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Navigating Severe Thrombocytopenia in End-Stage Liver Disease: A Pre-transplant Management Dilemma
Fares Jamal1, Amani Elshaer2, Cody Eslinger1
1Hematology and Oncology, Mayo Clinic, Phoenix, USA.
End-stage liver disease (ESLD) due to autoimmune causes may be complicated by immune thrombocytopenia (ITP), making liver transplantation challenging. We present a case of refractory ITP in a liver transplant candidate and outline therapeutic strategies used to manage critical thrombocytopenia. A 60-year-old woman with ESLD from primary biliary cholangitis and autoimmune hepatitis was evaluated for liver and kidney transplants. Her platelet count declined from 45 K/µL to 12 K/µL, prompting hematology involvement. Despite intravenous immunoglobulin (IVIG) and dexamethasone, the platelet response was limited. Rituximab had no effect, and splenectomy was too risky pre-transplant due to portal hypertension. Thrombopoietin receptor agonists were limited by thrombotic risk. Subdural hematomas further complicated her course. Ultimately, partial splenic artery embolization improved her platelet count to 25 K/µL, allowing combined liver-kidney transplantation with splenectomy. Postoperatively, her platelet count increased to 854 K/µL without complications. Managing refractory ITP in ESLD requires a multifaceted approach. While corticosteroids and IVIG are first-line therapies, options like thrombopoietin agonists pose thrombotic risks. Splenic artery embolization may be a viable strategy to increase platelet counts before transplantation. Further research is needed to guide treatment in this complex population.
End-stage liver disease (ESLD) due to autoimmune causes may be complicated by immune thrombocytopenia (ITP), making liver transplantation challenging. We present a case of refractory ITP in a liver transplant candidate and outline therapeutic strategies used to manage critical thrombocytopenia. A 60-year-old woman with ESLD from primary biliary cholangitis and autoimmune hepatitis was evaluated for liver and kidney transplants. Her platelet count declined from 45 K/µL to 12 K/µL, prompting hematology involvement. Despite intravenous immunoglobulin (IVIG) and dexamethasone, the platelet response was limited. Rituximab had no effect, and splenectomy was too risky pre-transplant due to portal hypertension. Thrombopoietin receptor agonists were limited by thrombotic risk. Subdural hematomas further complicated her course. Ultimately, partial splenic artery embolization improved her platelet count to 25 K/µL, allowing combined liver-kidney transplantation with splenectomy. Postoperatively, her platelet count increased to 854 K/µL without complications. Managing refractory ITP in ESLD requires a multifaceted approach. While corticosteroids and IVIG are first-line therapies, options like thrombopoietin agonists pose thrombotic risks. Splenic artery embolization may be a viable strategy to increase platelet counts before transplantation. Further research is needed to guide treatment in this complex population.
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