Salicylate-induced rhabdomyolysis

Interactions of Human Organic Anion Transporters and Human Organic Cation Transporters with Nonsteroidal Anti-Inflammatory Drugs

“…Acetaminophen, salicylate, diclofenac, and ibuprofen were reported to induce rhabdomyolysis in humans (Ross and Hoppel, 1987;Leventhal et al, 1989;Delrio et al, 1996). In this regard, hOAT3 was shown to be expressed in the skeletal muscle using Northern blot analysis (Cha et al, 2001).…”

“…Although the chemical diversity yields a broad range of pharmacokinetic characteristics (Frust and Munster, 2000), they have some general properties in common. NSAIDs have been shown to induce various forms of adverse drug reactions including adverse gastrointestinal effects (Day et al, 2000), renal dysfunction and nephrotoxicity (Day et al, 2000), liver damage (Zimmerman, 1981;Wood et al, 1985;Purcell et al, 1991;Day et al, 2000), adverse neurological effects (Hoppman et al, 1991;Day et al, 2000), and rhabdomyolysis (Ross and Hoppel, 1987;Leventhal et al, 1989;Delrio et al, 1996).…”

“…Although the chemical diversity yields a broad range of pharmacokinetic characteristics (Frust and Munster, 2000), they have some general properties in common. NSAIDs have been shown to induce various forms of adverse drug reactions including adverse gastrointestinal effects (Day et al, 2000), renal dysfunction and nephrotoxicity (Day et al, 2000), liver damage (Zimmerman, 1981;Wood et al, 1985;Purcell et al, 1991;Day et al, 2000), adverse neurological effects (Hoppman et al, 1991;Day et al, 2000), and rhabdomyolysis (Ross and Hoppel, 1987;Leventhal et al, 1989;Delrio et al, 1996).The secretion of numerous organic anions and cations, including endogenous metabolites, drugs, and xenobiotics, is an important physiological function of the renal proximal tubule. The process of secreting organic anions and cations through the proximal tubule cells is achieved via unidirectional transcellular transport involving the uptake of organic anions and cations into the cells from the blood across the basolateral membrane, followed by extrusion across the brush-border membrane into the proximal tubule fluid (Pritchard and Miller, 1993).…”

Rhabdomyolysis among hospitalized patients for salicylate intoxication in the United States: Nationwide inpatient sample 2003–2014

“…The neuromuscular effect of salicylate is uncommon. Rhabdomyolysis has been infrequently reported as a complication of salicylate intoxication [4,5]. The specific mechanism of rhabdomyolysis in salicylate intoxication is still unclear.…”

“…The specific mechanism of rhabdomyolysis in salicylate intoxication is still unclear. The uncoupling of oxidative phosphorylation leading to increase in heat production might be responsible the development of rhabdomyolysis [4]. Also, severe systemic inflammation and muscle rigidity might occur in salicylate intoxication, resulting in further heat production and muscle injury [3,5].…”