A technique to avoid atrophy in combined intralesional excision and steroid injection for keloids

Patel, Irshad A.; Hall, Per

doi:10.1054/bjps.1999.3306

Cited by 2 publications

(2 citation statements)

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“…These modalities, which ameliorate or eradicate keloid scar formation, have all obtained controversial outcomes for regression and arresting of keloid scar development (Shaffer et al, 2002). Intra-lesional corticosteroid as a monotherapy or combined with surgery for large keloids has proven efficient for flattening and reducing keloids (Kiil, 1977;Boyadjiev et al, 1995;Patel and Hall, 2000). However, the mechanistic role of steroids in moderating keloid formation remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone Induction of Keloid Regression through Effective Suppression of VEGF Expression and Keloid Fibroblast Proliferation

Wang

Yang

et al. 2006

Journal of Investigative Dermatology

145

155

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The biological mechanism underlying steroid therapy for treating keloids remains unclear. Analytical results demonstrated that topical intra-lesional steroid injections suppress vascular endothelial growth factor (VEGF) expression in keloid tissue and induce its regression in vivo. This study investigated whether glucocorticoid (dexamethasone) downregulates VEGF expression and hinders keloid fibroblast (KF) proliferation in keloid regression. Primary KF cultures were treated with various concentrations of dexamethasone, glucocorticoid receptor (GR) antagonist (mifeprostone, RU-486), VEGF-A antibody, VEGF receptor-2 (VEGF-R2) antagonist (SU-5416), and VEGF protein. Analytical results demonstrated that dexamethasone retarded KFs proliferation. However, suppression of fibroblast proliferation by dexamethasone pre-treatment was reduced by adding exogenous VEGF protein. Dexamethasone suppressed endogenous VEGF mRNA induction, protein expressed by KFs, and angiogenesis activity detected by a tube-forming assay of human umbilical vein endothelial cells co-cultured fibroblasts. These effects were reversed by pre-treatment with RU-486, and not by pre-treatment with SU-5416. Thus, dexamethasone induces keloid regression via interaction with the GR and suppresses endogenous VEGF expression and fibroblast proliferation. However, exogenous VEGF promotes fibroblast proliferation through the GR-independent pathway. Modulation of VEGF production may comprise a valuable treatment modality for keloids.

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Section: Introductionmentioning

confidence: 99%

Dexamethasone Induction of Keloid Regression through Effective Suppression of VEGF Expression and Keloid Fibroblast Proliferation

Wang

Yang

et al. 2006

Journal of Investigative Dermatology

145

155

View full text Add to dashboard Cite

show abstract

“…The appearance of mild side effects from the treatment, such as telangectasias and tissue atrophy, should be regularly followed to determine whether the therapy should be interrupted 19 . Pregnancy or plans for pregnancy are major contraindications to treatment.…”

Section: Treatment Protocolmentioning

confidence: 99%

Treatment of scars by steroid injections

Giovannini

2002

Wound Repair Regeneration

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A technique to avoid atrophy in combined intralesional excision and steroid injection for keloids

Cited by 2 publications

References 0 publications

Dexamethasone Induction of Keloid Regression through Effective Suppression of VEGF Expression and Keloid Fibroblast Proliferation

Dexamethasone Induction of Keloid Regression through Effective Suppression of VEGF Expression and Keloid Fibroblast Proliferation

Treatment of scars by steroid injections

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