Major suppression of pro-alpha1(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). Surgical excision is also common; often a glucocorticosteroid is injected weeks after excision when wound repair has already begun.


OBJECTIVE
Our purpose was to determine the efficacy of TA in reducing the pro-alpha1(I) type I collagen mRNA in the dermis, when TA is injected into the wound bed immediately after surgical excision of the keloid.


METHODS
Six patients with previously untreated keloids were studied. Three were treated with 10 mg/ml of TA immediately after excision of the keloid (experimental group); the other three patients were not treated with TA until 2 weeks after excision (control). Punch biopsy specimens were obtained from the TA-treated sites 2 weeks after removal of the keloid and from the wounds of the control group of patients before they were treated with TA. Sections were prepared for in situ hybridization analysis of the pro-alpha1(I) collagen mRNA, as well as for histochemical analysis of collagen fibers.


RESULTS
All keloids showed greatly elevated levels of pro-alpha1(I) type I collagen mRNA in the dermis. Postsurgical wounds injected with TA after removal of the keloid expressed decreased pro-alpha1(I) collagen transcripts, compared with skin not treated with TA. The collagen bundles were also thinner and less dense in the TA-treated skin.


CONCLUSIONS
Downregulation of the type I collagen gene expression is elicited by immediate TA injection after keloid excision. This suggests that prevention of recurrent keloid growth is possible if surgical excision is accompanied by immediate TA injection into the wound bed and that healing of the wound is not apparently compromised by inhibition of type I collagen gene expression.
Kauh
Y C
YC
Department of Dermatology and Cutaneous Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Rouda
S
S
Mondragon
G
G
Tokarek
R
R
diLeonardo
M
M
Tuan
R S
RS
Tan
E M
EM
D000287:Administration, Topical; D000293:Adolescent; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001706:Biopsy; D003094:Collagen / Q000032:analysis / Q000187:drug effects* / Q000235:genetics / Q000648:ultrastructure; D004396:Coloring Agents; D003131:Combined Modality Therapy; D015536:Down-Regulation; D004427:Ear Diseases / Q000188:drug therapy / Q000601:surgery; D004431:Ear, External / Q000601:surgery; D005786:Gene Expression Regulation / Q000187:drug effects; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D015552:Injections, Intralesional; D007627:Keloid / Q000601:surgery*; D011347:Procollagen / Q000032:analysis / Q000187:drug effects* / Q000235:genetics / Q000648:ultrastructure; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics; D012867:Skin / Q000187:drug effects*; D013909:Thorax / Q000473:pathology; D014158:Transcription, Genetic / Q000187:drug effects; D014222:Triamcinolone Acetonide / Q000008:administration & dosage / Q000627:therapeutic use*; D014945:Wound Healing / Q000187:drug effects
D000893:Anti-Inflammatory Agents; D004396:Coloring Agents; D005938:Glucocorticoids; D011347:Procollagen; D012333:RNA, Messenger; D003094:Collagen; D014222:Triamcinolone Acetonide