3.2.4 Keloid

Incidence in dark-pigmented populations 4.5-16% (African, Asian, and Hispanic descent), higher compared to Caucasians. Higher incidence during puberty and pregnancy. A positive family history increases the risk for the development of keloids although no specific gene has been identified. Rare genetic syndromes can confer increased risk for the development of keloids including Rubinstein-Taybi and Goeminne syndromes.

Keloids are a result of aberrant wound healing of surgical wounds, injuries (piercings, tattooing, insect bites, vaccinations), burns, skin-damaging infections, acne, increased skin tension, spontaneous (no trigger found). In keloids, the fibroblastic phase of wound healing continues unchecked, resulting in the clinical and histopathological findings. Keloidal fibroblasts have increased proliferative activity, persist for longer, and have lower rates of apoptosis compared to the ones in typical wound healing. Overproduction of collagen (20x greater than that of healthy skin and 3x greater than a hypertrophic scar). Transforming growth factor-β (promotes chemotaxis of fibroblasts to the site of inflammation and produces collagen) and platelet-derived growth factor are the primary drivers of this process.

Increased whorls of thickened, hyalinized collagen bundles widely known as keloidal collagen (up to 55% of specimens). Random organization of Type I and Type III collagen fibers. Horizontal fibrous band in the upper reticular dermis.

Keloids remain a therapeutic dilemma. Not only are they difficult to treat but incomplete therapy can lead to a keloid worsening. Predisposed individuals should avoid elective procedures, if possible, especially ear piercing and tattooing (primary prevention).

In accidental trauma or required surgical interventions, rapid primary closure, adequate haemostasis and reduction of wound tension reduce the risk for keloid development (secondary prevention).

Compression therapy with pressures of 15-45 mmHg for more than 23 hours per day for at least 6 months may reduce keloid development (tertiary prevention).

Intralesional corticosteroids (2 mg/cm2) 4 to 6 sessions at 15-30-day intervals alone or in monthly sessions after contact (pressure) (30 sec), cryocontact surgery (edema inducing for easier insertion) followed by intralesional corticosteroids, intralesional cryosurgery, surgical excision accompanied with post-surgical radiation or intralesional steroid injections (due to recurrence rates of 45-100% after surgery alone), radiotherapy (adjuvant therapy 24 h following excision), LASER treatment (Pulse-dye, 585 nm, Nd-YAG, 1065 nm) can be considered. Other treatments (topical imiquimod following excision, intralesional botulinum toxin, intralesional bleomycin or 5-fluorouracil, silicone gel tapes) may alleviate symptoms and reduce the volume of existing keloids.

It is important to manage patient expectations.