Eric Van Cutsem, MD, PhD | Authors

Clinical Management of EGFRI Dermatologic Toxicities: The European Perspective

October 01, 2007

Dermatologic treatment of epidermal growth factor receptor inhibitor (EGFRI) skin toxicity is supportive and aims at maintaining quality of life while continuing EGFRI therapy. Despite the lack of randomized controlled trials or evidence-based guidelines, most cases of acneiform eruption are well controlled by topical metronidazole and oral minocycline 100 mg qd. For severe reactions, the minocycline dose is doubled and saline compresses are used. For superinfection with Staphylococcus aureus, oral cefuroxime axetil can be added for a short term. Emollients and topical steroids can be administered for skin dryness or eczema. Paronychia is the hardest to treat but antiseptic soaks and a corticosteroid paste can alleviate symptoms to some degree.

Clinical Presentation and Pathophysiology of EGFRI Dermatologic Toxicities

October 01, 2007

This review summarizes the pathophysiology and clinical presentation of the cutaneous toxicities associated with EGFR inhibition. Such effects include papulopustular reactions, xerosis, pruritus, fissures, nail changes, hair changes, telangiectasias, hyperpigmentation, and mucositis. Most management strategies for these toxicities have been based on anecdotal experience; clinical trials are needed to provide uniform characterization to allow for evidence-based treatment strategies.

Clinical Research of EGFR Inhibitors and Related Dermatologic Toxicities

October 01, 2007

An acneiform-like skin toxicity is commonly observed in patients with solid tumors treated with epidermal growth factor receptor inhibitors (EGFRIs). This symptomatic rash is related to epidermal growth factor receptor (EGFR) inhibition in the skin. A positive relation between the presence and severity of treatment-related rash and survival has been consistently observed with all EGFRIs approved for clinical use. These findings suggest that rash may be a useful surrogate marker of successful EGFR inhibition and clinical benefit and therefore of possible use in identifying patients most likely to benefit from therapy, as well as to guide dose adjustments. Increasing drug dose until skin toxicity appears is being studied. Further studies are needed to thoroughly evaluate the value of skin toxicity as a surrogate marker for clinical benefit. Current treatments of the skin toxicity are empirical and oriented toward mitigating symptoms and not validated by well-controlled clinical trials. Rational treatments based on the biological mechanisms of the skin toxicity must be developed and tested in well-controlled clinical trials.