Eryhtropoetin induced ¹⁸F-PSMA-11 bone marrow sink effect

A patient with metastasized prostate adenocarcinoma underwent ¹⁸F-PSMA-11 PET/CT restaging following ¹⁷⁷Lu-PSMA-617 treatment and rising PSA-level. The maximum intensity projection image (right-side of the figure) demonstrated an intense homogenous tracer uptake throughout the bone marrow containing skeleton, whereas CT images showed specific bone metastases but no diffuse involvement, and previously known lymph node and liver metastases exhibited significantly reduced or absent uptake (see also left-side of the image, ¹⁸F-PSMA-11 MIP prior to ¹⁷⁷Lu-PSMA-617 therapy). None of the patients that underwent imaging with the same tracer-batch demonstrated similar findings excluding free ¹⁸F as a potential cause for the imaging findings. Furthermore, the patient did not suffer from any bone marrow disorder previously reported to present with diffuse bone marrow uptake on PSMA-targeting PET/CT imaging [1, 2]. Of interest, the patient had received recombinant human erythropoietin, 100 µg of Aranesp, 24 h prior to imaging to treat his renal failure associated anemia. At this dose, Aranesp reaches a nanomolar concentration in the bone marrow resulting in stimulation of the Tissue Protective Receptor on endothelial cells leading to the creation of a massive systemic reservoir of PSMA-positive neovasculature that outcompetes PSMA-expressing prostate carcinoma lesions for radiotracer availability [3, 4]. This may explain the diffuse marrow uptake and the decreased visibility of known metastases [4]. The effect of erythropoietin on bone marrow mobilization and neovascularization can persist for 7–10 days [5]. This should be taken into consideration in order to avoid erroneous interpretation of ¹⁸F-PMSA-11 PET/CT imaging and unnecessary bone marrow toxicity of ¹⁷⁷Lu-PSMA-617 treatment.