Kernel Medical Sub-website : www.kerneluvb.com
UV phototherapy treatment duration was restricted to less than one year
Type:Uv phototherapy Time:2016-02-01 10:14:04The 2009 British guidelines for vitiligo management suggest that treatment regimens for patients with skin types I to III should not exceed 200 treatments with NB-UVB or 150 treatments with PUVA. The evidence is deficient to set an upper limit for NB-UVB or PUVA for patients with skin types IV to VI.
Only 50% of the dermatologists always calculated the cumulative PUVA dose. However, 50% do not bother about it. Therefore, the issue of awareness of phototherapy-induced skin cancer risk needs to be addressed.
Based on our earlier survey concerning the general management of vitiligo, it was clear that the phototherapy treatment duration was restricted to less than one year by 46% of respondents due to the fear of increasing the patients' risks of developing skin cancer. To date, there have been no reports of skin cancer in Saudi vitiligo patients treated with phototherapy, as confirmed by the results of the present survey. Dermatologists with a mean work experience duration of more than 10 years and an average of 18 vitiligo patients per week did not observe any skin cancer in their phototherapy-treated vitiligo patients. This is very reassuring for dermatologists who use phototherapy to treat their vitiligo patients.
Only a very few cases of phototherapy-induced (or-related) skin cancer have been reported in vitiligo patients. Interestingly, Schallreuter et al.reported the absence of an increased risk of sun-induced damage and skin cancer in a study of 136 sun-exposed Caucasian patients with vitiligo.
Hexsel et al.reported the incidence of nonmelanoma skin cancer (NMSC) in a cohort of 477 patients with vitiligo. NMSC was found on sun-exposed sites of Caucasian patients with vitiligo in both vitiligo-affected and unaffected skin. Two of the six cancers arose in vitiliginous skin; the other four were found in skin containing melanocytes. The authors concluded that NMSC is as common or more so in patients with vitiligo than in the white population at large.
Nordlund later challenged this finding by reporting that there are few reports of skin cancer in vitiliginous skin. Many points described by Hexsel were disregarded, and none of the 91 nonwhite patients presented with NMSC in his study.
All vitiligo skin is considered to be of the Fitzpatrick skin type I. This indicates that the depigmented skin of all ethnic groups should be equally susceptible to skin cancer if melanin is the major determinant. These six cancers occurred only in the white people. Only two of these cancers occurred on true vitiliginous skin; the others were present on normal skin. Nordlund further commented that one would predict the converse to be true: that vitiliginous skin is more prone to skin cancer. The prevalence rates calculated by Hexsel et al. for basal cell carcinoma should be only one in four for depigmented skin and one in two for squamous-cell carcinomas (SCCs); this is lower than the rates anticipated for depigmented skin compared with normal skin.
Vitiliginous skin is less likely to be sun damaged than normal skin. There is a scarcity of reports of skin cancers in depigmented, vitiliginous skin treated with all modalities, including PUVA. Sun exposure is a known carcinogen in patients with psoriasis, but it has been the treatment of choice for vitiligo for many decades.
The cause of the low incidence of skin cancers in vitiligo patients remains unclear. One study has demonstrated the overexpression of a functional wild-type p53 protein in both the depigmented and the normal-pigmented epidermis of patients with vitiligo compared that of healthy controls. Surprisingly, long-term NB-UVB (311 nm) treatment does not alter this expression. This increase in epidermal p53 in vitiligo supports the hypothesis of a low incidence of actinic damage and basal cell carcinoma and SCC in vitiligo patients.