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Hypomagnesaemia and targeted anti-epidermal growth factor receptor (EGFR) agents
Andreia Costa1, Sabine Tejpar, Hans Prenen
1Digestive Oncology, University Hospital Gasthuisberg, Leuven, Belgium.
Abstract:
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.
Insights
Targeted anti-epidermal growth factor receptor (EGFR) agents can cause hypomagnesaemia and hypocalcaemia. This review details the mechanisms, clinical findings, and management of these electrolyte disorders in cancer patients.
Area of Science:
- Oncology
- Nephrology
- Pharmacology
Background:
- Targeted anti-epidermal growth factor receptor (EGFR) agents are crucial in cancer therapy.
- These therapies, especially monoclonal antibodies, can lead to electrolyte disturbances like hypomagnesaemia and hypocalcaemia.
- Early recognition of magnesium deficiency is challenging, yet severe cases can manifest as cardiac arrhythmias or convulsions.
Purpose of the Study:
- To review clinical trial findings on hypomagnesaemia induced by anti-EGFR agents.
- To discuss the underlying mechanisms of EGFR inhibitor-related electrolyte disorders.
- To outline treatment strategies for hypomagnesaemia in patients receiving anti-EGFR therapy.
Main Methods:
- Literature review of peer-reviewed journals.
- Analysis of clinical trial data.
- Discussion of pharmacological mechanisms.
Main Results:
- Anti-EGFR agents can cause urinary magnesium and calcium wasting due to inhibition of the transient receptor potential cation channel, subfamily M, member 6 (TRPM6).
- The risk of hypomagnesaemia correlates with treatment duration.
- This toxicity is reversible, with magnesium levels typically normalizing 4-6 weeks after treatment cessation.
Conclusions:
- Hypomagnesaemia is a significant, albeit reversible, side effect of anti-EGFR targeted therapies.
- Understanding the mechanism involving renal EGF/EGFR expression and TRPM6 is key to managing this toxicity.
- Prompt identification and management are essential for patient safety during cancer treatment.
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