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Bioimpact of EGFR antagonists on the pilosebaceous follicles
Gérald E Pierard1, Claudine Pierard-Franchimont, Philippe Humbert
1Laboratory of Skin Bioengineering and Imaging, Department of Dermatopathology, University Hospital Sart Tilman, Liège, Belgium. Gerald.pierard@ulg.ac.be
Abstract:
Cancer patients under targeted chemotherapy to the epidermal growth factor receptor (EGFR) frequently suffer from unusual skin adverse events. In the past, these changes were globally qualified as a rash. Our aim was to assess objectively by non invasive bioinstrumentation some early structural and functional skin changes associated with EGFR inhibitor treatment. A series of 27 cancer patients aged 58-66 years were assessed using two ultraviolet light emitting CCD cameras, Visioscan(®) and Visiopor(®). Assessments were performed on the foreheads at inclusion and therefore at weekly intervals for 2 months at most. No topical treatment was applied during the assessment period. The Visioscan(®) camera revealed specular light reflectance at the site of follicular plugging. The interfollicular stratum corneum showed occasional focal hyperkeratosis. These features increased in severity with the EGFR inhibitor treatment, indicating follicular involvement as an early adverse event of the therapy. The follicular fluorescence revealed by the Visiopor(®) camera remained unchanged over the treatment period. The present findings suggest an EGFR inhibitor-induced kerosis (follicular hyperkeratosis) possibly responsible for acneiform reactions.
Insights
Epidermal growth factor receptor (EGFR) inhibitors cause early skin changes, specifically follicular plugging and hyperkeratosis, leading to acneiform reactions in cancer patients. These findings highlight a condition termed EGFR inhibitor-induced kerosis.
Area of Science:
- Dermatology
- Oncology
- Bioinstrumentation
Background:
- Targeted cancer therapies, particularly epidermal growth factor receptor (EGFR) inhibitors, frequently cause skin adverse events.
- Previously, these skin changes were broadly categorized as a rash, lacking specific characterization.
Purpose of the Study:
- To objectively assess early structural and functional skin changes induced by EGFR inhibitor treatment using non-invasive bioinstrumentation.
- To identify specific skin alterations associated with EGFR inhibitor therapy beyond generalized rash.
Main Methods:
- A cohort of 27 cancer patients (aged 58-66 years) undergoing EGFR inhibitor treatment were evaluated.
- Non-invasive bioinstrumentation, including Visioscan® and Visiopor® ultraviolet light emitting CCD cameras, was used for assessments.
- Forehead skin was assessed weekly for up to 2 months, with no topical treatments applied.
Main Results:
- Visioscan® imaging revealed specular light reflectance indicative of follicular plugging and occasional focal hyperkeratosis in the interfollicular stratum corneum.
- These observed skin changes, particularly follicular plugging and hyperkeratosis, increased in severity with continued EGFR inhibitor treatment.
- Visiopor® imaging showed no significant changes in follicular fluorescence throughout the treatment period.
Conclusions:
- The study suggests that EGFR inhibitor treatment leads to follicular hyperkeratosis, a condition termed EGFR inhibitor-induced kerosis.
- This induced kerosis, characterized by follicular plugging, is proposed as a potential cause of acneiform reactions observed in patients.
- Non-invasive bioinstrumentation provides objective data for characterizing early-onset skin adverse events in targeted cancer therapy.
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