Assessment of sun‑related behavior and serum vitamin D in basal cell carcinoma: Preliminary results

Abstract

Ultraviolet radiation (UV), mainly from sunlight, is the main risk factor of the most common human skin cancer, basal cell carcinoma (BCC). A positive effect of UV on the skin is its contribution to the synthesis of vitamin D, which is important in sustaining general health, but having high levels of vitamin D is considered a risk factor for BCC. However, vitamin D receptor has antagonistic effects to UV radiation in regulating Sonic Hedgehog pathway. This is a pilot study aimed at characterizing the sun-related behavior and vitamin D status of 52 BCC patients and 59 controls from our geographical area. Patients were included in 4 subgroups: Single, multiple, recurrent, and both multiple and recurrent BCCs. Patients, more than controls, had at least one sunburn in childhood and lentigines (P<0.001). Also, they spent daily, on average, more time in the sun than controls (P<0.001) (3.00-8.00 and 1.50-4.00 h respectively). Outdoor work was similar in both groups. Participants had lower vitamin D serum levels than expected. Due to the small number of cases, no statistically significant differences were found between the subgroups but some tendencies were noted. Patients with only one recurrent BCC had less sunburns than the ones who also developed tumors at multiple sites (P=0.2). Patients with multiple and recurrent tumors had slightly lower vitamin D levels compared with single BCC patients (P=0.1) although they used more vitamin D supplements after the BCC diagnosis (P=0.2). Having a diagnosis of BCC, made patients more compliant to the use of sunscreen cream, but even so, half of them still did not use it. In conclusion, more effort should be invested in sun-related education and public health actions should focus on vitamin D deficiencies.

The Relationship between Vitamin D and Basal Cell Carcinoma: A Systematic Review

“…Skin cancer is the most common malignancy among Caucasians, with basal cell carcinoma (BCC) being the commonest among them in 2012 [1,2]. Its prevalence in the United States has risen to 800 to 1000 cases per 100,000 people [1,3,4].…”

“…With a dramatic increase in the incidence of both melanoma and non-melanoma skin cancers over the past 50 years, more than one million new diagnoses of BCC appear each year [5]. According to the World Health Organization (WHO) in 2006, light skin types (Fitzpatrick I, II) are more prone to developing keratinocyte-derived cancer as they are predisposed to sunburns after exposure to ultraviolet rays (UVR) [2].…”

“…Both natural and artificial ultraviolet (UV) radiation, particularly ultraviolet-B (UV-B) with a wavelength range between 280 and 320 nm, is the most important risk factor for BCC, especially for light skin types (Fitzpatrick I, II) [2,3]. Modifiable risks that increase UV exposure include wearing sleeveless or light clothing, participating in outdoor activities, taking suntan baths, and not applying sunscreen.…”

“…Modifiable risks that increase UV exposure include wearing sleeveless or light clothing, participating in outdoor activities, taking suntan baths, and not applying sunscreen. Other nonmodifiable risk factors are increased life expectancy, ozone depletion [6], genetic alterations, and UV radiation used for treating some skin conditions like psoriasis and vitiligo [2,6,7]. Sunlight exposure has a dual effect; it helps our skin produce vitamin D, exerting a protective effect against the development of skin cancer as well as causing deoxyribonucleic acid (DNA) damage to our skin cells [3].…”

“…These genes encode the vitamin D receptor (VDR) and methylenetetrahydrofolate reductase (MTHFR) [6,7,8,18,19]. The VDR is a member of the transacting transcriptional regulatory factor superfamily that includes steroid and thyroid hormone receptors, as well as retinoid-X receptors and retinoic acid receptors [3], and it is expressed on a variety of cells, including epidermal basal keratinocytes [2,19,20]. 1,25-Dihydroxy vitamin D3 (1,25(OH)2D3) exerts its action by binding to VDR, which then translocates to the nucleus where it regulates the expression of VDRresponsive genes.…”