Sinusoidal obstruction syndrome pathophysiology

Jump to navigation Jump to search

Sinusoidal obstruction syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Sinusoidal obstruction syndrome from Other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Sinusoidal obstruction syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Sinusoidal obstruction syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Sinusoidal obstruction syndrome pathophysiology

CDC on Sinusoidal obstruction syndrome pathophysiology

Sinusoidal obstruction syndrome pathophysiology in the news

Blogs on 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

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

  • 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]

References

  1. 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.
  2. 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.
  3. 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.
  4. 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.

Template:WS Template:WH