Vol 8, No 4 (2012)
Review paper
Published online: 2012-10-08
The mechanisms of magnesium wasting during the treatment with cetuximab and panitumumab
Onkol. Prak. Klin 2012;8(4):143-150.
Abstract
Cetuximab and panitumumab are monoclonal antibodies (mAbs) against epidermal growth factor receptor
(EGFR). Their function is to bind specifically to the extracellular domain of EGFR on both neoplastic
and normal cells which blocks the influence of EGF on the receptor. The important side effect of the
treatment with those drugs, apart from skin toxicity, infusion reactions or nausea, is hypomagnesemia.
Studies show that the mechanism responsible for this effect is the inhibition of EGFR by mAbs in distal
convoluted tubule of the nephron. The EGFR blockage through Ras and mitogen-activated protein kinase
suppress transient receptor potential melastatin submember 6 ion channel responsible for magnesium
reabsorption. The inhibition results in magnesium wasting and secondary hypomagnesemia. Almost all
patients treated with mAbs anty-EGFR have decreased level of blood serum magnesium but only few
develop severe hypomagnesemia.
(EGFR). Their function is to bind specifically to the extracellular domain of EGFR on both neoplastic
and normal cells which blocks the influence of EGF on the receptor. The important side effect of the
treatment with those drugs, apart from skin toxicity, infusion reactions or nausea, is hypomagnesemia.
Studies show that the mechanism responsible for this effect is the inhibition of EGFR by mAbs in distal
convoluted tubule of the nephron. The EGFR blockage through Ras and mitogen-activated protein kinase
suppress transient receptor potential melastatin submember 6 ion channel responsible for magnesium
reabsorption. The inhibition results in magnesium wasting and secondary hypomagnesemia. Almost all
patients treated with mAbs anty-EGFR have decreased level of blood serum magnesium but only few
develop severe hypomagnesemia.