An adolescent girl seeks medical advice for managing recurrent nodules on her ear lobes. The diagnosis is keloids.
Figure: Scar tissue originating from the ear lobe.
The CaseAn adolescent girl seeks your advice for managing recurrent nodules on her ear lobes. They were removed by a surgeon 3 years ago, only to return soon after surgery. The one on the left is quite massive, while the other is small.
Following a full-thickness injury to the skin, healing usually occurs with a scar confined to the area of the initial injury. When fibrosis thickens above that area, the lesion is referred to as a hypertrophic scar. Lesions that become dramatically thickened and extend beyond the injury margins are called keloids. Keloids may grow for months to years after healing of the primary insult.1-3
Clinically, keloids appear as firm rubbery to rock-hard, spherical or irregularly shaped, skin-colored or hyperpigmented nodules or tumors, some with claw-like projections at the base. They range in size from 0.5 cm to more than 20 cm. Keloids are composed of fibrous bundles of primarily type I and some type III collagen. Although many lesions are asymptomatic and pose only a cosmetic problem, some keloids, particularly large lesions in strategic locations, can be painful and interfere with normal function.
EPIDEMIOLOGY
Keloids are triggered by injuries to skin, including scratches, scrapes, insect bites, lacerations, hot water and thermal burns, bacterial infections (folliculitis, furuncles), viral infections (varicella, herpes simplex virus infection), and inflammatory dermatologic disorders (acne vulgaris). Deliberate injuries to the skin such as body piercing and tattooing have become a common cause of keloid formation during the past few decades.1-3
For reasons that are not fully understood, African Americans, Chinese, and Polynesians between the ages of 10 and 30 years are particularly predisposed to the development of keloids. Although any area of the body can be affected, the most common sites include the ear, presternal area, deltoid region, mid-abdomen, and upper back. The palms, soles, eyelids, and genitalia are only rarely affected.1-3
PATHOGENESIS
On histologic examination, keloids are found to have increased collagen and glycosaminoglycan deposition, both major components of the extracellular matrix. The collagen in keloids consists of thickened whorls of hyalinized collagen bundles in a haphazard array, known as keloidal collagen. This is in contrast to normal scars, where collagen bundles are oriented in parallel.
Transforming growth factor beta (TGF-beta) has been implicated in the pathogenesis of keloids. The 3 TGF-beta isoforms identified in mammals (TGF-beta 1, -beta 2, and -beta 3) are thought to have different biological activities in wound healing. TGF-beta 1 and TGF-beta 2 are believed to promote fibrosis and scar formation.4
Recent studies suggest that carriers of specific major histocompatibility complex alleles may be particularly predisposed to the development of keloids.5 In addition, distinct immunophenotypical profiles can be use to distinguish between hypertrophic and keloidal scarring.5 As a consequence, both of these lesions probably represent an abnormal response to environmental injury in genetically predisposed individuals at predisposed sites in the skin.
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