Tissue alpha-globulins in keloid formation.
The deposition of alpha-1-antitrypsin and alpha-2-macroglobulin, both known to be inhibitors of human skin collagenase, is significantly increased in keloids and in hypertrophic scars (as compared to normal skin). However, following intralesional triamcinolone treatment, a marked resorption of these abnormal scars occurs along with a significant reduction of the alpha-1-antitrypsin deposits. These findings suggest that alpha-globulins are involved in abnormal scar formation, and that triamcinolone may remove collagenase and/or protease inhibitors--thereby allowing activation of the collagenase with subsequent breakdown and resorption of the excessive collagen.
D000510:Alpha-Globulins / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism; D006801:Humans; D007627:Keloid / Q000188:drug therapy / Q000378:metabolism*; D003012:Microbial Collagenase / Q000378:metabolism; D014221:Triamcinolone / Q000627:therapeutic use; D000515:alpha 1-Antitrypsin / Q000378:metabolism; D000511:alpha-Macroglobulins / Q000378:metabolism
D000510:Alpha-Globulins; D000515:alpha 1-Antitrypsin; D000511:alpha-Macroglobulins; D014221:Triamcinolone; D003094:Collagen; D003012:Microbial Collagenase