Impaired wound healing secondary to bevacizumab

Abstract

Bevacizumab is a monoclonal antibody that exerts its antitumor activity by inhibiting vascular endothelial growth factor. Consequently, it suppresses endothelial cell proliferation, vascular permeability, and angiogenesis. This inhibitory effect contributes to tumour size reduction but causes wound-healing delay, specifically during the proliferative phase, in patients receiving bevacizumab. Although surgical wound-healing complications (WHC) associated with bevacizumab have been extensively reported, there is limited literature on peripheral WHC. More importantly, the histopathology of bevacizumab-associated WHC has not been described. We present the histopathology findings of a non-healing ulcer in a patient receiving bevacizumab, providing insight into the possible aetiology of this drug's adverse reaction. Furthermore, our patient's positive response to hyperbaric oxygen suggests its possible use for treatment of bevacizumab-associated non-healing wounds.

Keywords: VEGF-inhibitor; bevacizumab; dermal matrix; epithelialisation; wound-healing complication.

Figure 1

Bevacizumab‐associated wound‐healing failure: 2.5 cm × 1.5 cm punched‐out ulcer is seen with undermining borders and purulent discharge on the right dorsal mid‐forearm

Figure 2

Histopathology of bevacizumab‐associated wound‐healing complication. A, At lower magnification (H&E, ×20), the ulceration is not associated with appropriate dermal connective tissue regeneration, and the subcutaneous fat is pushing into the reticular dermis. B, At higher magnification (H&E, ×40), there is a lack of reepithelisation on the edge of the ulceration and lack of vascularisation on the base of the ulceration