Therapeutic Update on Actinic Keratosis

July 2014 | Volume 13 | Issue 7 | Features | 785 | Copyright © July 2014


Deborah S. Sarnoff MD FAAD FACP

5. Photodynamic Therapy (PDT) with 5-aminolevulinic acid (ALA) – (Levulan®, Kerastick®) or methyl-aminolevulinate (MAL) – Metvix® PDT uses a combination of a topical photosensitizer such as ALA or MAL and a visible light source, such as a blue or red lightemitting diode, pulsed dye laser, or intense pulsed light. Upon exposure to visible light, the photosensitizer is converted to protoporphyrin IX, which generates reactive oxygen species and ultimately induces apoptosis and necrosis.10,11 Use of PDT is limited to superficial lesions and less effective in hypertrophic AK.12

Conclusion

5.2 million office visits in the US each year can be attributed to AKs.13 Eradication of these common lesions will lower the incidences of invasive squamous cell carcinoma. Regimens that combine targeted destructive therapy with field-directed medical therapy to treat and prevent these premalignant lesions yield the most success. Future research will focus on finding agents with increased efficacy and fewer side effects and downtime.

Disclosure

Dr. Sarnoff has no relevant conflicts of interest to disclose.

References

  1. Glogau RG. The risk of progression to invasive disease. J Am Acad Dermatol. 2000;42(1 Pt 2):23-24.
  2. Spencer JM, Hazan C, Hsuing SH, Robins P. Therapeutic decision making in the therapy of actinic keratoses. J Drugs Dermatol 2005;4:296-301.
  3. Longley DB, Harkin DP, Johnston PG. 5-fluorouracil: mechanisms of action and clinical strategies. Nat Rev Cancer. 2003;3(5):330-338.
  4. Sauder DN. Immunomodulatory and pharmacologic properties of imiquimod. J Am Acad Dermatol. 2000;43(1 Pt 2):S6-11.
  5. Maltusch A, Röwert-Huber J, Matthies C et al. Modes of action of diclofenac 3%/ hyaluronic acid 2.5% in the treatment of actinic keratosis. J Deutschen Dermatologischen Gasellschaft. 2011;9(12):1011-1017.
  6. Tripp CS, Blomme EA, Chinn KS et al. Epidermal COX-2 induction following ultraviolet irradiation: suggested mechanism for the role of COX-2 inhibition in photoprotection. J Invest Dermatol. 2003;121(4):853-861.
  7. Fecker LF, Stockfleth E, Braun FK et al. Enhanced death ligand-induced apoptosis in cutaneous SCC cells by treatment with diclofenac/hyaluronic acid correlates with downregulation of c-FLIP. J Invest Dermatol. 2010;130(8):2098-2109.
  8. Green AC, Beardmore GL. Home treatment of skin cancer and solar keratoses. Australas J Dermatol. 1988;29(3):127-130.
  9. Rosen RH, Gupta AK, Tyring SK. Dual mechanism of action of ingenol mebutate gel for topical treatment of actinic keratoses: rapid lesion necrosis followed by lesion-specific immune response. J Am Acad Dermatol. 2012;66(3):486-493.
  10. Miller IM, Nielsen JS, Lophaven S, Jemec GB. Factors related to pain during routine photodynamic therapy: a descriptive study of 301 patients. J Eur Acad Dermatol Venereol. 2011;25(11):1275-1281.
  11. Nakaseko H, Kobayashi M, Akita Y et al. Histological changes and involvement of apoptosis after photodynamic therapy for actinic keratoses. Br J Dermatol. 2003;148(1):122-127.
  12. Wiegell SR, Fabricius S, Gniadecka M et al. Daylight-mediated photodynamic therapy of moderate to thick actinic keratoses of the face and scalp: a randomized multicentre study. Br J Dermatol. 2012;166(6):1327-1332.
  13. Warino L, Tusa M, Camacho F, et al. Frequency and cost of actinic keratosis treatment. Dermatol Surg. 2006;32(8):1045-1049.

AUTHOR CORRESPONDENCE

Deborah S. Sarnoff MD FAAD FACPAndrew.Sarnoff@gmail.com
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