Actinic keratosis

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Actinic keratosis (also called solar keratosis, or AK) is a premalignant condition of thick, scaly, or crusty patches of skin. It is most common in fair-skinned people who are frequently exposed to the sun, because their pigment isn't very protective. It usually is accompanied by solar damage. Since some of these pre-cancers progress to squamous cell carcinoma, they should be treated.

When skin is exposed to the sun constantly, thick, scaly, or crusty bumps appear. The scaly or crusty part of the bump is dry and rough. The growths start out as flat scaly areas, and later grow into a tough, wart-like area.

An actinic keratosis site commonly ranges in between 2 to 6 millimeters, and can be dark or light, tan, pink, red, a combination of all these, or the same pigment of one's skin. It may appear on any sun-exposed area, such as the face, ears, neck, scalp, chest, back of hands, forearms, lips etc.

Prevention

Preventative measures recommended for AK are similar to those for skin cancer:

  • Not staying in the sun for long periods of time without protection (e.g.:sunscreen, clothing, hats).
  • Frequently applying powerful sunscreens with SPF ratings greater than 15 and that also block both UVA and UVB light.
  • Using sunscreen even in winter sun exposure.
  • Wearing sun protective clothing such as hats, long-sleeved shirts, long skirts, or pants.
  • Avoiding sun exposure during noon hours is very helpful because ultraviolet light is the most powerful at that time.

Diagnosis

Doctors can usually identify AK by doing a thorough examination. A biopsy may be necessary when the keratosis is large and/or thick, to make sure that the bump is a keratosis and not a skin cancer. Seborrheic keratoses are other bumps that appear in groups like the actinic keratosis but are not caused by sun exposure, and are not related to skin cancers. Seborrheic keratoses may be mistaken for an actinic keratosis.

Treatment

Various modalities are employed in the treatment of actinic keratosis:

Regular follow-up after treatment is advised by many doctors. The regular checks are to make sure new bumps have not developed and that old ones haven't become thicker and/or have skin disease.

Experimental treatments

As of 2008 a company in Australia named Clinuvel Pharmaceuticals Limited is performing clinical trials with a melanocyte-stimulating hormone named melanotan (which they refer to as CUV1647) for actinic keratosis in organ transplant patients.[1]

External links

References

Additional Resources

  • Abel EA (1989). "Cutaneous manifestations of immunosuppression in organ transplant recipients". J Am Acad Dermatol. 21 (2 Pt 1): 167–79. PMID 2671063.
  • Fitzpatrick TB (1988). "The validity and practicality of sun-reactive skin types I through VI". Arch Dermatol. 124 (6): 869–71. PMID 3377516.
  • Glogau RG (2000). "The risk of progression to invasive disease". J Am Acad Dermatol. 42 (1 Pt 2): 23–4. PMID 10607353.
  • Gordon D, Silverstone H. (1969). "The biologic effects of ultraviolet radiation". In Ubach F, editor. The Biologic Effects of Ultraviolet Radiation. Oxford (UK): Pergamon Press. pp. p. 625.
  • Lookingbill DP, Lookingbill GL, Leppard B (1995). "Actinic damage and skin cancer in albinos in northern Tanzania: findings in 164 patients enrolled in an outreach skin care program". J Am Acad Dermatol. 32 (4): 653–8. PMID 7896957.
  • Marshall V (1974). "Premalignant and malignant skin tumours in immunosuppressed patients". Transplantation. 17 (3): 272–5. PMID 4592184.
  • Scotto J, Fears TR, Fraumeni JF. Incidence of nonmelanoma skin cancer in the United States. Publication No (NIH) 82-2433. Washington, DC: US Dept Health and Human Services; 1983.


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