Kvaskoff Marina, Pandeya Nirmala, Green Adèle C, Perry Susan, Baxter Catherine, Davis Marcia B, Mortimore Rohan, Westacott Lorraine, Wood Dominic, Triscott Joe, Williamson Richard, Whiteman David C
Population Health Department, QIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia; Inserm U1018, Centre for Research in Epidemiology and Population Health (CESP), "Nutrition, Hormones and Women's Health" Team, F-94805, Villejuif, France; Univ. Paris Sud 11, UMRS 1018, F-94807, Villejuif, France; Gustave Roussy, F-94805, Villejuif, France; Channing Division of Network Medicine, Department of Medicine, Brigham & Women's Hospital and Harvard Medical School, Boston, MA, 02115.
Int J Cancer. 2015 Jun 15;136(12):2900-11. doi: 10.1002/ijc.29335. Epub 2014 Nov 26.
Cutaneous melanomas are postulated to arise through at least two causal pathways, namely the "chronic sun exposure" and "nevus" pathways. While chronic sun exposure probably causes many head/neck melanomas, its role at other sites is unclear. In a population-based, case-case comparison study conducted in Brisbane, Australia, we determined the prevalence and epidemiologic correlates of chronic solar damage in skin adjacent to invasive, incident melanomas on the trunk (n = 418) or head/neck (n = 92) among patients aged 18-79 in 2007-2010. Participants self-reported information about environmental and phenotypic factors, and a dermatologist counted nevi and actinic keratoses. Dermatopathologists assessed solar elastosis adjacent to each melanoma using a four-point scale (nil, mild, moderate, marked), and noted the presence or absence of adjacent neval remnants. We measured associations between various factors and solar elastosis using polytomous logistic regression. Marked or moderate solar elastosis was observed in 10% and 27%, respectively, of trunk melanomas, and 60% and 17%, respectively, of head/neck melanomas. At both sites, marked elastosis was positively associated with age (p(trend) < 0.0001) and inversely associated with neval remnants (p(trend) < 0.001). For trunk melanomas, marked elastosis was associated with highest quartiles of total sun exposure [odds-ratio (OR) = 5.47, 95% confidence interval (CI) = 1.08-27.60] and facial freckling (OR = 2.98, 95% CI = 1.17-7.56), and inversely associated with deeply tanning skin (OR = 0.29, 95% CI = 0.08-1.11) and high nevus counts (OR = 0.08, 95% CI = 0.01-0.66). Mostly similar associations were observed with moderate solar elastosis. About one in three trunk melanomas in Queensland have evidence of moderate-to-marked sun damage, and they differ in risk associations from those without.
皮肤黑色素瘤被认为至少通过两种因果途径产生,即 “长期阳光照射” 和 “痣” 途径。虽然长期阳光照射可能导致许多头颈部黑色素瘤,但其在其他部位的作用尚不清楚。在澳大利亚布里斯班进行的一项基于人群的病例对照研究中,我们确定了2007年至2010年18至79岁患者躯干(n = 418)或头颈部(n = 92)侵袭性新发黑色素瘤邻近皮肤的慢性日光损伤的患病率及其流行病学相关因素。参与者自行报告有关环境和表型因素的信息,皮肤科医生对痣和光化性角化病进行计数。皮肤病理学家使用四点量表(无、轻度、中度、重度)评估每个黑色素瘤邻近部位的日光性弹力组织变性,并记录邻近痣残余的存在与否。我们使用多分类逻辑回归测量各种因素与日光性弹力组织变性之间的关联。分别在10% 和27% 的躯干黑色素瘤以及60% 和17% 的头颈部黑色素瘤中观察到重度或中度日光性弹力组织变性。在两个部位,重度弹力组织变性均与年龄呈正相关(p趋势<0.0001),与痣残余呈负相关(p趋势<0.001)。对于躯干黑色素瘤,重度弹力组织变性与总阳光暴露的最高四分位数相关 [比值比(OR)= 5.47,95% 置信区间(CI)= 1.08 - 27.60] 和面部雀斑相关(OR = 2.98,95% CI = 1.17 - 7.56),与深肤色呈负相关(OR = 0.29,95% CI = 0.08 - 1.11)以及与高痣计数呈负相关(OR = 0.08,95% CI = 0.01 - 0.66)。中度日光性弹力组织变性也观察到大致相似的关联。昆士兰州约三分之一的躯干黑色素瘤有中度至重度阳光损伤的证据,并且它们在风险关联方面与没有此类损伤的黑色素瘤不同。