Digestive Oncology, University Hospital Gasthuisberg, Leuven, Belgium.
Target Oncol. 2011 Dec;6(4):227-33. doi: 10.1007/s11523-011-0200-y. Epub 2011 Nov 24.
Currently, targeted anti-epidermal growth factor receptor (EGFR) agents have an important role in the treatment of various cancers. These drugs, particularly anti-EGFR monoclonal antibodies, may induce electrolyte disorders, such as hypomagnesaemia and hypocalcaemia. Early symptoms of magnesium deficiency can easily go unrecognized. However, hypomagnesaemia can in rare cases lead to serious clinical manifestations, including cardiac arrhythmias or convulsions. The elective tubular expression of renal EGF/EGFR explains the mechanism of this class-related drug side effect. Inhibition of the EGFR induces a mutated-like transient receptor potential cation channel, subfamily M, member 6 (TRPM6) syndrome, characterized by urinary magnesium and calcium wasting. The risk of hypomagnesaemia is associated with treatment duration. It is a reversible toxicity; the recovery of magnesium serum levels is usually seen 4-6 weeks of stopping the anti-EGFR antibody. Using literature from peer-reviewed journals, this review reports the clinical trials findings and discusses the mechanisms and the treatment of hypomagnesaemia induced by anti-EGFR targeted agents.
目前，靶向表皮生长因子受体 (EGFR) 的药物在各种癌症的治疗中具有重要作用。这些药物，特别是抗 EGFR 单克隆抗体，可能会引起电解质紊乱，如低镁血症和低钙血症。镁缺乏的早期症状很容易被忽视。然而，低镁血症在极少数情况下可导致严重的临床表现，包括心律失常或抽搐。肾脏 EGF/EGFR 的选择性管状表达解释了这种与药物相关的副作用的机制。EGFR 的抑制会诱导一种类似突变的瞬时受体电位阳离子通道，亚家族 M，成员 6（TRPM6）综合征，其特征是尿镁和钙流失。低镁血症的风险与治疗持续时间有关。它是一种可逆的毒性；停止使用抗 EGFR 抗体后 4-6 周通常会看到血清镁水平的恢复。本文使用同行评议期刊的文献，报告了临床试验结果，并讨论了抗 EGFR 靶向药物引起的低镁血症的机制和治疗方法。
