# Navigating Severe Thrombocytopenia in End-Stage Liver Disease: A Pre-transplant Management Dilemma

**Authors:** Fares Jamal, Amani Elshaer, Cody Eslinger, Sailendra Naidu, Rolland C Dickson, Leslie J Padrnos

PMC · DOI: 10.7759/cureus.85811 · Cureus · 2025-06-11

## TL;DR

This paper discusses the challenges of managing severe low platelet counts in a patient with end-stage liver disease before a transplant.

## Contribution

The paper presents a novel case of refractory immune thrombocytopenia and outlines a successful pre-transplant management strategy.

## Key findings

- Partial splenic artery embolization improved platelet count to 25 K/µL, enabling transplantation.
- Post-transplant platelet count increased to 854 K/µL without complications.
- Corticosteroids and IVIG had limited effectiveness, while splenic artery embolization was a viable alternative.

## Abstract

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.

## Linked entities

- **Chemicals:** dexamethasone (PubChem CID 5743)
- **Diseases:** end-stage liver disease (MONDO:0100193), primary biliary cholangitis (MONDO:0005388), autoimmune hepatitis (MONDO:0016264), immune thrombocytopenia (MONDO:0002048), portal hypertension (MONDO:0005080)

## Full-text entities

- **Genes:** MPL (MPL proto-oncogene, thrombopoietin receptor) [NCBI Gene 4352] {aka C-MPL, CD110, MPLV, THCYT2, THPOR, TPOR}, THPO (thrombopoietin) [NCBI Gene 7066] {aka CAMT2, MGDF, MKCSF, ML, MPLLG, THC9}
- **Diseases:** thrombotic (MESH:D013927), autoimmune hepatitis (MESH:D019693), primary biliary cholangitis (MESH:D008105), hematomas (MESH:D006406), Thrombocytopenia (MESH:D013921), portal hypertension (MESH:D006975), ESLD (MESH:D058625), ITP (MESH:D016553)
- **Chemicals:** dexamethasone (MESH:D003907), Rituximab (MESH:D000069283)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12254519/full.md

## References

20 references — full list in the complete paper: https://tomesphere.com/paper/PMC12254519/full.md

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Source: https://tomesphere.com/paper/PMC12254519