Sinusoidal obstruction syndrome pathophysiology
|
Sinusoidal obstruction syndrome Microchapters |
|
Differentiating Sinusoidal obstruction syndrome from Other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Sinusoidal obstruction syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Sinusoidal obstruction syndrome pathophysiology |
|
Directions to Hospitals Treating Sinusoidal obstruction syndrome |
|
Risk calculators and risk factors for Sinusoidal obstruction syndrome pathophysiology |
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.