Cyclosporine's immunosuppressive effects, entwined toxicity, and clinical modulations of an organ transplant drug.

The discovery and use of cyclosporine since its inception into the clinics in the '70s and up have played a crucial role in the advancement of transplant therapy and containment of immune-based rejections. The drug had improved rates of acute rejections, and supported early graft survival. However, the long-term survival of renal allografts is still less prevalent, and an in-depth analysis and reported findings led us to believe that there is a chronic irreversible component to the drug that is tackled through its metabolites, and causes toxicity, which led to new therapies, including monoclonal antibody based medications. A recap of the immunosuppressive effects and entwined toxicity of the drug, now relegated to solid transplants, overviews the past protocols used to minimize and avoid, or use in combination with this calcineurin inhibitor class drug with other drugs. The current review circumvents the cyclosporine's mechanism of action, pathophysiology, cytochrome roles, and other factors associated with acute and chronic toxicity. It also attempts to find conclusive strategies reported in recent studies to avoid its toxic side effects and develop a safe-use strategy for the drug. Gastrointestinal decontamination, supporting the airway, monitoring for signs of respiratory insufficiency, monitoring for severe reactions such as seizures, administration of oxygen, and avoiding the administration of drugs that increase the blood levels of cyclosporine are beneficial interventions when encountering cyclosporine toxicity cases. The constrained therapeutic outcome has also led to redesign, and combine formulation to review the pharmacokinetics of the drug.