Vascular Disorders of the Liver

Genetic predisposition resulting in sinusoidal obstruction syndrome in a patient with resected sigmoid cancer on adjuvant oxaliplatin

“…SOS is characterised by sinusoidal dilation and congestion, centrilobular vein fibrosis and obstruction, perisinusoidal fibrosis, necrosis of pericentral hepatocytes, parenchymal extinction lesions, hepatocyte plate disruption and nodular regenerative hyperplasia 10 12–16…”

Sinusoidal obstruction syndrome after oxaliplatin-based chemotherapy

“…SOS has been described in association with drugs including oxaliplatin, azathioprine, cysteamine, dacarbazine, dactinomycin, carmustine (BCNU), 6-mercaptopurine, 6-thioguanine, busulfan, dimethyl busulfan, cytosine arabinoside, cyclophosphamide, indicine-N-oxide, mustine-HCl, doxorubicin, urethane, vincristine, mitomycin-C, etoposide, arsenic, thorium dioxide (Thorotrast), and intra-arterial flurodeoxyuridine. 10 SOS related to oxaliplatin administration was first described by Rubbia-Brandt et al, 5 and is characterized by the following histologic findings: sinusoidal dilatation and congestion, centrilobular vein fibrosis and obstruction, perisinusoidal fibrosis, necrosis of pericentral hepatocytes, PELs, hepatocyte plate disruption, and nodular regenerative hyperplasia. 2 , 3 , 4 , 6 , 10 , 11 These changes are generally irregularly distributed within the hepatic parenchyme; however, if the changes are more extensive it is possible to recognize SOS on gross examination, where the liver appears diffusely "nodular" due to alternating areas of congestion/hemorrhage with relatively normal-looking areas.…”

Grandes nódulos hepatocelulares benignos em fígados cirróticos por bloqueio crônico do efluxo venoso

“…São nódulos regenerativos grandes, maiores do que os nódulos cirróticos adjacentes e que por isso se destacam em meio ao fígado cirrótico. Podem surgir em fígados com cirrose por diferentes etiologias, sendo encontrados em cerca de 50% dos pacientes com cirrose associada à síndrome de Budd-Chiari (10).…”

“…A obstrução do efluxo venoso pode se dar em qualquer ponto, desde as vênulas hepáticas, até a junção da veia cava inferior com o átrio direito (2,9), resultando em aumento da pressão nos sinusóides hepáticos, congestão sinusoidal, hepatomegalia, dor hepática, hipertensão portal e ascite (2,3). Nos estágios iniciais, a perfusão venosa portal do fígado é diminuída, o que pode resultar em trombose portal em 10-20% dos casos (10).…”