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Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Class Summary

These agents have profound and varied metabolic effects. They possess anti-inflammatory and immunosuppressive properties. The most commonly used corticosteroid is triamcinolone acetonide (TAC).

Triamcinolone (Aristospan, Kenalog-10)

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Triamcinolone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It is approved by US Food and Drug Administration (FDA) for use in keloids.

Class Summary

This is a family of glycoproteins produced mainly by eukaryotic cells when induced by viral and nonviral triggers. Antiviral properties include induction of 2'-5' A synthetase, ribonuclease L, and protein kinase P1. Antiproliferative properties include induction of 2'-5' A synthetase, inhibition of growth factors, enhancement of p53, and down-regulation of c-myc, c-fos, and certain c-ras. Immunoregulatory properties include induction of class I and II MHC antigens, increase of natural killer cells, and inhibition of the production of TH-2 cytokines.

Interferon alfa-2b (Intron-A)

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This is a protein product manufactured by recombinant DNA technology. Its mechanism of antitumor activity is not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles. Its immunomodulatory effects include suppression of tumor cell proliferation, enhancement of macrophage phagocytic activity, and augmentation of lymphocyte cytotoxicity. It is not approved by the FDA for use in hypertrophic scars and keloids.

Interferon beta 1a (Avonex, Rebif)

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Interferon alfa-n3 (Alferon N)

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Interferon alfa is a protein product either manufactured from a single-species recombinant DNA process or obtained from pooled units of donated human leukocytes that have been induced by incomplete infection with a murine virus.

The mechanisms by which interferon alfa exerts antiviral activity are not understood clearly. However, modulation of the host immune response may play an important role.

Peginterferon alfa 2b (PEG Intron, PegIntron Redipen, Sylatron)

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PEG-IFN consists of IFN alfa-2b attached to a single 12-kd PEG chain. It is excreted by the kidneys. PEG-IFN has sustained absorption, a slower rate of clearance, and a longer half-life than unmodified IFN, which permits more convenient once-weekly dosing and significantly improves quality of life for patients.

Pegylated interferon alfa-2a (Pegasys)

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PEG-IFN alfa-2a consists of IFN alfa-2a attached to a 40-kd branched PEG molecule. PEG-IFN has sustained absorption, a slower rate of clearance, and a longer half-life than unmodified IFN, which permits more convenient once-weekly dosing and significantly improves quality of life for patients.

Class Summary

Treatment of keloids and hypertrophic scars with verapamil has shown a reduction in vascularity, pliability, height, and width of the lesions.

Verapamil (Isoptin, Calan, Verelan PM)

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Verapamil blocks the synthesis and secretion of extracellular matrix molecules and increases fibrinase. It is not approved by the FDA for use in hypertrophic scars and keloids.

Class Summary

These agents inhibit cell growth and proliferation.

Bleomycin

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Injections cause necrosis of keratinocytes. It is not approved by the FDA for use in hypertrophic scars and keloids.

Fluorouracil topical (Adrucil)

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Fluorouracil is a pyrimidine analog that inhibits fibroblastic proliferation in tissue culture and is believed to reduce postoperative scarring by decreasing fibroblast proliferation. It is not approved by the FDA for use in hypertrophic scars and keloids.

Doxorubicin (Adriamycin)

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Doxorubicin irreversibly inactivates prolyl 4-hydroxylase in human skin fibroblasts and inhibits collagen alpha-chain assembly. It is not approved by the FDA for use in hypertrophic scars and keloids.

Tamoxifen

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Tamoxifen competitively binds to estrogen receptors, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects.

Class Summary

These agents decrease normal tonofilament and keratohyalin synthesis, increase the production of mucoid substances and the epidermal cell growth rate, and inhibit DNA synthesis in vitro.

Tretinoin topical (Retin-A, Retin-A Micro, Renova)

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Although the exact mechanism of action is unknown, retinoids decrease the cohesiveness of abnormal hyperproliferative keratinocytes, modulate keratinocyte differentiation, and have anti-inflammatory properties. It is not approved by the FDA for use in hypertrophic scars and keloids.

Class Summary

These agents inhibit immune processes that promote inflammation.

Tacrolimus ointment (Protopic)

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Tacrolimus suppresses release of cytokines from T cells. It also inhibits transcription for genes that encode interleukin 3 (IL-3), IL-4, IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor–alpha (TNF-alpha), all of which are involved in the early stages of T-cell activation.

Additionally, tacrolimus may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of high-affinity IgE receptor (FCeRI) on Langerhans cells. It is not approved by the FDA for use in hypertrophic scars and keloids.

