Influence of Serum Vitamin D Level in the Response of Actinic Keratosis to Photodynamic Therapy with Methylaminolevulinate.

Ricardo Moreno,Ángeles Juarranz,Yolanda Gilaberte,Laura Nájera,Marta Mascaraque,Salvador González

doi:10.3390/jcm9020398

Abstract

In mouse models of squamous cell carcinoma, pre-treatment with calcitriol prior to photodynamic therapy with aminolevulinic acid (ALA) enhances tumor cell death. We have evaluated the association between vitamin D status and the response of actinic keratoses to photodynamic therapy with methylaminolevulinate. Twenty-five patients with actinic keratoses on the head received one session of photodynamic therapy with methylaminolevulinate. Biopsies were taken at baseline and six weeks after treatment. Immuno-histochemical staining was performed for VDR, P53, Ki67 and β-catenin. Basal serum 25(OH)D levels were determined. Cases with a positive histological response to treatment had significantly higher serum 25(OH)D levels (26.96 (SD 7.49) ngr/mL) than those without response (18.60 (SE 7.49) ngr/mL) (p = 0.05). Patients with a complete clinical response displayed lower basal VDR expression (35.71% (SD 19.88)) than partial responders (62.78% (SD 16.735)), (p = 0.002). Our results support a relationship between vitamin D status and the response of actinic keratoses to photodynamic therapy with methylaminolevulinate.

Highlights

Vitamin D (VD) is a prohormone involved in a wide variety of functions in the organism, and has been related with several types of cancer [1]
This study supports the relationship between 25(OH)D serum levels and the response of Actinic keratoses (AKs) to MAL-Photodynamic therapy (PDT): VD deficient levels were found to be significantly associated to a lack of response in the reduction of the KIN grade of actinic keratoses, and patients whose AK exhibited a significantly lower VD receptor (VDR) basal expression showed a complete clinical response to the treatment
Our findings suggest that a poorer response of AK to MAL-PDT is likely to be expected under a deficient VD status

Summary

Introduction

Vitamin D (VD) is a prohormone involved in a wide variety of functions in the organism, and has been related with several types of cancer [1]. It has several known effects on epidermal carcinogenesis [2]: it regulates keratinocyte proliferation promoting its differentiation [3], and it prevents UV-induced mutations [4], enhancing mutation repair. Vitamin D is obtained mainly through exposure to sunlight which, in the epidermis, promotes transformation of 7-dehydrocholesterol into cholecalciferol or previtamin D3. In AK, the severity of keratinocytic dysplasia is classified, as in other intraepidermal carcinomas (CIN for cervical, VIN for vulvar, AIN for anal intraepithelial neoplasia) into KIN (keratinocytic intraepidermal neoplasia) grade 1, 2 or 3 according to the presence of dysplastic keratinocytes in one third, two thirds or the complete thickness of the epidermis [6]

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