Abstract
Hepatic sinusoidal obstruction syndrome (SOS)/veno-occlusive disease (VOD) is a complication after allogenic hematopoietic stem-cell transplantation (allo-HSCT) with high mortality. The purpose of this study was to assess the incidence and outcome of SOS in patients after allo-HSCT with the impact of ursodeoxycholic acid (UDCA) and low-dose heparin as SOS prophylaxis. Out of 1016 patients, 23 developed SOS, with a cumulative incidence of 2.3% (95% CI 1.3–3.3) 6 months after HSCT. Approximately one quarter of these patients (26.1%) had late-onset SOS. A high proportion were very severe SOS cases (74%), and 83% of the patients were treated with defibrotide (DF). In multivariate analysis, advanced disease (p = 0.003), previous HSCT (p = 0.025) and graft versus host disease (GvHD) prophylaxis by post-transplant cyclophosphamide (PTCy) (p = 0.055) were associated with the development of SOS. The 1-year overall survival (OS) was significantly lower in the SOS group compared to patients without SOS (13% versus 70%, p = 0.0001). In conclusion, we found a low incidence of SOS in patients receiving low-dose heparin and UDCA prophylactically, but among SOS patients, a high mortality. Low-dose heparin and UDCA might be a prophylactic approach for SOS.
Highlights
Hepatic sinusoidal obstruction syndrome (SOS) (formerly venoocclusive disease (VOD)) is a potentially life-threatening complication after allogenic hematopoietic stem cell transplantation [1]
Between 2006 and 2020, 1,163 allo-HSCTs were performed at the University Hospital of Basel
Transfusion support and infection prophylaxis Red blood cell transfusion was given to patients with hemoglobin concentrations
Summary
Hepatic sinusoidal obstruction syndrome (SOS) (formerly venoocclusive disease (VOD)) is a potentially life-threatening complication after allogenic hematopoietic stem cell transplantation (alloHSCT) [1]. An injury of the sinusoidal endothelium of the liver seems to be the underlying cause [1, 2], triggered by several factors including conditioning, drugs, allo-immunological reactions [3], and occurrence is favored by pre-existing liver damage [4]. Due to loss of integrity of the endothelium, erythrocytes, leukocytes and cellular debris penetrate into space of Disse [3], leading to an embolization of the centrilobular veins [2], resulting in hepatocellular damage and portal hypertension [5]. Clinical manifestations are unspecific [1], with hyperbilirubinemia, weight gain, painful hepatomegaly and ascites [5, 6]. The clinical course is ranging from mild forms spontaneously resolving, to severe forms with organ damage and multiorgan failure (MOF) [2]. The diagnosis is based on clinical presentation, supported by ultrasound, or, if the risk of invasive procedure is acceptable, confirmed histologically [1]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
