Sinusoidal obstruction syndrome pathophysiology: Difference between revisions
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{{CMG}}; {{AE}} {{HS}} | {{CMG}}; {{AE}} {{HS}} | ||
==Overview== | ==Overview== | ||
The development of sinusoidal obstruction syndrome begins with the injury to hepatic venous [[endothelium]]. It is thought that preexisting liver disease increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of drug metabolism which predisposes to the [[Endothelial|endothelial injury]]. The endothelial cells in patients with hepatitis may have abnormal expression of [[Adhesion molecule|adhesion molecules]] and | The development of sinusoidal obstruction syndrome begins with the injury to [[Hepatic veins|hepatic venous]] [[endothelium]]. It is thought that preexisting [[Liver diseases|liver disease]] increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of [[drug metabolism]] which predisposes to the [[Endothelial|endothelial injury]]. The endothelial cells in patients with [[hepatitis]] may have abnormal expression of [[Adhesion molecule|adhesion molecules]] and pro-coagulant factors. The deposition of [[fibrinogen]] and [[factor VIII]] within the [[Sinusoid (blood vessel)|sinusoids]] leads to their dilation and congestion by [[erythrocytes]]. The progressive occlusion of venules leads to widespread zonal liver disruption and centrilobular hemorrhagic necrosis. Hepatic sinusoidal obstruction syndrome (SOS) is mainly seen in patients of [[Hematopoietic stem cell transplantation|hematopoietic cell transplantation]]. | ||
==Pathogenesis== | ==Pathogenesis== | ||
* Sinusoidal obstruction syndrome (SOS) occurs due to obstruction of the [[Hepatic veins|hepatic venules]] and [[sinusoids]] rather than hepatic vein or [[inferior vena cava]] as seen in [[Budd Chiari syndrome]]. | * Sinusoidal obstruction syndrome (SOS) occurs due to obstruction of the [[Hepatic veins|hepatic venules]] and [[sinusoids]] rather than [[hepatic vein]] or [[inferior vena cava]] as seen in [[Budd Chiari syndrome]]. | ||
* Hepatic sinusoidal obstruction syndrome (SOS) is mainly seen in hematopoietic cell transplantation. | * Hepatic sinusoidal obstruction syndrome (SOS) is mainly seen in patients who have undergone [[hematopoietic stem cell transplantation]]. | ||
* The development of sinusoidal obstruction syndrome (SOS) begins with the injury to the hepatic venous endothelium. It is thought that preexisting liver disease increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of drug metabolism which predisposes to the endothelial injury. | * The development of sinusoidal obstruction syndrome (SOS) begins with the injury to the hepatic venous [[endothelium]]. It is thought that preexisting [[Liver diseases|liver disease]] increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of [[drug metabolism]] which predisposes to the [[Endothelial cells|endothelial injury]]. | ||
* The endothelial cells in patients with hepatitis may have abnormal expression of adhesion molecules and | * The [[endothelial cells]] in patients with [[hepatitis]] may have abnormal expression of adhesion molecules and pro-coagulant factors. | ||
* The deposition of fibrinogen and factor VIII within the sinusoids leads to their dilation and congestion by erythrocytes. The progressive occlusion of venules leads to widespread zonal liver disruption and centrilobular hemorrhagic necrosis. | * The deposition of [[fibrinogen]] and [[factor VIII]] within the [[sinusoids]] leads to their dilation and congestion by [[erythrocytes]]. The progressive occlusion of venules leads to widespread zonal liver disruption and centrilobular [[hemorrhagic]] necrosis. | ||
* The later changes in sinusoids include deposition of collagen, sclerosis of venular walls, fibrosis of the | * The later changes in [[sinusoids]] include deposition of [[collagen]], sclerosis of venular walls, [[fibrosis]] of the lumen and ultimately occlusion of hepatic venules. | ||
