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Liver

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Room: E-Poster Hall

P-12.06 Treatment of antibody mediated rejection after liver transplant: What do we know?

CRISTINA DOPAZO, Spain

CONSULTANT SURGEON
DEPARTMENT OF HPB SURGERY AND TRANSPLANTS
HOSPITAL UNIVERSITARIO VALL D´HEBRON, UNIVERSIDAD AUTONOMA DE BARCELONA

Abstract

Treatment of antibody mediated rejection after liver transplant: What do we know?

Cristina Dopazo1, Inmaculada Concepcion Gomez-Gavara1, Francisco Morseo2, Maria Teresa Salcedo3, Lluis Castells4, Mireia Caralts1, Isabel Campos4, Ernest Hidalgo1, Ramon Charco1, Itxarone Bilbao1.

1Department of HPB Surgery and Transplants, Hospital Universitario Vall D´Hebron, Barcelona, Spain; 2Department of Nephrology, Hospital Universitario Vall D´Hebron, Barcelona, Spain; 3Department of Histopathology, Hospital Universitario Vall D´Hebron, Barcelona, Spain; 4Liver Unit, Department of Internal Medicine, Hospital Universitario Vall D´Hebron, Barcelona, Spain

Acute antibody-mediated rejection (AMR) is having been well reported in the literature however the adequate treatment remains controversial and not extensively studied. 
Between 2015-2019, we performed 160 liver transplants (LT). Our acute cellular rejection rate was 32% and two cases (1,2%) were AMR with different response to the same treatment.
The first case is a 46 years-old female who underwent ABO compatible LT for hepatitis C and negative viral load, MELD score 16. Donor-recipient crossmatch was negative and his panel-reactive antibody rate was 0%. The initial immunosuppression therapy was based on tacrolimus (TAC) and steroids.  Nine days after LT, liver dysfunction due to de novo donor-specific antibody (DSA)-driven AMR was diagnosed. Liver biopsy revealed signs of expansion of the portal tracts with an intense plasma cell infiltrate, bile duct injury and focal C4d staining in 20% of the portal microvascular endothelial. Luminex® (Luminex SA; One Lambda, Canoga Park, CA) single-antigen assay was used for testing DSAs. The result was positive for one HLA class II DSA anti-DPB1 and mean fluorescence intensity (MFI) over 20,000. She he was treated with plasmapheresis and 100mg/kg of human normal iv immunoglobulin (7 courses) without retuximab. Progressive improvement of liver function was observed achieving normal function 6 months post-LT.
The second case is a 69 years-old male transplanted due to HCC and hepatitis C and positive viral load. He received antiviral treatment with elbasvir/grazoprevir one month after LT with sustained viral response. Seven months after LT, the patient presented severe liver dysfunction and liver biopsy showed also signs of AMR with a C4d deposition in 20% of the portal endothelial and HLA class II DSA DQB1*03 with MFI over 20,000. Despite of 9 sessions immunoadsorption and iv immunoglobulins, no response was observed and he was retransplanted with a negative crossmatch and a PRA rate of 21%. He received induction immunosupression with policlonal antibodies and conventional triple therapy (TAC+MMF+steroids). Outcome was uneventful and DSA DQB1*03 after 3 months of retransplant are over 6,000 with normal function 9 months post-retransplant.
Despite de low incidence of AMR, the rapid decision to carry out specific strategies overcoming AMR, including retransplantation, was crucial to achieving success in these cases.

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