A 67‑year‑old man with advanced prostate cancer died after starting a hormone drug (degarelix) that blocks the GnRH system. Within days he developed tumor lysis syndrome (TLS), a dangerous condition where dying cancer cells flood the blood with harmful chemicals, leading to kidney failure and death. All similar cases in prostate cancer have been fatal, showing that GnRH‑blocking drugs can trigger TLS in patients with a huge tumor load.

Tumor lysis syndrome (TLS) is a life-threatening oncological emergency resulting from massive cellular destruction. Although most frequently associated with chemotherapy in hematologic malignancies, TLS is uncommon in solid tumors due to their typically slower proliferation rates and treatment response. We report a case of a 67-year-old male with a history of untreated prostate cancer diagnosed two years earlier, who presented with abdominal pain, anorexia, and weight loss. Physical examination revealed painful hepatomegaly. Laboratory tests showed a cholestatic pattern, elevated lactate dehydrogenase, and elevated prostate-specific antigen (PSA) levels. Computed tomography (CT) revealed findings suggestive of pulmonary, hepatic, and adrenal metastases, multiple mediastinal and abdominal lymphadenopathies, and osteolytic bone lesions. Despite the relatively modest increase in PSA levels compared to the extensive disease burden, repeat prostate biopsy confirmed a high-grade prostate adenocarcinoma (Gleason score 9). Hormone therapy with degarelix was initiated. On the third day after treatment initiation, the patient developed both laboratory and clinical features consistent with TLS, including hyperuricemia, hyperphosphatemia, hyperkalemia, and acute kidney injury (Acute Kidney Injury Network (AKIN) stage III). A mediastinal lymph node biopsy obtained via endobronchial ultrasound was subsequently performed but was inconclusive. TLS management was initiated, which included aggressive intravenous hydration, hypouricemic therapy with rasburicase, and correction of electrolyte disturbances. No additional disease-directed therapy, namely, renal replacement therapy, was pursued, given the rapid clinical deterioration, extensive metastatic disease, and absence of feasible oncologic treatment options, with an overall poor prognosis. The patient ultimately died 17 days after the onset of TLS. The literature consistently shows that TLS occurring after initiation of hormonal therapy, including gonadotropin-releasing hormone-axis interventions, is associated with extremely poor outcomes. In all reported treatment-related TLS cases in prostate cancer, mortality was universal despite aggressive supportive management. This case illustrates a rare instance of TLS occurring after initiation of gonadotropin-releasing hormone antagonist therapy in metastatic prostate cancer, highlighting the need for careful risk assessment, close biochemical monitoring, and prompt recognition and management of TLS, especially in patients with high tumor burden.