* The severity of symptoms depends on the number of sinusoids involve and severity of the histologic changes. | * The severity of symptoms depends on the number of [[sinusoids]] involve and severity of the histologic changes. | ||
[[Image:Hepatic sinusoids.png|thumb|center|750px|Originally by Frevert U, Engelmann S, Zougbédé S, Stange J, Ng B, et al https://commons.wikimedia.org/wiki/File:Hepatic_structure2.svg]] | [[Image:Hepatic sinusoids.png|thumb|center|750px|Originally by Frevert U, Engelmann S, Zougbédé S, Stange J, Ng B, et al https://commons.wikimedia.org/wiki/File:Hepatic_structure2.svg]] | ||
==Gross Pathology== | ==Gross Pathology== | ||
* On gross pathology, the liver has diffusely mottled appearance with areas of congestion and normal appearing hepatic parenchyma.<ref name="pmid24757663">{{cite journal| author=Seo AN, Kim H| title=Sinusoidal obstruction syndrome after oxaliplatin-based chemotherapy. | journal=Clin Mol Hepatol | year= 2014 | volume= 20 | issue= 1 | pages= 81-4 | pmid=24757663 | doi=10.3350/cmh.2014.20.1.81 | pmc=3992335 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24757663 }} </ref> | * On gross pathology, the liver has diffusely mottled appearance with areas of [[congestion]] and normal appearing hepatic parenchyma.<ref name="pmid24757663">{{cite journal| author=Seo AN, Kim H| title=Sinusoidal obstruction syndrome after oxaliplatin-based chemotherapy. | journal=Clin Mol Hepatol | year= 2014 | volume= 20 | issue= 1 | pages= 81-4 | pmid=24757663 | doi=10.3350/cmh.2014.20.1.81 | pmc=3992335 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24757663 }} </ref> | ||
==Microscopic Pathology== | ==Microscopic Pathology== | ||
The most important histopathological characteristics of sinusoidal obstruction syndrome are:<ref name="pmid6363247">{{cite journal |vauthors=McDonald GB, Sharma P, Matthews DE, Shulman HM, Thomas ED |title=Venocclusive disease of the liver after bone marrow transplantation: diagnosis, incidence, and predisposing factors |journal=Hepatology |volume=4 |issue=1 |pages=116–22 |year=1984 |pmid=6363247 |doi= |url=}}</ref><ref name="pmid2438942">{{cite journal |vauthors=Shulman HM, Gown AM, Nugent DJ |title=Hepatic veno-occlusive disease after bone marrow transplantation. Immunohistochemical identification of the material within occluded central venules |journal=Am. J. Pathol. |volume=127 |issue=3 |pages=549–58 |year=1987 |pmid=2438942 |pmc=1899766 |doi= |url=}}</ref><ref name="pmid8175139">{{cite journal |vauthors=Shulman HM, Fisher LB, Schoch HG, Henne KW, McDonald GB |title=Veno-occlusive disease of the liver after marrow transplantation: histological correlates of clinical signs and symptoms |journal=Hepatology |volume=19 |issue=5 |pages=1171–81 |year=1994 |pmid=8175139 |doi= |url=}}</ref> | The most important [[histopathological]] characteristics of sinusoidal obstruction syndrome are:<ref name="pmid6363247">{{cite journal |vauthors=McDonald GB, Sharma P, Matthews DE, Shulman HM, Thomas ED |title=Venocclusive disease of the liver after bone marrow transplantation: diagnosis, incidence, and predisposing factors |journal=Hepatology |volume=4 |issue=1 |pages=116–22 |year=1984 |pmid=6363247 |doi= |url=}}</ref><ref name="pmid2438942">{{cite journal |vauthors=Shulman HM, Gown AM, Nugent DJ |title=Hepatic veno-occlusive disease after bone marrow transplantation. Immunohistochemical identification of the material within occluded central venules |journal=Am. J. Pathol. |volume=127 |issue=3 |pages=549–58 |year=1987 |pmid=2438942 |pmc=1899766 |doi= |url=}}</ref><ref name="pmid8175139">{{cite journal |vauthors=Shulman HM, Fisher LB, Schoch HG, Henne KW, McDonald GB |title=Veno-occlusive disease of the liver after marrow transplantation: histological correlates of clinical signs and symptoms |journal=Hepatology |volume=19 |issue=5 |pages=1171–81 |year=1994 |pmid=8175139 |doi= |url=}}</ref> | ||
*Sinusoidal dilation | *[[Sinusoid (blood vessel)|Sinusoidal]] dilation | ||
