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June 2004

LE Magazine June 2004
Sun damage

Recent trends in cutaneous melanoma incidence among whites in the United States.
BACKGROUND: It is not yet clear whether increasing melanoma incidence is real or whether recent incidence trends mainly reflect improved diagnosis. To address this question, we examined the most recent melanoma incidence patterns among the white population stratified by sex, age, tumor stage, and tumor thickness by use of data from the Surveillance, Epidemiology, and End Results Program. METHODS: We examined log-transformed age-specific rates for melanoma by 5-year age groups and time periods by year of diagnosis and birth cohort. Melanoma trends were further examined among broader age groups (<40 years, 40-59 years, and > or =60 years) by tumor stage and tumor thickness. Rates were age-adjusted to the 1970 U.S. standard population, and trends were tested by use of a two-sided Student's t test. RESULTS: Melanoma incidence increased in females born since the 1960s. From 1974-1975 through 1988-1989, upward trends for the incidence of localized tumors and downward trends for the incidence of distant-stage tumors occurred in the age group under 40 years. In the more recent time period, 1990-1991 through 1996-1997, age specific rates among females compared with males generally remained stable or declined more for distant-stage tumors and increased less for local-stage tumors. Thin tumors (<1 mm) increased statistically significantly in all age groups (P<.05 for all), except in men under age 40 years. In contrast, rates for thick tumors (> or =4 mm) increased statistically significantly (P =.0003) only in males aged 60 years and older. CONCLUSION: Melanoma incidence may well continue to rise in the United States , at least until the majority of the current population in the middle-age groups becomes the oldest population. The recent trends may reflect increased sunlight exposure.

J Natl Cancer Inst. 2001 May 2;93(9):678-83

Ultraviolet radiation: sun exposure, tanning beds, and vitamin D levels. What you need to know and how to decrease the risk of skin cancer.
This year, more than one million new cases of skin cancer will be diagnosed in the United States and an estimated 9800 individuals will die of the disease. Despite recent public education efforts and increased public awareness about the importance of the use of sunscreen and avoidance of ultraviolet radiation, the incidence of melanoma has more than tripled among white Americans from 1980 to 2001. This increase in cancer rates means that one person dies of melanoma in this country every hour of every day. The answer to this increasing problem is not a simple one, but public education seems to be a common starting point. The American Cancer Society and the American Academy of Dermatology have published recommendations with regard to sun exposure and sunscreen use. However, patients often ask questions that are not as easily answered. Questions such as, Which sunscreens are the safest? Are tanning beds safe? If I limit my sun exposure, do I need to take vitamin D supplements? If I tanned as a teenager, is the damage already done? How do I treat sunburn? This article provides a review of the current literature regarding these issues and provides the facts family physicians need to answer common patient questions. The author discusses the mechanisms of sun damage, the facts on tanning beds, and the importance of supplementing vitamin D.

Am Osteopath Assoc . 2003 Aug;103(8):371-5

Common skin disorders in the elderly.
Skin diseases commonly seen in the elderly are more often than not the effects of sun damage or vascular disease. The effects of a lifetime of even casual sun exposure can be dramatic. Chronically sun-exposed skin becomes thin, loses collagen, and has disrupted elastin and decreased glycosaminoglycans. The result is skin that breaks easily, bruises, sags, irritates easily, and itches. The spots and bumps that patients associate with age are all sun-induced. Consider how lesionless a 60-year-old's buttock is compared to the extensor forearm. The reason that bruising attributed to anticoagulation seems to occur exclusively on the extensor forearm and not the volar aspect of the arm is that sun-induced elastin degradation is greatest on the extensor forearm. Even trivial trauma will cause unsupported capillaries to shear and bleed whether the patient is anticoagulated or not. This article reviews the primary skin disorders associated with the elderly and some of the management approaches that the primary care physician can use.

Clin Cornerstone . 2001;4(1):39-44

Elderly and sun-affected skin. Distinguishing between changes caused by aging and changes caused by habitual exposure to sun.
OBJECTIVE: To review and distinguish between skin changes produced by aging and changes produced by habitual exposure to sun. QUALITY OF EVIDENCE: The literature was searched from 1969 to 1999 for articles on dermatoheliosis and sun-damaged skin. Surprisingly few were found comparing the difference between elderly skin and sun-damaged skin. A few articles focused on certain small aspects of sun-damaged skin. Many excellent articles described particular changes (e.g., actinic keratosis), but few covered all the changes due to aging and to sun. MAIN MESSAGE: Skin changes due to aging can be distinguished from those due to sun damage. All changes due to sun exposure can be grouped under the term dermatoheliosis; five parts of the skin are involved: epidermis (actinic keratosis), dermis (solar elastosis), blood vessels (telangiectasia), sebaceous glands (solar comedones), and melanocytes (diffuse or mottled brown patches). Habitual exposure to sun and a white skin are prerequisites for developing these changes. Knowing the difference between changes caused by sun and by aging can help physicians predict which patients are most likely to get skin cancers. CONCLUSION: Knowledge of these common skin changes will help physicians diagnose and manage the skin abnormalities of elderly people and of people with dermatoheliosis.

