A 35-year-old patient presents 6 months after a laparotomy with a raised, firm, erythematous scar that extends well beyond the boundaries of the original incision onto the chest wall. He has no personal or family history of keloid. The most likely diagnosis and its distinguishing molecular mechanism compared to hypertrophic scar is:

• A Hypertrophic scar — characterised by failure of collagen lysis in Type I collagen remodelling
• B Keloid — characterised by collagen III predominance and reduced MMP-1 activity only
• C Desmoid tumour — characterised by β-catenin mutation and fibrous tissue invasion
• D Keloid — characterised by invasion beyond wound margins, myofibroblast persistence, and upregulated TGF-β1/TGF-β2 driven collagen synthesis that extends clonally beyond original wound boundary ✓

Explanation

Keloids are distinguished from hypertrophic scars by extending beyond the original wound margins (hypertrophic scars remain within the wound boundary). Molecularly, keloids demonstrate persistent myofibroblast activity and markedly elevated TGF-β1 and TGF-β2 signalling driving excess Type I collagen synthesis. Keloid fibroblasts show clonal expansion beyond the wound edge, reduced apoptosis, and dysregulation of matrix metalloproteinases (decreased MMP-1, increased TIMP-1). Hypertrophic scars show similar but contained and self-limiting TGF-β activity. Race is a strong risk factor for keloids (higher incidence in people of African, Asian, and Hispanic descent). Treatment includes intralesional triamcinolone, silicone sheets, and radiotherapy.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.