Novel recently approved drugs can cause rhabdomyolysis, sometimes presenting with combined toxicity in both heart and skeletal muscle, which points to new target mechanisms.
This review highlights that some novel drugs can cause combined toxicity in both heart and skeletal muscle, challenging the dogma that cardiac tissue is only secondarily affected in rhabdomyolysis.
Rhabdomyolysis is a clinical condition of potential life threatening destruction of skeletal muscle caused by diverse mechanisms including drugs and toxins. Given the fact that structurally not related compounds cause an identical phenotype pinpoints to common targets or pathways, responsible for executing rhabdomyolysis. A drop in myoplasmic ATP paralleled with sustained elevations in cytosolic Ca²⁺ concentration represents a common signature of rhabdomyolysis. Interestingly, cardiac tissue is hardly affected or only secondary, as a consequence of imbalance in electrolytes or acid-base equilibrium. This dogma is now impaired by compounds, which show up with combined toxicity in heart and skeletal muscle. In this review, cases of rhabdomyolysis with novel recently approved drugs will be explored for new target mechanisms in the light of previously described pathomechanisms.
M. Hohenegger (Sat,) conducted a review in Drug-induced rhabdomyolysis. Novel recently approved drugs was evaluated. Novel recently approved drugs can cause rhabdomyolysis, sometimes presenting with combined toxicity in both heart and skeletal muscle, which points to new target mechanisms.