Fibrinogen Immunostaining in a Single Case of an Earlobe Keloid: A Case Report and Literature Review

Abnormal scars, such as keloids and hypertrophic scars, are fibroproliferative disorders that develop following wounds or infections extending into the reticular dermis, with cutaneous mechanical tension considered an aggravating factor. The detailed mechanisms underlying keloid formation and patterns of extension remain unclear. Recent studies suggest that microvascular hyperpermeability, potentially resulting from structural alterations in the vascular basement membrane and increased microvascular density in the superficial dermis, may contribute to keloid development. We report a single case of an earlobe keloid treated with surgical excision followed by postoperative radiotherapy (8 Gy in a single fraction). The resected tissue was histologically confirmed as a keloid. Immunohistochemical staining for fibrinogen and CD31 was performed on cryosections to evaluate vascular permeability. Fluorescence images were acquired using a confocal laser scanning microscope. The patient showed no recurrence during at least 12 months of follow-up. Fibrinogen deposition was observed predominantly in the superficial dermis at the keloid apex, with stronger signals than those in deeper regions of the keloid and adjacent normal skin. Fibrinogen is a key factor in wound healing and fibrosis, and its deposition within the extracellular matrix may reflect vascular hyperpermeability. Our findings suggest that areas of fibrinogen leakage may represent potential sites of future collagen deposition and keloid progression. However, this observation is based on a single case, and further studies are warranted to clarify the role of fibrinogen in keloid pathogenesis.