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Tissue alpha-globulins in keloid formation.

R F Diegelmann, C P Bryant, I K Cohen

    Plastic and Reconstructive Surgery
    |March 1, 1977
    PubMed
    Summary
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    Keloids and hypertrophic scars show increased alpha-globulin inhibitors of collagenase. Triamcinolone treatment reduces these deposits, suggesting a mechanism for scar resorption by enabling collagen breakdown.

    Area of Science:

    • Biochemistry
    • Dermatology
    • Wound Healing

    Background:

    • Keloids and hypertrophic scars involve abnormal collagen deposition.
    • Alpha-1-antitrypsin and alpha-2-macroglobulin inhibit human skin collagenase.
    • Increased levels of these inhibitors are observed in abnormal scars compared to normal skin.

    Purpose of the Study:

    • To investigate the role of alpha-globulins in abnormal scar formation.
    • To determine the effect of intralesional triamcinolone treatment on these scar types and associated protein deposits.

    Main Methods:

    • Quantification of alpha-1-antitrypsin and alpha-2-macroglobulin deposition in keloids, hypertrophic scars, and normal skin.
    • Assessment of scar changes following intralesional triamcinolone acetonide administration.

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    Main Results:

    • Significantly increased deposition of alpha-1-antitrypsin and alpha-2-macroglobulin was found in keloids and hypertrophic scars.
    • Intralesional triamcinolone treatment led to marked scar resorption.
    • A significant reduction in alpha-1-antitrypsin deposits was observed after triamcinolone treatment.

    Conclusions:

    • Alpha-globulins appear to play a role in the pathogenesis of abnormal scarring.
    • Triamcinolone may facilitate scar resorption by reducing collagenase inhibitors, potentially allowing collagenase activation and collagen breakdown.