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Cutaneous Toxicity from Epidermal Growth Factor Receptor Inhibitors: Would a Subcutaneous Desensitization be Helpful? Case Report

Authors :
Daniela Di Mauro
Andrea D'Alessio
Davide Resta
Carmelo Fortugno
Simonetta Villa
Luca Geroli
S. Cecchini
Antonello Quadri
Source :
Tumori Journal. 102:S65-S68
Publication Year :
2016
Publisher :
SAGE Publications, 2016.

Abstract

Purpose Cetuximab and panitumumab are monoclonal antibody inhibitors that bind the epidermal growth factor receptor (EGFR) currently used in the treatment of metastatic colorectal cancer. The main adverse event related to EGFR inhibitors (EGFR-Is) is cutaneous toxicity, which can cause dosage reduction and interruption of treatment. State-of-the-art management of skin toxicity associated with EGFR-Is therapy involves the topical administration of corticosteroids and oral antibiotics, but is not completely effective in the management of toxicity. Subcutaneous desensitization with increasing concentrations of monoclonal antibodies can induce a tolerance to drug administration and reduce cutaneous adverse effects. To our knowledge, this is the first case in which a reduction or a disappearance of skin toxicity caused by EGFR-Is through subcutaneous desensitization has been achieved. Case Report We present cases of 2 Caucasian patients with adenocarcinoma of the colon treated with EGFR-Is who developed severe cutaneous toxicity. A 73-year-old man presented grade 4 skin toxicity of the face and grade 3 skin toxicity of the trunk during treatment with cetuximab. A 68-year-old woman developed G2 rash on the face after the first administration of cetuximab. These patients underwent subcutaneous desensitization with increasing concentrations of EGFR-Is. After this procedure, patients restarted therapy at the optimal dosage with reduction or disappearance of skin toxicity. Conclusions These cases suggest that by giving rising doses of antibody it is possible to obtain desensitization able to prevent severe cutaneous adverse events in patients treated with EGFR-Is.

Details

ISSN :
20382529 and 03008916
Volume :
102
Database :
OpenAIRE
Journal :
Tumori Journal
Accession number :
edsair.doi.dedup.....2f2eba71793a3d621c5f83af0db0226f
Full Text :
https://doi.org/10.5301/tj.5000579