Role of Sodium-Glucose Co-Transporter-2 Inhibitor During Anthracycline Use: An Updated Review.

The coalescence of anthracycline-induced cardiotoxicity and the evolving role of sodium-glucose co-transporter-2 (SGLT-2) inhibitors in oncology and cardiology has prompted a comprehensive review of their mechanisms, clinical implications, and future directions. Anthracyclines, potent chemotherapeutic agents, have been integral in cancer treatment, yet their potential for cardiac harm necessitates careful monitoring and management. We explore the multifactorial nature of anthracycline-induced cardiotoxicity, encompassing diverse patient populations, cumulative doses, and interplay with other treatments. While advancements in imaging and biomarker assessments aid in early detection, the lack of standardized criteria poses challenges. The emergent role of SGLT-2 inhibitors, initially developed for diabetes management, presents a novel avenue for cardioprotection. Beyond glycemic control, these inhibitors exhibit pleiotropic effects, including enhanced diuresis, anti-inflammatory actions, and modulation of energy sources. Consequently, SGLT-2 inhibitors are being investigated for their potential to mitigate cardiotoxic effects, promising an innovative approach in cardio-oncology. Despite these advancements, limitations in data interpretation and patient-specific considerations persist. The future of anthracycline-induced cardiotoxicity research lies in predictive biomarkers, precision medicine, multidisciplinary collaboration, and tailored treatment regimens. By navigating these challenges and harnessing emerging strategies, we aim to optimize cancer treatment efficacy while safeguarding cardiovascular health, ultimately paving the way for a new era of personalized and comprehensive oncologic care.

Toxicities of CAR T-cell therapy: a review of current literature.

The chimeric antigen receptor (CAR) design, first invented by Zelig Eshhar, paved the way for the use of genetically modified T-cells in targeted therapy against cancer cells. Since then, it has gone through many generations, especially with the integration of co-stimulation in the second and third-generation CARs. However, it also mounts a hyperactive immune response named as cytokine release syndrome with the release of several cytokines eventually resulting in multiple end-organ toxicities. The severity of cytokine release syndrome depends upon certain factors such as the tumor burden, choice of co-stimulation, and degree of lymphodepletion, and can manifest as pulmonary edema, vascular leak, renal dysfunction, cardiac problems, hepatic failure, and coagulopathy. Many grading criteria have been used to define these clinical manifestations but they lack harmonization. Neurotoxicity has also been significantly associated with CAR T-cell therapy but it has not been studied much in previous literature. This review aims to provide a comprehensive account of the clinical manifestations, diagnosis, management, and treatment of CAR T-cell associated neurotoxicity.