Are We Using Too Much Triamcinolone Acetonide for Intralesional Keloid Therapy?
Nina Zamani1, M.Sc., Michael Tirgan2, M.D., Akash Gunjan1*, Ph.D.
BACKGROUND
Keloids are fibroproliferative skin lesions that develop during wound healing and are characterized by excessive dermal fibroblast proliferation and extracellular matrix deposition, leading to tissue growth far beyond the original wound boundaries. Intralesional corticosteroids remain the cornerstone of therapy for keloid disorder, yet dosing practices vary widely, and high concentrations of Triamcinolone Acetonide (TA) are frequently used without a clearly defined biological rationale, often resulting in significant adverse effects including localized skin atrophy, hypopigmentation, acneiform eruptions, telangiectasia and necrosis. We hypothesize that clinically used doses of TA exceed the dose required to achieve maximal biological effect on keloid fibroblasts.
CONCLUSION
TA exhibits a dose-dependent inhibitory effect on fibroblast viability and the levels of fibrotic biomarkers that plateaus between 50–100μM in vitro. QIVIVE analysis indicates that the concentrations required for maximal biological effect (50–100μM) correspond to approximately 0.022–0.043 mg/cm3 of TA, which are between ~500-1000-fold lower than the intralesional doses (20–40mg) commonly used in the clinic currently. Our results suggest that standard high dose intralesional TA regimens for keloid therapy may far exceed the dose necessary for maximal therapeutic effect and may be primarily contributing to the commonly observed adverse effects. Based on our findings, we recommend testing TA doses of 0.1-1mg/cm3 in future clinical trials for keloid therapy.
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