Anticoagulation therapy with warfarin was administered at a dose of 3 mg/d

Anticoagulation therapy with warfarin was administered at a dose of 3 mg/d. of liver function and liver pathology. During the 17-mo follow-up period, she was in good condition with normal liver function and no ascites. CONCLUSION Gramine SOS can be a recurrent disease after LT, and autoimmune antibody and genetic sequencing should be screened before LT. For susceptible patients, anticoagulant drugs should be used for an extended period, and tacrolimus or other pathogenic agents should be avoided. Early diagnosis and treatment can improve the prognosis of patients and avoid graft failure or death. strong class=”kwd-title” Keywords: Sinusoidal obstructive syndrome, Liver transplantation, Recurrence, Sinusoidal dilatation and congestion, Patchy enhancement, Gramine Case report Core Tip: Sinusoidal obstructive syndrome (SOS) is usually a complex entity with incompletely defined pathogenesis. It Gramine is also an uncommon complication after liver transplantation. We reported a rare case of SOS that recurred twice in liver allografts. We believed that this condition is usually uncommon and has rarely been reported in liver transplant recipients. INTRODUCTION Sinusoidal obstructive syndrome (SOS) is usually a rare disorder with a unique etiopathogenesis Gramine related to endothelial toxicity leading to fibrotic obliteration of the hepatic centrilobular veins with congestion and hemorrhage[1,2]. Liver transplantation (LT) is an effective treatment for SOS patients with severe liver failure. SOS after LT is very rare with an incidence of 1 1.9%-2.9%, but it includes a risk for graft failure. Some cytotoxic drugs and/or immunologic responses may be associated with this entity, but the causes and pathophysiological processes of SOS after LT are not well known[3]. Onset of SOS is usually characterized by ascites, hepatomegaly and jaundice. Here, we describe an unusual case of second-time recurrence of SOS after liver retransplantation (rLT). CASE PRESENTATION Chief complaints A 27-year-old woman came to our center due to aggravated abdominal distension and ascites for 1 mo. History of present illness Two months ago, she received rLT from a donation after cardiac death in our center for recurrence of SOS after LT. She recovered well and was discharged on postoperative day 25 under treatment with methylprednisolone, tacrolimus, mycophenolate mofetil and warfarin. One month later, XCL1 she developed progressive abdominal distension and moderate elevation of transaminase with no apparent cause. Abdominal ultrasound showed massive ascites without vascular abnormality. History of past illness Five years ago, she underwent a living donor LT for SOS (Physique ?(Figure1).1). Initially she recovered well with an immunosuppressive regimen of cyclosporine A and mycophenolate mofetil. One year ago, she developed abdominal distension and ascites. She was diagnosed with recurrence of SOS by computed tomography (CT) and histopathology (Figures ?(Figures11 and ?and2).2). She was treated with diuretics and anticoagulants, but her ascites and abdominal distension were aggravated, along with jaundice. She had no abnormal personal and family history. Open in a separate window Physique 1 Hepatic venography. A and B: Native liver showed marked sinusoidal dilatation and congestion in centrilobular regions and extensive bridging fibrosis and necrosis linking central to central areas; C: Explanted first liver graft characterized by massive perivenular congestion and hemorrhage with marked sinusoidal dilatation. Portal tract was not remarkable; D: Two months after liver retransplantation, liver biopsy was performed to clarify the diagnosis. The second liver graft liver pathology showed sinusoidal dilatation and congestion; E: In addition to warfarin, tacrolimus was switched to cyclosporine A. Two months after treatment, perivenular congestion and sinusoidal dilation were alleviated and were only observed in the focal perivenular area; F: Nine months later, there was no perivenular congestion and only moderate sinusoidal dilatation. Open in a separate window Physique 2 Computed tomography image. A: Before liver retransplantation, computed tomography (CT) showed hepatomegaly and heterogeneous, patchy enhancement; B: Two months later, the patient complained of abdominal distension. CT revealed hepatomegaly with patchy enhancement and ascites; C: Two months after treatment with anticoagulation and immunosuppressant conversion, CT showed alleviation of hepatomegaly and heterogeneous enhancement. Physical examination Her body temperature, blood pressure, heart rate and breathing rate were within normal limits. Main positive indicators were cutaneous and sclera icterus with Gramine abdominal bulge and shifting dullness. Laboratory examinations Laboratory results suggested that alanine aminotransferase was 61 IU/L, glutamic oxaloacetylase was 39.9 IU/L, alkaline phosphatase was 90 IU/L, glutamyl transpeptidase was 103 IU/L, total bilirubin was 40.85 mol/L, direct bilirubin was 31.7 moL/L.