Invisible colonic dysplasia: Difference between revisions
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Created page with "'''Invisible colonic dysplasia''' is colonic dysplasia that is not seen on endoscopy. ==General== *The reason for random biopsies in inflammatory bowel disease. *Relatively..." |
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==General== | ==General== | ||
*The reason for random biopsies in inflammatory bowel disease. | *The reason for random biopsies in inflammatory bowel disease. | ||
*Relatively uncommon - one series of [[ulcerative colitis]] patients estimated ~12% of lesions are "invisible".<ref>{{cite journal | | *Relatively uncommon - one series of [[ulcerative colitis]] patients estimated ~12% of lesions are "invisible".<ref>{{cite journal |authors=Blonski W, Kundu R, Lewis J, Aberra F, Osterman M, Lichtenstein GR |title=Is dysplasia visible during surveillance colonoscopy in patients with ulcerative colitis? |journal=Scand J Gastroenterol |volume=43 |issue=6 |pages=698–703 |date=2008 |pmid=18569987 |doi=10.1080/00365520701866150 |url=}}</ref> | ||
==Gross== | ==Gross== | ||
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==Microscopic== | ==Microscopic== | ||
Features: | Features: | ||
* | #Nuclear changes at the surface of the mucosa - '''key feature'''. | ||
#*Size and shape ''or'' size change: | |||
#**Cigar-shaped (elongated) nucleus (usu. length:width > 3:1) with nuclear hyperchromasia (more blue). | |||
#**Large round nuclei +/- [[vesicular nuclei|vesicular]] appearance (clearing) -- nuclei have white space. | |||
#*Nuclear crowding/pseudostratification - '''important'''. | |||
#*+/-Loss of nuclear polarity (nuclei no longer on basement membrane). | |||
#Loss/decrease of goblet cells (common). | |||
#Cytoplasmic hyperchromasia. | |||
Notes: | |||
*Nuclear changes deep to the surface are non-neoplastic if normal appearing mucosa (with small round nuclei) is superficial to it; mucosa that is more blue and atypical deep ''and'' less blue without nuclear atypia at the surface is said to be "maturing". | |||
**Classically, adenomatous polyps have "reverse maturation": | |||
***The surface is more hyperchromatic (more blue). | |||
***The base is more mature (more globlet cells, no nuclear changes -- less blue). | |||
*[[Ampullary adenoma]]s often have less prominent pseudostratification and fine chromatin. | |||
DDx: | |||
*Reactive changes due to inflammation. | |||
*Invasive adenocarcinoma. | |||
==See also== | ==See also== | ||
Revision as of 19:27, 9 March 2021
Invisible colonic dysplasia is colonic dysplasia that is not seen on endoscopy.
General
- The reason for random biopsies in inflammatory bowel disease.
- Relatively uncommon - one series of ulcerative colitis patients estimated ~12% of lesions are "invisible".[1]
Gross
- Not visible - definitional.
Microscopic
Features:
- Nuclear changes at the surface of the mucosa - key feature.
- Size and shape or size change:
- Cigar-shaped (elongated) nucleus (usu. length:width > 3:1) with nuclear hyperchromasia (more blue).
- Large round nuclei +/- vesicular appearance (clearing) -- nuclei have white space.
- Nuclear crowding/pseudostratification - important.
- +/-Loss of nuclear polarity (nuclei no longer on basement membrane).
- Size and shape or size change:
- Loss/decrease of goblet cells (common).
- Cytoplasmic hyperchromasia.
Notes:
- Nuclear changes deep to the surface are non-neoplastic if normal appearing mucosa (with small round nuclei) is superficial to it; mucosa that is more blue and atypical deep and less blue without nuclear atypia at the surface is said to be "maturing".
- Classically, adenomatous polyps have "reverse maturation":
- The surface is more hyperchromatic (more blue).
- The base is more mature (more globlet cells, no nuclear changes -- less blue).
- Classically, adenomatous polyps have "reverse maturation":
- Ampullary adenomas often have less prominent pseudostratification and fine chromatin.
DDx:
- Reactive changes due to inflammation.
- Invasive adenocarcinoma.
See also
- DALM.
References
- ↑ Blonski W, Kundu R, Lewis J, Aberra F, Osterman M, Lichtenstein GR (2008). "Is dysplasia visible during surveillance colonoscopy in patients with ulcerative colitis?". Scand J Gastroenterol 43 (6): 698–703. doi:10.1080/00365520701866150. PMID 18569987.