MAJOR SUPPRESSION OF PRO-ALPHA-1(I) TYPE-I COLLAGEN GENE-EXPRESSION IN THE DERMIS AFTER KELOID EXCISION AND IMMEDIATE INTRAWOUND INJECTION OF TRIAMCINOLONE ACETONIDE

Background: A keloid is a benign tumor that contains excess collagen, primarily type I collagen. A common therapy is intralesional injection of a glucocorticosteroid, such as triamcinolone acetonide (TA). Surgi cal excision is also common; often a glucocorticosteroid is injected w eeks after excision when wound repair has already begun. Objective: Ou r purpose was to determine the efficacy of TA in reducing the pro-alph a 1(I) type I collagen mRNA in the dermis, when;TA is injected into th e wound bed immediately after surgical excision of the keloid. Methods : Six patients with previously untreated keloids were studied. Three w ere treated with 10 mg/ml of TA immediately after excision of the kelo id (experimental group); the other three patients were not treated wit h TA until 2 weeks after excision (control). Punch biopsy specimens we re obtained from the TA-treated sites 2 weeks after removal of the kel oid and from the wounds of the control group of patients before they w ere treated with TA. Sections were prepared for in situ hybridization analysis of the pro-alpha 1(I) collagen mRNA, as well as for histochem ical analysis of collagen fibers. Results: All keloids showed greatly elevated levels of pro-alpha 1(I) type I collagen mRNA in the dermis. Postsurgical wounds injected with TA after removal of the keloid expre ssed decreased pro-alpha 1(I) collagen transcripts, compared with skin not treated with TA. The collagen bundles were also thinner and less dense in the TA-treated skin. Conclusion: Downregulation of the type I collagen gene expression is elicited by immediate TA injection after keloid excision. This suggests that prevention of recurrent keloid gro wth is possible if surgical excision is accompanied by immediate TA in jection into the wound bed and that healing of the wound is not appare ntly compromised by inhibition of type I collagen gene expression.