*Portal tract changes of fibrosis and bile ductular reaction | *[[Portal triad|Portal tract]] changes of [[fibrosis]] and [[Bile duct|bile ductular]] reaction | ||
*Sclerosis of venular walls | *[[Sclerosis]] of venular walls | ||
*Sinusoidal endothelial cell detachment from the space of Disse can be seen on electron microscopy | *[[Sinusoid (blood vessel)|Sinusoidal]] endothelial cell detachment from the [[space of Disse]] can be seen on [[electron microscopy]] | ||
==References== | ==References== | ||
Latest revision as of 15:33, 28 February 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Husnain Shaukat, M.D [2]
Overview
The development of sinusoidal obstruction syndrome begins with the injury to hepatic venous endothelium. It is thought that preexisting liver disease increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of drug metabolism which predisposes to the endothelial injury. The endothelial cells in patients with hepatitis may have abnormal expression of adhesion molecules and pro-coagulant factors. The deposition of fibrinogen and factor VIII within the sinusoids leads to their dilation and congestion by erythrocytes. The progressive occlusion of venules leads to widespread zonal liver disruption and centrilobular hemorrhagic necrosis. Hepatic sinusoidal obstruction syndrome (SOS) is mainly seen in patients of hematopoietic cell transplantation.
Pathogenesis
- Sinusoidal obstruction syndrome (SOS) occurs due to obstruction of the hepatic venules and sinusoids rather than hepatic vein or inferior vena cava as seen in Budd Chiari syndrome.
- Hepatic sinusoidal obstruction syndrome (SOS) is mainly seen in patients who have undergone hematopoietic stem cell transplantation.
- The development of sinusoidal obstruction syndrome (SOS) begins with the injury to the hepatic venous endothelium. It is thought that preexisting liver disease increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of drug metabolism which predisposes to the endothelial injury.
- The endothelial cells in patients with hepatitis may have abnormal expression of adhesion molecules and pro-coagulant factors.
- The deposition of fibrinogen and factor VIII within the sinusoids leads to their dilation and congestion by erythrocytes. The progressive occlusion of venules leads to widespread zonal liver disruption and centrilobular hemorrhagic necrosis.
- The later changes in sinusoids include deposition of collagen, sclerosis of venular walls, fibrosis of the lumen and ultimately occlusion of hepatic venules.
- The severity of symptoms depends on the number of sinusoids involve and severity of the histologic changes.
Gross Pathology
- On gross pathology, the liver has diffusely mottled appearance with areas of congestion and normal appearing hepatic parenchyma.[1]
Microscopic Pathology
The most important histopathological characteristics of sinusoidal obstruction syndrome are:[2][3][4]
- Sinusoidal dilation
- Portal tract changes of fibrosis and bile ductular reaction
- Sclerosis of venular walls
- Sinusoidal endothelial cell detachment from the space of Disse can be seen on electron microscopy
References
- ↑ Seo AN, Kim H (2014). "Sinusoidal obstruction syndrome after oxaliplatin-based chemotherapy". Clin Mol Hepatol. 20 (1): 81–4. doi:10.3350/cmh.2014.20.1.81. PMC 3992335. PMID 24757663.
- ↑ McDonald GB, Sharma P, Matthews DE, Shulman HM, Thomas ED (1984). "Venocclusive disease of the liver after bone marrow transplantation: diagnosis, incidence, and predisposing factors". Hepatology. 4 (1): 116–22. PMID 6363247.
- ↑ Shulman HM, Gown AM, Nugent DJ (1987). "Hepatic veno-occlusive disease after bone marrow transplantation. Immunohistochemical identification of the material within occluded central venules". Am. J. Pathol. 127 (3): 549–58. PMC 1899766. PMID 2438942.
- ↑ Shulman HM, Fisher LB, Schoch HG, Henne KW, McDonald GB (1994). "Veno-occlusive disease of the liver after marrow transplantation: histological correlates of clinical signs and symptoms". Hepatology. 19 (5): 1171–81. PMID 8175139.