Treatment with an epidermal growth factor receptor inhibitor (EGFRI) in patients having non-small-cell lung cancer can cause frequent and diverse skin toxicities, an acneiform rash being one of the commonest. Although the exact pathophysiology of this rash and its development mechanisms remain unknown, investigators have noted that EGFRI induced skin toxicity might be partly associated with sebaceous gland function. Sebum is composed mainly of the lipids squalene (SQ), wax ester (WE), triglyceride, free fatty acid, and cholesterol, which are secreted mostly from the sebaceous glands and by keratinocytes. We therefore investigated the lipid composition of sebum before and after administration of EGFRI and whether sebum composition was associated with the development of acneiform rash. To investigate any associated changes in sebum gland activity, we focused especially on alterations in the amounts of SQ and WE, which are secreted solely from the sebaceous glands. In contrast to our expectations, we observed no substantial changes in the lipid composition of sebum before and after administration of EGFRI. Composition varies with the individual; however, the proportion of SQ and WE derived from the sebaceous glands was significantly lower in regions that did not develop acneiform rash than in regions that did. Our results suggest that development of an acneiform rash after administration of EGFRI could be related to sebaceous gland activity. Measurement of the lipid composition of sebum before therapy with EGFRI might predict which patients will be prone to acneiform rash.
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