# Navigating Cytomegalovirus Retinitis in a Patient With Myelodysplastic Syndromes Transitioning to Acute Myeloid Leukemia Post Transplant: A Case Study

**Authors:** Steven A Benyahia, Sunny Kahlon, Srijit Paul, Yusuf Aboul-Nasr, Kevin Harvey, Mamta Patel, Shivan Shah, Enas Abdallah

PMC · DOI: 10.7759/cureus.78491 · 2025-02-04

## TL;DR

A patient with myelodysplastic syndromes and acute myeloid leukemia faced complex treatment challenges due to CMV retinitis and drug resistance.

## Contribution

This case study highlights the management of CMV retinitis with UL97 resistance in a patient transitioning from MDS to AML post-transplant.

## Key findings

- The patient's CMV PCR levels decreased with combination therapies but required letermovir for sustained control.
- AML relapse treatment led to undetectable TP53 mutations and reduced CD34+ blasts.
- Foscarnet treatment caused acute kidney injury, requiring hydration and careful management.

## Abstract

We present a case of cytomegalovirus (CMV) retinitis with UL97 resistance in a patient undergoing treatment for acute myeloid leukemia (AML), highlighting the complex interplay between hematological malignancies and CMV management. A 49-year-old female patient with myelodysplastic syndromes (MDS) with 4.5% blasts and TP53 mutations ((variant allele frequency (VAF)) 5.2%) underwent an allogeneic stem cell transplant complicated by acute graft versus host disease (GvHD) and subsequent CMV viremia. Her UL97 resistance posed significant challenges to CMV management, necessitating a transition from ganciclovir to foscarnet and maribavir. The CMV polymerase chain reaction (PCR) levels initially >10,000 copies/mL decreased to <300 copies/mL with combination therapies, though fluctuations persisted until letermovir prophylaxis was initiated. Six months after the transplant, AML relapse was treated with cladribine, cytarabine, granulocyte-colony-stimulating factor/filgrastim, and mitoxantrone (CLAG-M) and venetoclax, leading to measurable clearance of TP53 mutations to undetectable levels by NGS and reduction of CD34+ blasts from 25% to 0%. However, the patient developed vision loss and was diagnosed with CMV retinitis, requiring intravitreal and systemic foscarnet alongside laser prophylaxis for retinal detachment. The complexity of her case was compounded by foscarnet-induced acute kidney injury (AKI), requiring intravenous hydration and suspected GvHD, managed with steroids and supportive care. This case illustrates the aggressive nature of MDS-AML progression, the critical role of vigilant CMV surveillance, and the nuanced approach needed for treatment, balancing efficacy against potential side effects. The successful navigation of these complexities offers valuable insights for similar cases.

## Linked entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157]
- **Chemicals:** ganciclovir (PubChem CID 135398740), foscarnet (PubChem CID 3415), maribavir (PubChem CID 471161), cladribine (PubChem CID 20279), cytarabine (PubChem CID 6253), mitoxantrone (PubChem CID 4212), venetoclax (PubChem CID 49846579)
- **Diseases:** cytomegalovirus retinitis (MONDO:0000878), myelodysplastic syndromes (MONDO:0018881), acute myeloid leukemia (MONDO:0015667), graft versus host disease (MONDO:0013730), acute kidney injury (MONDO:0002492)

## Full-text entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, CD34 (CD34 molecule) [NCBI Gene 947]
- **Diseases:** GvHD (MESH:D006086), CMV retinitis (MESH:D017726), CMV viremia (MESH:D014766), AML (MESH:D015470), AKI (MESH:D058186), MDS (MESH:D009190), vision loss (MESH:D014786), hematological malignancies (MESH:D019337), retinal detachment (MESH:D012163)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11884420/full.md

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Source: https://tomesphere.com/paper/PMC11884420