The Efficacy of a Sunscreen With SPF30 and a After-sun-lotion in the Prevention of Polymorphic Light Eruption
The Efficacy of a Sunscreen With SPF30 and a After-sun-lotion in the Prevention of Polymorphic Light Eruption
Polymorphic light eruption (PLE) is a common photodermatosis characterized by the appearance of itching, erythema, papules or vesicles on sun-exposed skin. Though etiology is unclear it is hypothesized that it is an abnormal immune response to autologous antigens generated by ultraviolet radiation (UVR). This randomized, double blinded left-right body side experimental comparison study was designed to assess the preventive effect of a sunscreen and topical DNA repair enzyme-containing after-sun lotion in PLE.
A SPF 30 sunscreen (containing chemical and physical UV filters), an after-sun lotion containing liposomal encapsulated micrococcus luteus lysate with endonuclease activity and photolyase (active AS), and an after-sun placebo formulation (containing no DNA repair enzymes) (placebo AS) has been used in this study. Fourteen PLE patients were enrolled. On day 1, the individual minimal erythema dose (MED) was assessed on patients' buttock skin by exposure to a test ladder of solar-simulated UVR (xenon arc source, Oriel Corp. Darmstadt, Germany). From day 2 to 5, 0.75 individual MED exposures (increased by 0 to 25% per exposure, depending on the erythema response to a preceding dose) were given to a total of four 5-by-5 cm skin test fields on symmetrically located, individual PLE predilection sites on the trunk or extremities. The test fields were treated in randomized and double-blinded fashion either with SPF30 sunscreen 20 min before UVR exposure, active AS or placebo AS (all creams at a concentration of 2mg/cm2) immediately after UVR exposure, or left untreated. Sixty minutes after UVR exposure all test areas were treated with visible light (400 to 450nm, 5J/cm2) to activate the light dependent photolyase DNA repair mechanism. The photo test procedure led to the appearance of PLE symptoms in unprotected test fields of 12/14 (86%) patients, active AS-treated test fields of 6/14 (43%) patients (p<0.05), placebo AS-treated test fields of 10/14 (71%) patients (p, ns), and no (0%) sunscreen-protected test fields of any patient (p<0.0001 vs. unprotected test fields, Fisher exact test). These results provide evidence that i) DNA damage is a trigger of PLE, ii) increasing DNA repair can prevent induction of PLE symptoms, and iii) the use of sun care preparations containing DNA repair enzymes may be clinically useful for PLE patients.
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