Rabacfosadine-Induced Mucocutaneous Toxicity and Multi-Organ Failure in a Dog with Multicentric B-Cell Lymphoma

Canine B-cell lymphomas often develop resistance to standard cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy, necessitating effective salvage options.While the temozolomide-based THOP protocol and rabacfosadine (Tanovea ® ) are recognized rescue therapies for refractory cases, detailed clinical reports documenting their severe systemic toxicities remain scarce.An 11-year-old mixed-breed dog with CHOP-refractory multicentric B-cell lymphoma experienced rapid disease progression despite sequential rescue attempts, including a temozolomide-based THOP protocol.As a last-line salvage therapy, rabacfosadine was administered, which induced rapid and marked tumor reduction within 1 week.Despite this initial potent response, the tumor regrew shortly after administration, and the clinical course was complicated by a severe and ultimately fatal toxicity cascade.The patient developed profound dermatopathy and gastrointestinal mucosal shedding.This extensive mucocutaneous barrier disruption likely precipitated hypovolemia and systemic inflammatory response syndrome (SIRS).Consequently, this acute hemodynamic collapse led to fatal secondary ischemic injuries, specifically acute pancreatitis and Grade IV acute kidney injury (AKI).This case highlights the critical potential for rabacfosadine to induce a fatal toxicity cascade initiated by barrier failure.It emphasizes the urgent need for rigorous monitoring and early intervention for dermatologic and gastrointestinal adverse events to prevent systemic hemodynamic collapse in heavily pre-treated patients.