Severe intracellular magnesium and potassium depletion in patients after treatment with cisplatin.
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 approximately 500 mg (270 mg m(-2) surface area) cisplatin over 80 days was associated with reductions in muscle [Mg] (95% CI) (8.95 (8.23-9.63) to 7.76 (7.34-8.18) mumol g(-1) wet wt. (P<0.01), and muscle [K] (90.81 (83.29-98.34) to 82.87 (78.74-87.00) mumol g(-1) wet wt. (P<0.05), as well as in P-Mg 0.82 (0.80-0.85) to 0.68 (0.64-0.73) mmol l(-1) (P<0.01 but not in P-K (4.0 (3.8-4.1) vs 3.8 (3.7-4.0) mmol l(-1)). No simple correlations were observed between P-Mg and muscle [Mg], or between P-K and muscle [K], either before (n=65) or after (n=26) treatment with cisplatin. The changes in [Mg] and [K] were not associated with changes in the muscle Na,K-ATPase concentration. Following treatment with cisplatin, an approximately 15% decline in P-Mg was accompanied by an approximately 15% loss of muscle [Mg], as well as an approximately 10% 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.
Department of Oncology 5072, Rigshospitalet, University of Copenhagen, The Finsen Center, Blegdamsvej 9, Copenhagen DK-2100, Denmark. H.LAJER@rh.dk
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H
Lajer
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Bundgaard
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Secher
H H
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Hansen
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Kjeldsen
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Daugaard
D000251:Adenosine Triphosphatases / Q000032:analysis / Q000187:drug effects; D017301:Ca(2+) Mg(2+)-ATPase / Q000032:analysis / Q000187:drug effects; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy; D027682:Cation Transport Proteins; D002945:Cisplatin / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007424:Intracellular Fluid / Q000187:drug effects*; D008175:Lung Neoplasms; D008274:Magnesium / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000737:chemistry / Q000187:drug effects*; D011188:Potassium / Q000032:analysis*; D011237:Predictive Value of Tests; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis / Q000187:drug effects; D013736:Testicular Neoplasms / Q000188:drug therapy
D027682:Cation Transport Proteins; D000251:Adenosine Triphosphatases; D017301:Ca(2+) Mg(2+)-ATPase; C022761:potassium transporting ATPase; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D002945:Cisplatin; D011188:Potassium