Extreme Phenotype of Epidermal Growth Factor Receptor Inhibitor-induced Destructive Folliculitis

Abstract

Due to the increasingly widespread use and side effect profile of epidermal growth factor receptor inhibitors (EGFRIs), cutaneous side effects of these drugs are frequently encountered. The EGFR is expressed on keratinocytes and fibroblasts. Inhibition of EGFR can produce a range of cutaneous adverse effects, the most frequent being a characteristic acneiform skin eruption. As the latter is associated with good anti-neoplastic responses, the onset of EGFRI-induced acneiform skin eruption is typically viewed as a positive sign by patients and physicians. It can usually be treated well with standard acne drugs, but in rare cases, the skin eruption can be so severe that systemic therapy and/or interruption of EGFRI treatment are required. One of the severest forms of EGFRI-induced skin eruption occurring on the head and neck area resembles folliculitis decalvans. Here, we discuss the management of such a case seen in our department. In addition, we present an analysis of tumor necrosis factor-α, interleukin-1β (IL-1β), and IL-17A expression based on immunohistochemical stains and qPCR.

Keywords: Epidermal growth factor receptor-inhibitor; folliculitis; folliculitis decalvans; interleukin-17A; interleukin-1β; tumor necrosis factor-α.

Figure 1

(a) After 4 weeks of treatment with cetuximab (b) 6 weeks into the epidermal growth factor receptor-inhibitor-inhibiting treatment. (c) After treatment with topical steroids and antiseptics, almost 2½ months treatment have been started

Figure 2

Immunohistochemical stainings with antibodies against (a) IL-17, (b) tumor necrosis factor-α, and (c) IL-1β

Figure 3

mRNA level of IL-17A, tumor necrosis factor-α, and IL-1β in lesional skin of the patient. Relative mRNA levels have been normalized to healthy skin (n= 2)