A Case of Myelodysplastic Syndrome in a Liver Transplant Patient

Abstract

Purpose: There is a known increased incidence of myelodysplastic syndrome (MDS) after heart and lung transplant. There is, however, only one reported case of MDS in a liver transplant (LT) patient. This abstract presents the second known case of MDS in a LT patient and discusses the role of immunosuppression in development of MDS after LT. Methods: PubMed search using keywords “myelodysplastic syndrome” and “liver transplant” was done to identify any previous reported case of MDS in LT. Patient data was gathered from the patient and the medical record. Results: A 54-year-old white man underwent LT in 2003 for hepatitis C (HCV) related cirrhosis and hepatocellular carcinoma and in 2004 for recurrence of his HCV. He developed pancytopenia in 2006 which was attributed to his pegylated interferon treatment for HCV. The peg-interferon dose was intitally decreased, later stopped entirely and erythropoietin was initiated. In January 2007, the patient presented to his hepatologist complaining of weakness, malaise, and shortness of breath. WBC was 3.47 × 1000/μl, hemoglobin 10.6 gm/dL, Hct 33.8%, platelets 21 × 1000/μl, and neutrophils were 1.61 × 1000/μl. A liver biopsy revealed bridging fibrosis and recurrent hepatitis C. A bone marrow biopsy revealed myelodysplastic syndrome, type refractory anemia with excess blasts (RAEB)-1. He underwent 4 cycles of azacitidine from February to May 2007 with no improvement on repeat bone marrow biopsy in May 2007. Prograf dose was lowered and the patient underwent 3 cycles of decitabine. His last bone marrow biopsy done in November 2007 continued to show MDS, RAEB-1 with hypocellular marrow. The patient underwent 1 more cycle of decitabine without significant improvement in his laboratory testing. Conclusion: This is only the second reported case of MDS occurring in a post-LT patient. Our patient developed MDS almost 2 years after his second LT, as compared to the previous report in which the patient developed MDS 3 months after LT with subsequent progression to acute myelogenous leukemia within 2 months of the MDS diagnosis. Our patient's MDS type carries a very poor prognosis and high likelihood of conversion to acute myelogenous leukemia. He was treated with chemotherapy and reduction in immunosuppression without a clinical response. Given the rarity of MDS after LT, further study is needed to optimize the medical management of these patients. Although rare, MDS should be considered in the evaluation of pancytopenia after LT.