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A Controlled Trial of Intralesional Recombinant Interferon- in the Treatment of Keloidal ScarringClinical and Histologic Findings
Richard D. Granstein, MD;
Alain Rook, MD;
Thomas J. Flotte, MD;
Andree Haas, MD;
Richard L. Gallo, MD, PhD;
Howard S. Jaffe, MD;
Edward P. Amento, MD
Arch Dermatol. 1990;126(10):1295-1302.
Abstract
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• Interferon- (IFN-) suppresses the synthesis of collagen by fibroblasts in vitro and the synthesis of collagen in vivo in animal models. Therefore, recombinant human IFN- was examined for its ability to clinically modify keloids. Subjects were treated by injection of either 0.01 or 0.1 mg of recombinant human IFN- into one lesional site and diluent alone into another lesional site three times per week for 3 weeks. Keloids were measured and photographed before beginning therapy and weekly thereafter. Three days after the final injection, biopsies were performed on treated and control sites. Six of eight subjects who finished the course of treatment demonstrated reduction in size at the treated site with an average reduction in height of 30.4% vs 1.1% for control sites. Lesions treated with recombinant human IFN- demonstrated alterations in both the epidermis and dermis. The epidermis showed thinning of the suprapapillary plates, compact hyperkeratosis, focal or diffuse parakeratosis, exocytosis of lymphocytes, and an increased quantity of mucin. The dermis contained a diminished quantity of thickened collagen bundles and active fibroblasts and an increased number of inflammatory cells and quantity of mucin. These results suggest the feasibility of using IFN- in the treatment of abnormal fibrosis. Dose-ranging studies are required to establish whether IFN- can fulfill a true clinical need in the treatment of keloidal scarring.
(Arch Dermatol. 1990;126:1295-1302)
Author Affiliations
From the Wellman Laboratories and Massachusetts General Hospital-Harvard Medical School Cutaneous Biology Research Center, Department of Dermatology, Harvard Medical School, Massachusetts General Hospital (Drs Granstein, Flotte, Haas, and Gallo), Boston; Department of Dermatology, University of Pennsylvania, Philadelphia (Dr Rook); and Clinical Research (Dr Jaffe) and Research and Development (Dr Amento), Genentech Inc, South San Francisco, Calif.
Footnotes
Accepted for publication June 7, 1990.
Presented in part at the National Meeting of the Society for Investigative Dermatology, Washington, DC, May 1990.
Reprint requests to the Department of Dermatology, Wellman 2, Massachusetts General Hospital, Boston, MA 02114 (Dr Granstein).
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