Angiodysplasia pathophysiology: Difference between revisions

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==Overview==
==Overview==
The exact [[pathogenesis]] of angiodysplasia is unknown. It has been proposed that chronic obstruction of submucosal veins coupled with the effect of [[aging]], ultimately lead to the formation of small arterio-venous collaterals. Angiogenic factors have also been found to play a role in the development of angiodysplasia.


==Pathophysiology==
==Pathophysiology==
The most widely quoted hypothesis in literature is the one by Boley et al in a study using resected colon specimens from patients with angiographic and clinical evidence of cecal vascular lesions. Histological evaluation revealed dilated and tortuous veins in the submucosa even without obvious mucosal lesion. It was suggested that those lesions develop with ageing due to chronic low‐grade intermittent obstruction of submucosal veins as a result of increased contractility at the level of muscularis propria. This leads to congestion of the capillaries and failure of the pre‐capillary sphincters, resulting in the formation of small arterio‐venous collaterals.


It is a degenerative lesion, acquired, probably resulting from chronic and intermittent contraction of the colon that is obstructing the venous drainage of the mucosa.  As time goes by the veins become more and more tortuous, while the capillaries of the mucosa gradually dilate and pre-capillary sphincter becomes incompetent. Thus is formed an arteriovenous malformation characterised by a small tuft of dilated vessels. This hypothesis accounts for the high prevalence of these lesions in the right colon and is based on the Laplace law.   
*The exact [[pathogenesis]] of angiodysplasia is still unknown.
*According to a theory, angiodysplasia develops due to chronic obstruction of submucosal veins coupled with the effect of [[ageing]], ultimately leading to the formation of small arterio-venous collaterals.<ref name="pmid24138285">{{cite journal| author=Sami SS, Al-Araji SA, Ragunath K| title=Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management. | journal=Aliment Pharmacol Ther | year= 2014 | volume= 39 | issue= 1 | pages= 15-34 | pmid=24138285 | doi=10.1111/apt.12527 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24138285  }} </ref>
*Some studies have revealed increased levels of angiogenic factors like vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang1), Ang2, etc., in [[small bowel]] and human colonic angiodysplasia.<ref name="pmid28868182">{{cite journal| author=Holleran G, Hussey M, Smith S, McNamara D| title=Assessment of serum angiogenic factors as a diagnostic aid for small bowel angiodysplasia in patients with obscure gastrointestinal bleeding and anaemia. | journal=World J Gastrointest Pathophysiol | year= 2017 | volume= 8 | issue= 3 | pages= 127-132 | pmid=28868182 | doi=10.4291/wjgp.v8.i3.127 | pmc=5561433 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28868182  }} </ref><ref name="pmid25319741">{{cite journal| author=Holleran G, Hall B, O'Regan M, Smith S, McNamara D| title=Expression of Angiogenic Factors in Patients With Sporadic Small Bowel Angiodysplasia. | journal=J Clin Gastroenterol | year= 2015 | volume= 49 | issue= 10 | pages= 831-6 | pmid=25319741 | doi=10.1097/MCG.0000000000000260 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25319741 }} </ref>
*It has also been proposed that [[aortic stenosis]], [[von Willebrand disease]], and [[chronic renal failure]] by various mechanisms contribute to development of angiodysplasia.<ref name="pmid24138285">{{cite journal| author=Sami SS, Al-Araji SA, Ragunath K| title=Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management. | journal=Aliment Pharmacol Ther | year= 2014 | volume= 39 | issue= 1 | pages= 15-34 | pmid=24138285 | doi=10.1111/apt.12527 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24138285  }} </ref><br />
 
==Associated Conditions==
The following conditions have been reported to be associated with angiodysplasia:
 
