Comparative Results in Treatment of Keloids With Intralesional 5-FU/Kenalog, 5-FU/Verapamil, Enalapril Alone,Verapamil Alone, and Laser: A Case Report and Review of the Literature

November 2016 | Volume 15 | Issue 11 | Original Article | 1442 | Copyright © 2016

Doru Alexandrescu MD,a Sabrina Fabi MD,b Lindsey C.Yeh MD MS, c Richard E. Fitzpatrick MD,b and Mitchel P. Goldman MDb

a Division of Dermatology, University of California at San Diego, CA bGoldman Butterwick Gro Fabi & Wu: Cosmetic Laser Dermatology, San Diego, CA c Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY

Abstract

BACKGROUND: The pathogenesis of keloids involves a hyperproliferative state due to molecular abnormalities, cellular driving pathways, such as TGF, VEGF, and the inactivation of proapoptotic genes. We reviewed the literature and compared various treatment combina- tions in the treatment of keloids in a one patient observation. METHODS AND MATERIALS: Treatment modalities consisted of: intralesional 5- uorouracil (5-FU)/triamcinolone (TMC), 5-FU/verapamil, enal- april alone, verapamil alone, and fractional carbon dioxide laser. Size, height, and softness of the keloid, pain, itching, and pain were assessed. RESULTS: 5-FU based treatments proved to be more ef cacious than the other modalities. 5-FU + TMC demonstrated the largest reduc- tion in keloid height and rmness. The greatest degree of scar softening and average size reduction was achieved with 5-FU/ TMC (80% and 70% reduction, respectively), followed by 5-FU/verapamil (50% and 33% reduction, respectively). The same combinations led to the greatest reduction in scar height (70% and 33%, respectively). All treatments led to resolution of pain and itching in the keloid. CONCLUSION: The favorable effects of the 5-FU + verapamil combination are new and deserve further exploration. J Drugs Dermatol. 2016;15(11):1442-1447.

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INTRODUCTION

Development of keloids is caused by an abnormal hyperproliferative state of dermal broblasts, which deposit increased amounts of collagen in the wound, with expansion beyond the boundaries of the initial insult.1 This process is driven by an imbalance favoring collagen production over matrix degradation.2 A host of molecular abnormalities and cellular driving pathways that promote a hyperproliferative state have been identified in the pathogenesis of keloids. Among them, transforming growth factor (TGF) β1 and 2, vas- cular endothelial growth factors (VEGF), and inhibition of apop- tosis through down regulation of proapoptotic genes, such as the p53 gene family, appear to play important roles.3,4 We sought to compare several pharmacological agents in the treat- ment of a patient with multiple keloids on his chest. The agents evaluated in this case report have well described molecular effects on broblast proliferation. Triamcinolone (TMC) and verapamil inhibit cell proliferation, TGF-β1 expression and induce keratinocyte apoptosis.5 Verapamil also inhibits the incorporation of proline into extracellular matrix (ECM) protein.6 5-fluorouracil (5-FU) inhibits TGF-β and type I collagen gene expression induces cell cycle G2 arrest and apoptosis in keloid broblasts.7, 8 Angiotensin converting enzyme (ACE) inhibition induces a decrease in metabolic activity and the ac- cumulation of brous tissue in non-infarcted myocardium, which correlates with the production of de novo angiotensin I and II, which in uence brous tissue contractility and myo- broblast collagen turnover.9 Laser irradiation targets scar tissue microvasculature,10 which interferes with the proliferation and ability to secrete VEGF from scar tissue. Pulse dye laser (PDL) signi cantly down-regulates the expression of connective tissue growth factors.11 The fractionated carbon dioxide (CO2) laser produces microscopic columns of thermal ablation.

CASE REPORT

A 30 year-old male presented for treatment of pruritic and painful chest keloids. Five keloids were selected and photo- graphed during the initial and all subsequent visits. Each of the five keloids were treated with different approaches: 1) intralesional 5-FU 50 mg/ml (APP Pharmaceuticals, Schaumberg, IL)/ TMC (Bristol-Myers Squibb Company, Princeton, NJ) 10 mg/ml (mixed as 0.9cc 5-FU/0.1cc TMC), 2) 5-FU 50 mg/ml/verapamil 2.5 mg/ml (mixed as 0.5cc 5-FU/0.5cc verapamil), 3) enala- pril (West-Ward Pharmaceuticals, Eatontown, NJ) 0.125mg/ ml alone, 4) verapamil 2.5 mg/ml (Hoopira Inc, Lake Forest, IL) alone, and 5) fractionated CO2 laser (Fraxel Re:pair, Solta

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