Can Fam Physician. 2001 Jun;47:1236-43

Cutaneous photobiology. The melanocyte vs. the sun: who will win the final round?
Solar ultraviolet radiation (UV) is a major environmental factor that dramatically alters the homeostasis of the skin as an organ by affecting the survival, proliferation and differentiation of various cutaneous cell types. The effects of UV on the skin include direct damage to DNA, apoptosis, growth arrest, and stimulation of melanogenesis. Long-term effects of UV include photoaging and photocarcinogenesis. Epidermal melanocytes synthesize two main types of melanin: eumelanin and pheomelanin. Melanin, particularly eumelanin, represents the major photoprotective mechanism in the skin. Melanin limits the extent of UV penetration through the epidermal layers, and scavenges reactive oxygen radicals that may lead to oxidative DNA damage. The extent of UV-induced DNA damage and the incidence of skin cancer are inversely correlated with total melanin content of the skin. Given the importance of the melanocyte in guarding against the adverse effects of UV and the fact that the melanocyte has a low self-renewal capacity, it is critical to maintain its survival and genomic integrity in order to prevent malignant transformation to melanoma, the most fatal form of skin cancer. Melanocyte transformation to melanoma involves the activation of certain oncogenes and the inactivation of specific tumor suppressor genes. This review summarizes the current state of knowledge about the role of melanin and the melanocyte in photoprotection, the responses of melanocytes to UV, the signaling pathways that mediate the biological effects of UV on melanocytes, and the most common genetic alterations that lead to melanoma.

Pigment Cell Res. 2003 Oct;16(5):434-47

Determinants of melanocyte density in adult human skin.
The distribution of melanocytes in human skin has been observed to vary within and among individuals, yet little is known of the factors that determine the density of these pigment cells. These factors were explored in a molecular epidemiological study conducted among a population-based sample of 97 male subjects aged over 50 years in Queensland , Australia . Information relating to environmental and phenotypic factors was collected through face-to-face interviews and physical examination of all participants. In addition, 2-mm biopsies of representative skin were taken from the dorsum of the hand and another anatomical site. Melanocytes were identified by cytoplasmic staining with the B8G3 (anti-TRP1) monoclonal antibody using standard immunohistochemical techniques. Melanocyte counts were performed blind by two observers. On crude analysis, melanocyte density decreased with advancing age (P = 0.0002), and increased with increasing number of naevi (P = 0.01). Other pigmentary characteristics (such as hair and eye colour and depth of tan) were not associated with epidermal melanocyte density. Melanocyte density varied significantly by anatomical site (P = 0.02), with highest densities observed on the back/shoulders (n = 50, 17.1 +/- 8.8 cells/mm, mean +/- SD) followed by the upper limbs (n = 11, 12.6 +/- 8.8 cells/mm) and lower limbs (n = 14, 14.4 +/- 5.9 cells/mm). Lowest melanocyte densities were recorded on the anterior trunk (n = 3, 3.2 +/- 2.4 cells/mm). These findings confirm the results of earlier studies in which site-specific differences in melanocyte density have been found. We speculate that the unequal distribution of melanocytes may partially explain the site-specific incidence of melanoma, offering fresh perspectives on the aetiology of this cancer.

Arch Dermatol Res. 1999 Sep;291(9):511-6

Epidemiology of ultraviolet-DNA repair capacity and human cancer.
The following conclusions are derived from an epidemiological study. Reduced repair of ultraviolet (UV)-induced DNA damage contributes directly to basal cell carcinoma (BCC) in individuals with prior sunlight overexposure. A family history of BCC is a predictor of low DNA repair. Repair of UV-damaged DNA declines at a fixed rate of approximately 1% per annum in noncancerous controls. The DNA repair differences between young BCC cases and their controls disappear as they age. Hence, BCC, in terms of DNA repair, is a premature aging disease. The persistence of photochemical damage because of reduced repair results in point mutations in the p53 gene and allelic loss of the nevoid BCC gene (Gorlin's syndrome) located on chromosome 9q. The fact that environmental vulnerability is gender oriented implicates hormones in regulating DNA repair. Xeroderma pigmentosum appears to be a valid paradigm for the role of DNA repair in BCC in the general population.

Environ Health Perspect . 1997 Jun;105 Suppl 4:927-30

Repair of UV light-induced DNA damage and risk of cutaneous malignant melanoma.
BACKGROUND: The mechanism underlying the role of UV light exposure from sunlight in the etiology of cutaneous malignant melanoma (CMM) is unclear. Patients with xeroderma pigmentosum, a disease characterized by severe sensitivity to UV radiation and a defect in nucleotide excision repair, have a high incidence of CMM, which suggests that DNA repair capacity (DRC) plays a role in sunlight-induced CMM in the general population as well. METHODS: We conducted a hospital-based case-control study of DRC and CMM among 312 non-Hispanic white CMM patients who had no prior chemotherapy or radiation therapy, and 324 cancer-free control subjects who were frequency-matched to case patients on age, sex, and ethnicity. Information on demographic variables, risk factors, and tumor characteristics was obtained from questionnaires and medical records. We used the host-cell reactivation assay to measure the DRC in study subjects' lymphocytes. All statistical tests were two sided. RESULTS: Case patients had a 19% lower mean (+/- standard deviation [SD]) DRC (8.5 +/- 3.4%) than control subjects (10.5 +/- 5.1%), a statistically significant difference (P<.001). DRC that was at or below the median value (i.e., 9.4%) in control subjects was associated with increased risk for CMM after adjustment for age, sex, and other covariates (odds ratio [OR] = 2.02, 95% confidence interval [CI] = 1.45 to 2.82). We observed a dose-response relationship between decreased DRC and increased risk of CMM (P(trend)<.001). Patients with tumors on sun-exposed skin had statistically significantly lower DRC than patients with tumors on unexposed skin (8.2 +/- 3.3% versus 9.5 +/- 3.5%; P =.004). CONCLUSIONS: Reduced DRC is an independent risk factor for CMM and may contribute to susceptibility to sunlight-induced CMM among the general population.

J Natl Cancer Inst. 2003 Feb 19;95(4):308-15