Persistent alteration of the skin microbiome in patients with skin rash after receiving EGFR inhibitor treatment

The pathological mechanism responsible for EGFR inhibitor (EGFRI)-induced skin rash remains unclear. Recent studies reveal associations between skin dysbiosis and skin inflammatory diseases. This study aimed to examine whether skin dysbiosis is associated with EGFRI-induced skin rash. Bacterial swabs were taken from the forehead of 17 cancer patients at baseline and at several time points after EGFRIs initiation, as well as from 20 healthy controls. The skin microbiome was analysed using 16S rRNA sequencing. The severity of the skin rash was assessed using the rash grade. Skin surface parameters (pH, water capacitance, and sebum level) were also measured. Compared with baseline, the abundance of Cutibacterium acnes decreased in 13 of 15 cases, and that of Staphylococcus aureus, Corynebacterium spp., Staphylococcus epidermidis or Proteobacteria increased in 13 of 15 cases after EGFRIs initiation. Skin pH increased significantly in parallel with a decrease in water capacitance after EGFRI initiation. Also, the composition of the skin microbiome of patients with severe rash was significantly different from that of healthy controls. In addition, the skin dysbiosis did not return to baseline during EGFRIs treatment for >1 year. These longitudinal observations indicate that skin dysbiosis is associated with development of skin rash.

Automated summary

This study aimed to investigate the association between skin dysbiosis and skin rash induced by EGFRI. The results showed that the abundance of Cutibacterium acnes decreased while Staphylococcus aureus, Corynebacterium spp., Staphylococcus epidermidis, or Proteobacteria increased after EGFRI initiation. Skin pH increased and water capacitance decreased. The skin microbiome composition of patients with severe rash was significantly different from that of healthy controls. Moreover, skin dysbiosis did not return to baseline during long-term EGFRI treatment.