This literature review explores atopic dermatitis and its management, with a focus on phototherapy as a treatment modality. The primary objectives are to elucidate the pathophysiological mechanisms, clinical manifestations, diagnostic criteria, and epidemiology of atopic dermatitis. Additionally, it seeks to explain phototherapy mechanisms, different modalities, and other therapeutic approaches. In this review, we comprehensively examine atopic dermatitis by synthesizing findings from diverse sources over the past 20 years. We investigate the epidemiology, pathophysiology, clinical manifestations, diagnostic criteria, and role of phototherapy in treatment. We conduct thematic analysis, compare phototherapy modalities, consider contextual factors, and integrate patient perspectives while upholding ethical considerations. Limitations include potential publication bias, language barriers, temporal constraints, subjectivity, and limited generalizability. Atopic dermatitis has a complex pathogenesis and can be managed with diverse modalities. Phototherapy emerges as an effective and safe treatment, particularly when other therapies prove ineffective.

Phototherapy is a standard treatment for moderate-to-severe psoriasis. However, concern remains regarding the associated cutaneous carcinogenic risk. Our objective is to conduct a systematic review of skin cancer risk for psoriasis patients treated with phototherapy. To achieve our goal, we searched Cochrane, PubMed, and Embase databases. We aimed to evaluate existing literature (from July 1, 2010, to December 31, 2020) on phototherapy for all Fitzpatrick skin phototypes (FSP) which includes 71 articles, and eight articles being categorized in this review. Five studies did not report an increased skin cancer risk with narrowband-ultraviolet blue (UVB) and unspecified UVB for FSP II through VI, with one study not reporting FSP. Three studies did report an increased risk of skin cancer with narrowband-UVB and broadband-UVB for FSP I-VI, with one study also not specifying skin phototypes or UVB phototherapy type. Additionally, a study with psoralen and ultraviolet A with and without narrowband-UVB demonstrated an increased risk of skin cancer in phototypes III and IV. The most commonly reported secondary outcomes with phototherapy were actinic keratosis (123) and solar lentigines (10). Numerous patients were also on additional therapies including methotrexate, acitretin, and biologics. Study limitations include publication bias due to limited number of studies published on this topic in the last ten years along with heterogeneity in reporting. The relationship between phototherapy, psoriasis, and cutaneous oncogenic risk remains contradictory. While phototherapy for psoriasis is an efficacious therapy, further studies are needed to understand the cutaneous oncogenic risk based on FSP to help clinicals tailor treatment recommendations based on skin phototypes.

BACKGROUND: Maximum cyclobutane pyrimidine dimer (CPD) formation in the skin induced by ultraviolet B (UVB) irradiation is thought to occur within a few minutes and is immediately decreased by the DNA repair system.
OBJECTIVE: We evaluated the time course and differential effects of narrowband (NB-UVB) and broadband (BB-UVB) UVB on CPD formation.
METHODS: We investigated CPD formation at various time-points in vivo, from 3 min to 72 h, after UVB irradiation using 2 mouse strains, C57BL/6 J and BALB/c. The backs of the mice were shaved and irradiated with NB-UVB or BB-UVB. Skin specimens were obtained and stained with anti-CPD antibody. Positive signals in the epidermis were measured using ImageJ. DNA was extracted from the isolated epidermis and subjected to quantitative CPD analysis by enzyme-linked immunosorbent assay (ELISA).
RESULTS: CPDs induced by UVB irradiation (1 minimum erythemal dose) in epidermal skin were detected in the nucleus. Although the CPD levels increased immediately after irradiation (3 min), the highest level was detected at 1 h and the increase lasted 24-48 h after irradiation. BB-UVB tended to induce greater CPD levels than NB-UVB in both mouse strains. The ELISA showed similar results.
CONCLUSIONS: CPDs were induced immediately after UV irradiation, with the maximum level observed 1 h after irradiation. BB-UVB irradiation tended to induce greater levels of CPD formation. In addition to the direct effects of UVB, the presence of CPDs in hair follicles, which were not irradiated by UVB, suggests that reactive oxygen species are also involved in CPD formation in the skin.

Phototherapy using narrowband ultraviolet-B (NB-UVB) has been shown to be more effective than conventional broadband UVB (BB-UVB) in treating a variety of skin diseases. To assess the difference in carcinogenic potential between NB-UVB and BB-UVB, we investigated the cytotoxicity via colony formation assay, genotoxicity via sister chromatid exchange (SCE) assay, mutagenicity via hypoxanthine phosphoribosyltransferase (HPRT) mutation assay, as well as cyclobutane pyrimidine dimer (CPD) formation and reactive oxygen species (ROS) generation in Chinese hamster ovary (CHO) and their NER mutant cells. The radiation dose required to reduce survival to 10% (D10 value) demonstrated BB-UVB was 10 times more cytotoxic than NB-UVB, and revealed that NB-UVB also induces DNA damage repaired by nucleotide excision repair. We also found that BB-UVB more efficiently induced SCEs and HPRT mutations per absorbed energy dosage (J/m2) than NB-UVB. However, SCE and HPRT mutation frequencies were observed to rise in noncytotoxic dosages of NB-UVB exposure. BB-UVB and NB-UVB both produced a significant increase in CPD formation and ROS formation (p < 0.05); however, higher dosages were required for NB-UVB. These results suggest that NB-UVB is less cytotoxic and genotoxic than BB-UVB, but can still produce genotoxic effects even at noncytotoxic doses.

Ascorbic acid 2-glucoside (AA2G), glucosylated ascorbic acid (AA), has superior properties for bioavailability and stability compared to AA. Although AA2G has shown radioprotective properties similar to AA, effects for UV light, especially UVC and UVB, are not studied. AA2G was tested for cytotoxicity and protective effects against ionizing radiation, UVC, and broadband and narrowband UVB in Chinese hamster ovary (CHO) cells and compared to AA and dimethyl sulfoxide (DMSO). Pretreatment with DMSO, AA, and AA2G showed comparative protective effects in CHO wild type and radiosensitive xrs5 cells for cell death against ionizing radiation with reducing the number of radiation-induced DNA damages. Pretreatment with AA and AA2G protected CHO wild type and UV sensitive UV135 cells from UVC and broadband UV, but not from narrowband UVB. DMSO showed no protective effects against tested UV. The UV filtration effects of AA and AA2G were analyzed with a spectrometer and spectroradiometer. AA and AA2G blocked UVC and reduced short wavelengths of UVB, but had no effect on wavelengths above 300nm. These results suggest that AA2G protects cells from radiation by acting as a radical scavenger to reduce initial DNA damage, as well as protecting cells from certain UVB wavelengths by filtration.

Ultraviolet (UV) radiation contributes to the development of skin cancer through direct and indirect DNA damage, production of reactive oxygen species, and local immunomodulation. The association between UV radiation and skin cancer has raised concern for the risk of carcinogenesis following phototherapy. The photocarcinogenic impact of psoralen and UVA radiation (PUVA) has been extensively studied, whereas limited safety studies exist for other phototherapy modalities, such as broadband and narrowband UVB and UVA1. Because of the as of yet unclear risk, patients who have undergone any type of phototherapy should be followed for age-appropriate skin cancer screening.