Abstract

INTRODUCTION: The Acute Graft-versus-Host Disease (GVHD) is one of the rare complications after liver transplant (LT) with prevalence up to 2%. Among solid organ transplant, intestinal transplant has the highest incidence followed by LT. Unfortunately, no universal treatment guidelines are available for this disease with poor outcomes and mortality up to 85%. CASE DESCRIPTION/METHODS: 67-year-old male underwent orthotopic LT for end-stage liver failure due to Nonalcoholic steatohepatitis. CMV- patient received ABO identical cadaveric donor liver with CMV + serology. He had no peri-operative complications and was started on immunosuppression and antimicrobial therapies. Within 40 days of LT, he developed leukopenia and early transplant rejection, which was treated with medications. Within 100 days, patient developed rash on extremities and trunk that later spread to face, palms and soles. His course was further complicated by CMV seroconversion around 130 days post-LT. On day 168, patient presented with pancytopenia and continuing skin rash. The initial skin biopsy indicated drug induced reaction, but subsequent biopsy was consistent with GVHD. His treatment regime included steroid, tacrolimus, and rabbit Anti-thymocyte globulin (ATG) with broad-spectrum antimicrobials. Chimerism was initially 19% donor cells in the blood and it was 55% after 4 doses of ATG. He became septic and on day 209 succumbed to massive brain hemorrhage. DISCUSSION: GVHD after LT is in of the lethal complication that usually develops within 3-5 weeks. The key is to have a high index of suspicion with recognition of clinical signs; characteristic itchy palmar skin rash, diarrhea, fever, pancytopenia with normal LFTs. The symptoms are not specific and often diagnosed as infection or drug allergies. GVHD diagnosis can be established with skin lesion or GI tract biopsy and further confirmed with chimerism >30% in the blood of recipient. There is no consensus on treatment. Various strategies are adopted to suppress activated donor lymphocytes, including but not limited to, reduction or even withdrawal of immunosuppression, change in regimen with or without adding steroid boluses, IL-2 antagonist, antithymocyte/lymphocyte globulin, or use of OKT3. Broad-spectrum antimicrobial coverage is pivotal to prevent superimposed infection which is the main cause of death. Further studies are needed to raise the awareness among clinicians and to improve outcomes in patients who develop GVHD following LT.

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