Severe intracellular magnesium and potassium depletion in patients after treatment with cisplatin

Abstract

The purpose of this study is (1) to evaluate skeletal muscle magnesium (Mg) and potassium (K) during treatment with cisplatin; (2) to evaluate the predictive value of plasma (P)-Mg for intracellular Mg during cisplatin treatment; and (3) to evaluate whether changes in intracellular K influence skeletal muscle Na,K-ATPase. In all, 65 patients had a needle muscle biopsy obtained before and 26 patients both before and after cisplatin treatment. Biopsies were analysed for Mg, K, and Na,K-ATPase concentrations, and P-Mg and P-K determined. Treatment with a total dose of E500 mg (270 mg [K] were not associated with changes in the muscle Na,K-ATPase concentration. Following treatment with cisplatin, an E15% decline in P-Mg was accompanied by an E15% loss of muscle [Mg], as well as an E10% reduction of muscle [K] and fatigue and muscle weakness previously ascribed to hypomagnesaemia may therefore also be well explained by muscle K depletion observed despite normal levels of P-K. There was no correlation between P-Mg and SM-Mg or between P-K and SM-K. Thus, P-Mg and P-K are not reliable indicators for Mg and K depletion during treatment with cisplatin. However, the majority of patients will present Mg and K depletion after cisplatin therapy and of these only very few patients will present a low P-Mg or P-K. Therefore, routine supplementation should be considered in all patients receiving cisplatin.

Cisplatin increases urinary sodium excretion in rats: gender-related differences

“…Cisplatin has multiple intracellular effects, causing direct cytotoxicity with reactive oxygen species, activating mitogenactivated protein kinases, and stimulating inflammation and fibrogenesis. These events cause tubular damage and tubular dysfunction with Na, K, and Mg wasting (6,7). In addition to elevation of serum creatinine levels and uremia, electrolyte abnormalities are well-known adverse effects of cisplatin (8).…”

Metabolic syndrome in childhood leukemia survivors: a meta-analysis

“…Also intensive CT plays a role to increase the risk of MetS as some chemotherapeutic agents can lead to MetS through several mechanisms [39][40][41]. Alkylating agents and CRT may damage the testis and the pituitary gland, respectively, leading to testosterone deficiency in both of cases.…”

“…Alkylating agents and CRT may damage the testis and the pituitary gland, respectively, leading to testosterone deficiency in both of cases. Cisplatin treatment may cause at short-and longterm magnesium deficiency, increasing the risk for MetS, as magnesium intake is inversely associated with MetS and its individual components [39,40]. CT-related endothelial damage, exerted by platinum and bleomycin, is associated with insulin resistance [41,42] and increases the risk of MetS.…”

“…Even if the pathogenetic mechanisms have not yet been fully clarified, these modalities might lead to alterations in the endocrine and metabolic states [15,16,22,32,[35][36][37][38][39][40][41][42][43][44][45][46] causing MetS.…”

Serum and Tissue Concentrations of Magnesium, Calcium, Potassium and Sodium in Rats

“…It is therefore of great importance to detect magnesium deficiency in the organism (Feillet-Coudray et al 2003;Gong et al 2003;Hoane et al 2003;Lajer et al 2003;Rude et al 2003). Some authors recommend the use of magnesium concentrations in serum for assessment of deficiency, but others argue that the loading test will provide more exact results, because in the presence of normal serum values intracellular magnesium may be deficient (Stalnikowitz 2003).…”