*[[Von Willebrand disease]] (vWD)<ref name="pmid14571395">{{cite journal| author=Warkentin TE, Moore JC, Anand SS, Lonn EM, Morgan DG| title=Gastrointestinal bleeding, angiodysplasia, cardiovascular disease, and acquired von Willebrand syndrome. | journal=Transfus Med Rev | year= 2003 | volume= 17 | issue= 4 | pages= 272-86 | pmid=14571395 | doi=10.1016/s0887-7963(03)00037-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14571395  }} </ref>
*[[Aortic stenosis]] (Heyde syndrome)<ref name="pmid14571395">{{cite journal| author=Warkentin TE, Moore JC, Anand SS, Lonn EM, Morgan DG| title=Gastrointestinal bleeding, angiodysplasia, cardiovascular disease, and acquired von Willebrand syndrome. | journal=Transfus Med Rev | year= 2003 | volume= 17 | issue= 4 | pages= 272-86 | pmid=14571395 | doi=10.1016/s0887-7963(03)00037-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14571395  }} </ref><ref name="pmid15473466">{{cite journal| author=Pate GE, Chandavimol M, Naiman SC, Webb JG| title=Heyde's syndrome: a review. | journal=J Heart Valve Dis | year= 2004 | volume= 13 | issue= 5 | pages= 701-12 | pmid=15473466 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15473466  }} </ref>
*[[End-stage renal disease]] (ESRD)<ref name="pmid31798771">{{cite journal| author=Tariq T, Karabon P, Irfan FB, Goyal S, Mayeda MM, Parsons A | display-authors=etal| title=Secondary angiodysplasia-associated gastrointestinal bleeding in end-stage renal disease: Results from the nationwide inpatient sample. | journal=World J Gastrointest Endosc | year= 2019 | volume= 11 | issue= 10 | pages= 504-514 | pmid=31798771 | doi=10.4253/wjge.v11.i10.504 | pmc=6885446 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31798771  }} </ref>
*[[Systemic sclerosis]] (SSc)<ref name="pmid18498445">{{cite journal| author=Marie I, Ducrotte P, Antonietti M, Herve S, Levesque H| title=Watermelon stomach in systemic sclerosis: its incidence and management. | journal=Aliment Pharmacol Ther | year= 2008 | volume= 28 | issue= 4 | pages= 412-21 | pmid=18498445 | doi=10.1111/j.1365-2036.2008.03739.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18498445 }} </ref>


Dilated submucosal veins have been one of the most consistent histologic findings and may represent the earliest abnormality in colonic angiodysplasia. This histologic feature supports the theory of chronic venous obstruction in the genesis of angiodysplasia.
==Gross Pathology==


Investigators have observed that patients with AD are more likely to have underlying cardiac, vascular or pulmonary diseases and therefore suggested that mucosal ischemia from chronic hypoxia or hypo‐perfusion may contribute to the development of AD; however, these were small observational case–control studies with no histological correlation. This has led to the suggestion that the increased incidence of bleeding AD in patients with AS could be due to reduced cardiac output and tissue perfusion in this subgroup.
*Angiodysplasia is particularly difficult to recognise on [[gross examination]] of a resection specimen without the use of specific injection techniques.<ref name="pmid8877645">{{cite journal| author=Koga H, Iida M, Nagai E, Aoyagi K, Matsumoto T, Takesue M | display-authors=etal| title=Jejunal angiodysplasia confirmed by intravascular injection technique in vitro. Report of a case and review of the literature. | journal=J Clin Gastroenterol | year= 1996 | volume= 23 | issue= 2 | pages= 139-44 | pmid=8877645 | doi=10.1097/00004836-199609000-00017 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8877645  }} </ref>
*Angiodysplasia can be seen easily on [[endoscopy]]. The most common appearance on endoscopy is a flat, red lesion with a fern-like or regular margin.


Increased expression of angiogenic factors, like basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), is also believed to play a role in the pathogenesis of colonic angiodysplasia as the expression of VEGF is higher in patients with hypoxia than normoxia.
==Histology==


There is a role of VWF in regulating angiogenesis which has been studied recently. The link between the mechanical disruption of high molecular-weight multimers of von Willebrand factor, due to the turbulent blood flow through a narrowed valve in patients with aortic stenosis, and colonic angiodysplasia has been formed.
*Angiodysplastic lesions on histology appear as ectatic, thin-walled blood vessels in [[mucosa]] or [[submucosa]].<ref name="pmid1544666">{{cite journal| author=Thelmo WL, Vetrano JA, Wibowo A, DiMaio TM, Cruz-Vetrano WP, Kim DS| title=Angiodysplasia of colon revisited: pathologic demonstration without the use of intravascular injection technique. | journal=Hum Pathol | year= 1992 | volume= 23 | issue= 1 | pages= 37-40 | pmid=1544666 | doi=10.1016/0046-8177(92)90008-q | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1544666  }} </ref>
*[[Histopathology|Histopathologic]] findings on resected specimen are diagnostic.<ref name="pmid8532207">{{cite journal| author=Accordino R, Paties C, Inzani E, Civardi C, Cremonesi V, Lagasi L | display-authors=etal| title=[Angiodysplasia of the right colon]. | journal=Minerva Chir | year= 1995 | volume= 50 | issue= 7-8 | pages= 703-6 | pmid=8532207 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8532207  }} </ref>


==References==
==References==
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Latest revision as of 15:23, 30 June 2022

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nikita Singh, M.B.B.S.[2]

Overview

The exact pathogenesis of angiodysplasia is unknown. It has been proposed that chronic obstruction of submucosal veins coupled with the effect of aging, ultimately lead to the formation of small arterio-venous collaterals. Angiogenic factors have also been found to play a role in the development of angiodysplasia.

