Case Report: Zoledronic acid-induced hyperprogression in oncology: a case study of RET-driven neuroendocrine carcinoma treated with Selpercatinib - Report - MDSpire
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Case Report: Zoledronic acid-induced hyperprogression in oncology: a case study of RET-driven neuroendocrine carcinoma treated with Selpercatinib
Clinical Report: Hyperprogressive Disease Induced by Zoledronic Acid
Overview
This case study presents a 59-year-old woman with RET-driven neuroendocrine carcinoma who developed hyperprogressive disease after switching from denosumab to zoledronic acid. The rapid deterioration of her condition highlights the need for careful monitoring when changing bone-modifying agents during targeted therapy.
Background
Hyperprogressive disease (HPD) is a phenomenon where tumor growth accelerates following treatment, which can complicate management strategies for patients with advanced malignancies. Understanding the potential triggers of HPD, particularly in the context of bone-modifying agents like zoledronic acid, is crucial for optimizing treatment outcomes in patients with metastatic disease. This case underscores the importance of monitoring treatment responses in patients receiving targeted therapies.
Data Highlights
No numerical data or trial data presented in the article.
Key Findings
A 59-year-old woman with RET p.V804M mutation experienced HPD after switching to zoledronic acid.
Initial treatment with Selpercatinib and denosumab resulted in partial remission for 6 months.
After switching to zoledronic acid, the patient developed severe bone pain and elevated NSE levels within one month.
Radiological assessments showed significant disease progression after the switch to zoledronic acid.
The patient’s condition deteriorated rapidly, leading to her death 8 months post-diagnosis.
Clinical Implications
Clinicians should exercise caution when switching bone-modifying agents in patients undergoing targeted therapy, as this may trigger HPD. Close monitoring of symptoms and tumor markers is essential to identify any adverse effects promptly.
Conclusion
This case highlights the potential risks associated with changing bone-modifying agents during RET inhibitor therapy and emphasizes the need for further research to understand the mechanisms behind HPD.
