Ultrasound in the Management of Hepatic Veno-Occlusive Disease in Three Children Treated with Dactinomycin and Vincristine

Abstract

Three children, treated with dactinomycin and vincristine without radiotherapy showed hepatic toxicity consistent with diagnostic criteria for hepatic veno-occlusive disease (VOD). Two patients were affected with Wilms' tumor and the third with malignant fibromatosis. The clinical manifestations of VOD were mild and regressed in all patients after supportive therapy. Serial ultrasonography (US) was performed in all cases and was useful in confirming the diagnosis and in evaluating the severity of the disease. US features of VOD were hepatomegaly, gallbladder wall thickening, ill-defined borders of the hepatic vessels, and ascites. Parenchymal heterogeneity was still present after several months as a result of the hepatic injury. The hazy appearance of the portal vessels and the gallbladder wall thickening seemed directly correlated with the degree of hepatic involvement in the early phase of VOD.

Defibrotide for the treatment of hepatic veno‐occlusive disease/sinusoidal obstruction syndrome following nontransplant‐associated chemotherapy: Final results from a post hoc analysis of data from an expanded‐access program

“…An increased risk for development of VOD/SOS, with or without HSCT, also has been recognized in patients with AML treated with gemtuzumab ozogamicin . Thioguanine, vincristine, and high‐dose actinomycin‐D also have been reported to be associated with the development of VOD/SOS . The present analysis was not powered to investigate any possible associations with specific agents or regimens, and no inferences can be made from the results.…”

“…8 Thioguanine, vincristine, and high-dose actinomycin-D also have been reported to be associated with the development of VOD/SOS. [10][11][12][31][32][33] The present analysis was not powered to investigate any possible associations with specific agents or regimens, and no inferences can be made from the results.…”

“…The incidence and mortality rate of VOD/SOS following nontransplant‐associated chemotherapy are not known. A number of agents have been reported to be associated with an increased risk of VOD/SOS in the non‐HSCT setting, including inotuzumab and gemtuzumab ozogamicin, vincristine, and/or actinomycin D …”

“…3 The incidence and mortality rate of VOD/SOS following nontransplant-associated chemotherapy are not known. A number of agents have been reported to be associated with an increased risk of VOD/SOS in the non-HSCT setting, including inotuzumab and gemtuzumab ozogamicin, 8,9 vincristine, and/or actinomycin D. [10][11][12][13] In the context of HSCT, the primary event in the pathogenesis of VOD/SOS is injury to hepatic sinusoidal endothelial cells and hepatocytes, usually within the first 21 days post-HSCT, resulting in a prothrombotic-hypofibrinolytic state and sinusoid obstruction. 14 Clin-ically, VOD/SOS is typically characterized by hepatomegaly, hyperbilirubinemia, jaundice, ascites, and weight gain.…”

Ultrasound in radioembolization induced liver disease (REILD)

“…Only very few reports deal with alterations of the liver texture in VOD. Schiavetti [17] described three children suffering from VOD with slightly heterogeneous parenchymal echo texture, and increased echogenicity of portal triads, persisting for several months. Probably, this was due to fibrosis, and is not comparable to the transient increase in liver parenchymal echogenicity observed in our patients.…”