, Ravikumara M (April 2010). "Celiac disease and eosinophilic esophagitis: a true association". J. Pediatr. Gastroenterol. Nutr. 50 (4): 397–9. doi:10.1097/MPG.0b013e3181a70af4. PMID 19841598.
- ↑ Al-Hussaini, AA.; Semaan, T.; El Hag, IA.. "Esophageal trachealization: a feature of eosinophilic esophagitis.". Saudi J Gastroenterol 15 (3): 193-5. doi:10.4103/1319-3767.54747. PMID 19636182.
- ↑ URL: http://www.ajronline.org/cgi/reprint/164/4/900.pdf. Accessed on: 4 October 2010.
- ↑ 15.0 15.1 Dellon ES, Aderoju A, Woosley JT, Sandler RS, Shaheen NJ (October 2007). "Variability in diagnostic criteria for eosinophilic esophagitis: a systematic review". Am. J. Gastroenterol. 102 (10): 2300–13. doi:10.1111/j.1572-0241.2007.01396.x. PMID 17617209.
- ↑ PMID 19830560.
- ↑ Furuta GT, Liacouras CA, Collins MH, et al. (October 2007). "Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment". Gastroenterology 133 (4): 1342–63. doi:10.1053/j.gastro.2007.08.017. PMID 17919504.
- ↑ Liacouras CA, Spergel JM, Ruchelli E, et al. (December 2005). "Eosinophilic esophagitis: a 10-year experience in 381 children". Clin. Gastroenterol. Hepatol. 3 (12): 1198–206. PMID 16361045.
- ↑ Riddell, RH.; Odze, RD. (Oct 2009). "Definition of Barrett's esophagus: time for a rethink--is intestinal metaplasia dead?". Am J Gastroenterol 104 (10): 2588-94. doi:10.1038/ajg.2009.390. PMID 19623166.
- ↑ Chandrasoma, P.; Wijetunge, S.; DeMeester, S.; Ma, Y.; Hagen, J.; Zamis, L.; DeMeester, T. (Jan 2012). "Columnar-lined esophagus without intestinal metaplasia has no proven risk of adenocarcinoma.". Am J Surg Pathol 36 (1): 1-7. doi:10.1097/PAS.0b013e31822a5a2c. PMID 21959311.
- ↑ Voutilainen, M.; Färkkilä, M.; Juhola, M.; Mecklin, JP.; Sipponen, P. (Nov 1999). "Complete and incomplete intestinal metaplasia at the oesophagogastric junction: prevalences and associations with endoscopic erosive oesophagitis and gastritis.". Gut 45 (5): 644-8. PMID 10517897.
- ↑ Feng, W.; Zhou, Z.; Peters, JH.; Khoury, T.; Zhai, Q.; Wei, Q.; Truong, CD.; Song, SW. et al. (Aug 2011). "Expression of insulin-like growth factor II mRNA-binding protein 3 in human esophageal adenocarcinoma and its precursor lesions.". Arch Pathol Lab Med 135 (8): 1024-31. doi:10.5858/2009-0617-OAR2. PMID 21809994.
- ↑ Levine, DS. (Sep 1997). "Management of dysplasia in the columnar-lined esophagus.". Gastroenterol Clin North Am 26 (3): 613-34. PMID 9309409.
- ↑ Hamilton, SR.; Smith, RR. (Mar 1987). "The relationship between columnar epithelial dysplasia and invasive adenocarcinoma arising in Barrett's esophagus.". Am J Clin Pathol 87 (3): 301-12. PMID 3825997.
- ↑ 25.0 25.1 Sampliner RE (March 2009). "Endoscopic Therapy for Barrett's Esophagus". Clin. Gastroenterol. Hepatol.. doi:10.1016/j.cgh.2009.03.011. PMID 19306943.
- ↑ 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. 46. ISBN 978-0443066573.
- ↑ 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. 49. ISBN 978-0443066573.
- ↑ GAG. January 2009.
- ↑ 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. 54. ISBN 978-0443066573.
- ↑ Alikhan, M.; Rex, D.; Khan, A.; Rahmani, E.; Cummings, O.; Ulbright, TM. (Jul 1999). "Variable pathologic interpretation of columnar lined esophagus by general pathologists in community practice.". Gastrointest Endosc 50 (1): 23-6. PMID 10385717.
- ↑ URL: http://www.hopkins-gi.org/GDL_Disease.aspx?CurrentUDV=31&GDL_Disease_ID=46159D68-6ED3-4F76-895B-99D8BBBB46EF&GDL_DC_ID=E25BDF77-223D-4B6F-9700-5BE41DBDE28B. Accessed on: 7 August 2011.
- ↑ Lefkowitch, Jay H. (2006). Anatomic Pathology Board Review (1st ed.). Saunders. pp. 104 Q1. ISBN 978-1416025887.
- ↑ URL: http://www.cap.org/apps/docs/committees/cancer/cancer_protocols/2011/Esophagus_11protocol.pdf. Accessed on: 6 April 2012.
- ↑ 34.0 34.1 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 168. ISBN 978-0781765275.
- ↑ Pech, O.; May, A.; Rabenstein, T.; Ell, C. (Nov 2007). "Endoscopic resection of early oesophageal cancer.". Gut 56 (11): 1625-34. doi:10.1136/gut.2006.112110. PMC 2095648. PMID 17938435. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2095648/.
- ↑ Thosani, N.; Singh, H.; Kapadia, A.; Ochi, N.; Lee, JH.; Ajani, J.; Swisher, SG.; Hofstetter, WL. et al. (Nov 2011). "Diagnostic accuracy of EUS in differentiating mucosal versus submucosal invasion of superficial esophageal cancers: a systematic review and meta-analysis.". Gastrointest Endosc. doi:10.1016/j.gie.2011.09.016. PMID 22115605.
- ↑ 37.0 37.1 37.2 Carmack, SW.; Vemulapalli, R.; Spechler, SJ.; Genta, RM. (Dec 2009). "Esophagitis dissecans superficialis ("sloughing esophagitis"): a clinicopathologic study of 12 cases.". Am J Surg Pathol 33 (12): 1789-94. doi:10.1097/PAS.0b013e3181b7ce21. PMID 19809273.
- ↑ Coppola, D.; Lu, L.; Boyce, HW. (Oct 2000). "Chronic esophagitis dissecans presenting with esophageal strictures: a case report.". Hum Pathol 31 (10): 1313-7. doi:10.1053/hupa.2000.18470. PMID 11070124.
- ↑ 39.0 39.1 39.2 Lopes, S.; Figueiredo, P.; Amaro, P.; Freire, P.; Alves, S.; Cipriano, MA.; Gouveia, H.; Sofia, C. et al. (May 2010). "Glycogenic acanthosis of the esophagus: an unusually endoscopic appearance.". Rev Esp Enferm Dig 102 (5): 341-2. PMID 20524767.
- ↑ Zendehdel, K.; Nyrén, O.; Edberg, A.; Ye, W. (Jan 2011). "Risk of esophageal adenocarcinoma in achalasia patients, a retrospective cohort study in Sweden.". Am J Gastroenterol 106 (1): 57-61. doi:10.1038/ajg.2010.449. PMID 21212754.
- ↑ Kjellin, AP.; Ost, AE.; Pope, CE. (2005). "Histology of esophageal mucosa from patients with achalasia.". Dis Esophagus 18 (4): 257-61. doi:10.1111/j.1442-2050.2005.00478.x. PMID 16128783.