ACTINIC KERATOSES: -------------------------------------------- The issue raised with AK's is similar to that which Rick Sharpe alluded to with the melanoma which was destroyed as an SK at the primary care physicians office. Delays in the treatment of skin cancer wind up being very expensive for the patient and the insurance companies. On the other side of the coin is the dermatologist who believes that every AK needs to be destroyed. I see many patients who have AK's whose expression are triggered by inflammation such as sun exposure, seborrheic dermatitits and contact dermatitis where the AK flares up as the "locus minoris resistensae." These conditions are best treated for the underlying inflammatory trigger. Seborrheic dermatitis appears to be one of the most common AK promotors, therefore I favor the use of Nizoral in many patients with AK's. What the exact role of radiation dermatitis is in promoting AK's is unclear to me. Sunscreens have a role in this setting, but do they have a role in melanoma prevention or are sunscreens the emperor's new clothes, an opium of disregard for the sunbathing masses? AK's occur in a range of types and patient settings. Can we really afford to promote the use LN2 in the treatment of cutaneous horns in kidney transplant patients? Should I leave a very thin AK on the face of a 25 year old with red hair and blue eyes? Can I leave the same on an 85 year old? Do I treat the underlying inflammatory disease before assessing the appropriateness of AK's for treatment? In the end, there is a tremendous burden of skin cancer. All of us must every day attack the problem with our best thought and action. Perhaps it comes in the form of careful study the use of destruction in a trial of cure in most cutaneous keratoses. For my self, I will continue to ignore many AK's that don't appear to have aggressive potential. I will in all circumstance inform patients of the warning signs of transformation to SCC's, i.e. thickening, soreness, crusting and bleeding. I will seek to reduce the underlying inflammation which may be promoting the AK's. Ultimately, I spend alot of time watching the patients who are at high risk for metastatic skin cancer. Perhaps the use of light activated porphorins will be able to relieve my severe skin cancer patients of most of their skin cancer burden. I certainly wish there were a way to relieve the pain and mutilation that is imposed by my recurrent destructive treatments in these severely actinically damaged patients. I sincerely doubt that this is the motivation of in insurance carriers in the setting of AK therapy. Rhett Drugge, M.D. ---------------- A colleague came back recently from a conference in San Diego with the impression that peels were not as effective as portrayed in treatment of AK's because they do not reach the level of the hair follicle. So, we discussed the old 5 FU tactic, and were surprised to find out that one of us treats for 6 weeks, and the other of us treats for 2 weeks, or several days after crusting and oozing. One of us thought that the 5 FU does penetrate the hair follicle , and one of us didn't know. Could others please give us some sage advice on length of 5FU treatment? Does it get into the hairfollicle? Is this important? Diane Thaler ------------- Colleagues, I received this letter while rxderm was down. The writer asks for more interchange on the subject. Specifically the regimen and if there are remaining cells in the follicles which could become problematic that Five Flourouracil Five percent would or would not hit. Any studies or input of the malignant potential of actinic keratoses would also be appreciated. Diane Thaler --------------- Diane: Longitudinal studies on the malignant potential of AK's have been done by Robin Marks and colleagues from the Victoria Cancer Centre in Australia. First article was published in the BJD around 1986. Marks estimates that one would have to treat >1000 AK's to prevent one SCC. His studies show that 30% of AK's disappear within a year if untreated. Maybe he's on the list and will address this directly. Some of this was reviewed in an editorial by Robin Marks in the Archives (I believe it may have been this past September, but I could be wrong). David J. Elpern ------------------- For 15-20 years I have used a 2 week aggressive regimen for facial actinic keratoses in many hundreds of patients: 1% 5-FU solution AM & h.s., Retin A cream h.s., 10% TCA peel weekly. It does a great job on the AK's and the cosmetic benefit is dramatic. Believe it or not, I have never had a patient who didn't complete all or most of the regimen. This regimen which I presented at a national meeting was a cover story in Dermatology Times about 15 years ago. P.S. Don't try it on the neck. Philip Hughes, M.D. ------------------------- Have you compared this with simply five percent 5-fu BID for two weeks? Half face one, half face the other? Maybe even post treatment biopsies to see what is left behind ? Have you compared this with simply five percent 5-fu BID for two weeks? Half face one, half face the other? Maybe even post treatment biopsies to see what is left behind ? Diane Thaler --------------- AKS including Bowenoid AKs do not involve the follicular epithelium but do slightly cuff the infundibulum. AK-like lesions that recur after LN2 are often really Bowens. These lesions are best treated with excision, though 5-FU with occlusion, especially where the follicles are tiny,(such as on eyelids, penile shaft, etc), is almost always effective. Charles Fishman, M.D. ---------------------------- Many early AKs will disappear without specific treatment. The Australian sunscreen study did not treat AKs with anything other than SPF 17 sunscreen and many regressed [1] . I think this is analogous to the promoter dependent papillomas that have been described in the experimental mouse model of multistage chemical carcinogenesis [2] (in other words, with early preneoplastic lesions, all you may need to do is take away the promoting influence, in the case of human lesions, the sun. Other lesions probably don't regress as much as they are destroyed by the host immune response, which has a major role in protecting us from nascent cancers, including especially skin cancers. While many early lesions do regress or are destroyed by the immune response, many don't. The thicker the AK and the longer it has been there, the greater the potential for it becoming a fully malignant lesion (e.g. squamous cell carcinoma) so a lot depends on how impressive the lesion is clinically. Some are early and show mild dysplasia histologically and some are thick, large and potentially very dangerous "bowenoid" or hypertrophic lesions that are difficult to distinguish from a squamous cell carcinoma clinically or even histologically. AKs are not created equal, and there is no substitute for good clinical judgement in deciding which ones are dangerous. I am a bit disturbed that some managed care types have attempted to use the concept that early AKs will "self-destruct" or regress without specific therapy to justify a non-treatment policy. This is a very dangerous position to take for the reasons I have outlined, and a recipe for ensuring a dramatic increase in cases of metastatic non-melanoma skin cancer. Personally I treat the most clinically obvious AKs and leave the subtle ones for the sunscreen and/or a course of 5-FU (the best course of action when many early lesions are present) to mop up. The longer an AK hangs around, the more likely it is to do something nasty. Also, co-existing problems such as immunosuppression due to a transplant should make you even more aggressive about treating them. 1. Thompson SC, Jolley D, Marks R: Reduction of solar keratoses by regular sunscreen use. N Engl J Med 329(16):1147-1151, 1993. 2. Reddy AL, Caldwell M, Fialkow PJ: Sequential studies of skin tumorigenesis in phosphoglycerate kinase mosaic mice: effect of resumption of promotion on regressed papillomas. Cancer Res 47(7):1947-51, 1987. Mark Naylor, M.D. -----------------------