Class Summary

The agent imiquimod has been reported to show some efficacy. However, the mechanism of action of imiquimod cream in treating keratosis is unknown.

Imiquimod (Aldara, Zyclara)

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Imiquimod is an immune response modifier currently approved for the treatment of genital and perianal warts. It is capable of inducing IFN-alpha, TNF-alpha, IL-1, IL-6, and IL-8. Studies using 5% cream in mice showed significant induction of IFN-alpha at the application site occurring as early as 2 hours after treatment. At 4 hours after application, increases in IFN-alpha mRNA levels were found, indicating an increase in transcription. It is not approved by the FDA for use in hypertrophic scars and keloids.

Questions

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Media Gallery

Clawlike outline of a keloid. Courtesy of Dirk M. Elston, MD.
Keloid. Courtesy of Dirk M. Elston, MD.
Keloid. Courtesy of Dirk M. Elston, MD.
Keloid. Courtesy of Dirk M. Elston, MD.
Histology of keloid demonstrating central zone of hyalinized collagen (hematoxylin and eosin stain). Courtesy of Dirk M. Elston, MD.
Histology of keloid demonstrating thick hyalinized collagen bundles (hematoxylin and eosin stain). Courtesy of Dirk M. Elston, MD.

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Author

Brian Berman, MD, PhD Dermatologist and Partner, Skin and Cancer Associates; Professor Emeritus of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine

Brian Berman, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Aclaris; Bifrontera; Aiviva; Pulse; Celumigen; Dermira; DUSA Sun; Exeltis, Ferndale; Galderma; GSK; Halscion; Klara; Leo; Medimetriks; Miragen; Novan; Novartis; TopMD; Aclaris; Menlo; Cara; Lemonex; Mediwound; Almirall; Pfizer; Sirnaomics; Minolab<br/>Serve(d) as a speaker or a member of a speakers bureau for: Sun; Exeltis, Ferndale; Galderma; GSK; Halscion; Leo Pharmaceuticals; Medimetriks; Miragen; Novan; Novartis; Valeant Pharmaceuticals; Anacor; Clark; Aclaris; Sensus;Almirall<br/>Received research grant from: Dermira; DUSA; Exeltis, Ferndale; Galderma; Leo; Menlo; Anacor; Clark; Pulse; Miragen; Sensus; Minolab<br/>Received income in an amount equal to or greater than $250 from: Bifrontera; Aiviva; Pulse Biosciences; Dermira; DUSA; Sun; Menlo; Exeltis, Ferndale; Galderma; GSK; Halscion; Leo; Medimetriks; Miragen; Novan; Novartis; TopMD; Anacor;Aclaris; Sensus; Cara; Lemonex; Mediwound;Almirall;Minolab;.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven R Feldman, MD, PhD Professor, Departments of Dermatology, Pathology and Public Health Sciences, and Molecular Medicine and Translational Science, Wake Forest Baptist Health; Director, Center for Dermatology Research, Director of Industry Relations, Department of Dermatology, Wake Forest University School of Medicine

Steven R Feldman, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, North Carolina Medical Society, Society for Investigative Dermatology

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbvie for consulting; Received honoraria from Galderma for speaking and teaching; Received consulting fee from Lilly for consulting; Received ownership interest from www.DrScore.com for management position; Received ownership interest from Causa Reseasrch for management position; Received grant/research funds from Janssen for consulting; Received honoraria from Pfizer for speaking and teaching; Received consulting fee from No.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Sadegh Amini, MD Dermatologist, Skin Cancer Associates; Voluntary Assistant Professor, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine.

Sadegh Amini, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, International Society of Dermatology

Disclosure: Own stocks at NYSE for: AbbVie Inc.

Martha H Viera, MD Resident Physician, Department of Dermatology and Cutaneous Surgery, Jackson Memorial Hospital, University of Miami, Leonard M Miller School of Medicine

Martha H Viera, MD is a member of the following medical societies: American Medical Association, Women's Dermatologic Society

Disclosure: Nothing to disclose.

Arash Taheri, MD Research Fellow, Center for Dermatology Research, Department of Dermatology, Wake Forest University School of Medicine

Disclosure: Nothing to disclose.

Andrea D Maderal, MD Resident Physician, Department of Dermatology and Cutaneous Surgery, Jackson Memorial Hospital, University of Miami, Leonard M Miller School of Medicine

Andrea D Maderal, MD is a member of the following medical societies: American Academy of Dermatology, Florida Society of Dermatology and Dermatologic Surgery, Medical Dermatology Society, Miami Society for Dermatology, Rheumatologic Dermatology Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Whitney Valins, MD, to the development and writing of the source articles.