Results of Scalp Cooling to Prevent Chemotherapy-Induced Alopecia

By Charbel C. Khoury, MD
August 8, 2015

Being diagnosed with cancer can be devastating and life-changing. Furthermore, the side effects of chemotherapy are often very distressing, and hair loss is one of the more feared complications. When a patient, and particularly a woman, loses her hair to chemotherapy, she is faced with the stigma of the disease, and may feel that she is losing her identity, femininity, and sexuality.1 Patients with chemotherapy-associated alopecia are confronted with the lethal nature of cancer, and a minority of patients even choose to avoid chemotherapy for fear of losing their hair. Continue reading “Results of Scalp Cooling to Prevent Chemotherapy-Induced Alopecia”

Vancomycin as a Rare Cause of Drug-Induced Cytopenias

By Martina M. McGrath, MD
May 30, 2017

Vancomycin is a glycopeptide antibiotic, with activity against gram positive organisms, including MRSA. It is widely prescribed for hospital-acquired infections, device-related infections, and treatment of resistant organisms. While side effects such as red man syndrome, ototoxicity, and nephrotoxicity are well recognized, immune thrombocytopenia is a less common, but potentially severe, complication of vancomycin therapy. Indeed, because many affected patients are critically ill or treated with other potential culprit agents such as heparin, vancomycin-induced platelet destruction can go unrecognized. Continue reading “Vancomycin as a Rare Cause of Drug-Induced Cytopenias”

Immune Checkpoint Inhibitors: Collateral Damage and Organ Toxicities

By Martina M. McGrath, MD
February 3, 2017

Cancer immunotherapy has led to a paradigm shift in the treatment of a range of malignancies. Recently developed, immune checkpoint inhibitors (ICPI) are monoclonal antibodies, which specifically block immunological pathways involved in the control of T cell-mediated immune responses. Anti-CTLA4 (ipilimumab) blocks the interaction of CTLA-4, expressed by regulatory T cells, with its ligand, B7, allowing for increased T cell activation via CD28-B7 signalling. Similarly anti-PD-1 (nivolumab, pembrolizumab, pidilizumab) prevents interaction between PD-1 and its ligand PD-L1, another critical negative T cell costimulatory pathway. By ‘removing the brake’ for T cell activation, these agents increase anti-tumor immunity and overcome some of the mechanisms by which tumors evade the immune response. Management of diseases such as metastatic melanoma have been transformed by the availability of these agents and studies continue to show benefit in an increasing number of malignancies. Continue reading “Immune Checkpoint Inhibitors: Collateral Damage and Organ Toxicities”