Pathophysiology

  • The exact pathogenesis of angiodysplasia is still unknown.
  • According to a theory, angiodysplasia develops due to chronic obstruction of submucosal veins coupled with the effect of ageing, ultimately leading to the formation of small arterio-venous collaterals.[1]
  • Some studies have revealed increased levels of angiogenic factors like vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang1), Ang2, etc., in small bowel and human colonic angiodysplasia.[2][3]
  • It has also been proposed that aortic stenosis, von Willebrand disease, and chronic renal failure by various mechanisms contribute to development of angiodysplasia.[1]

Associated Conditions

The following conditions have been reported to be associated with angiodysplasia:

Gross Pathology

  • Angiodysplasia is particularly difficult to recognise on gross examination of a resection specimen without the use of specific injection techniques.[8]
  • Angiodysplasia can be seen easily on endoscopy. The most common appearance on endoscopy is a flat, red lesion with a fern-like or regular margin.

Histology

References

  1. ↑ 1.0 1.1 Sami SS, Al-Araji SA, Ragunath K (2014). "Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management". Aliment Pharmacol Ther. 39 (1): 15–34. doi:10.1111/apt.12527. PMID 24138285.
  2. ↑ Holleran G, Hussey M, Smith S, McNamara D (2017). "Assessment of serum angiogenic factors as a diagnostic aid for small bowel angiodysplasia in patients with obscure gastrointestinal bleeding and anaemia". World J Gastrointest Pathophysiol. 8 (3): 127–132. doi:10.4291/wjgp.v8.i3.127. PMC 5561433. PMID 28868182.
  3. ↑ Holleran G, Hall B, O'Regan M, Smith S, McNamara D (2015). "Expression of Angiogenic Factors in Patients With Sporadic Small Bowel Angiodysplasia". J Clin Gastroenterol. 49 (10): 831–6. doi:10.1097/MCG.0000000000000260. PMID 25319741.
  4. ↑ 4.0 4.1 Warkentin TE, Moore JC, Anand SS, Lonn EM, Morgan DG (2003). "Gastrointestinal bleeding, angiodysplasia, cardiovascular disease, and acquired von Willebrand syndrome". Transfus Med Rev. 17 (4): 272–86. doi:10.1016/s0887-7963(03)00037-3. PMID 14571395.
  5. ↑ Pate GE, Chandavimol M, Naiman SC, Webb JG (2004). "Heyde's syndrome: a review". J Heart Valve Dis. 13 (5): 701–12. PMID 15473466.
  6. ↑ Tariq T, Karabon P, Irfan FB, Goyal S, Mayeda MM, Parsons A; et al. (2019). "Secondary angiodysplasia-associated gastrointestinal bleeding in end-stage renal disease: Results from the nationwide inpatient sample". World J Gastrointest Endosc. 11 (10): 504–514. doi:10.4253/wjge.v11.i10.504. PMC 6885446 Check |pmc= value (help). PMID 31798771.
  7. ↑ Marie I, Ducrotte P, Antonietti M, Herve S, Levesque H (2008). "Watermelon stomach in systemic sclerosis: its incidence and management". Aliment Pharmacol Ther. 28 (4): 412–21. doi:10.1111/j.1365-2036.2008.03739.x. PMID 18498445.
  8. ↑ Koga H, Iida M, Nagai E, Aoyagi K, Matsumoto T, Takesue M; et al. (1996). "Jejunal angiodysplasia confirmed by intravascular injection technique in vitro. Report of a case and review of the literature". J Clin Gastroenterol. 23 (2): 139–44. doi:10.1097/00004836-199609000-00017. PMID 8877645.
  9. ↑ Thelmo WL, Vetrano JA, Wibowo A, DiMaio TM, Cruz-Vetrano WP, Kim DS (1992). "Angiodysplasia of colon revisited: pathologic demonstration without the use of intravascular injection technique". Hum Pathol. 23 (1): 37–40. doi:10.1016/0046-8177(92)90008-q. PMID 1544666.
  10. ↑ Accordino R, Paties C, Inzani E, Civardi C, Cremonesi V, Lagasi L; et al. (1995). "[Angiodysplasia of the right colon]". Minerva Chir. 50 (7–8): 703–6. PMID 8532207.

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