UVA-1 is a modality of phototherapy with a long wavelength, which allows it to achieve greater penetration and makes it especially effective for the treatment of sclerotic skin diseases [2
]. This longer wavelength is also associated with a lower risk of burning during treatment than other phototherapy modalities. The main mechanism of action is the activation of fibroblasts, which produce metalloproteinases, with the consequent reduction in collagen production [3
]. Other mechanisms include immediate and retarded apoptosis (due to the generation of reactive oxygen species), neovascularization, activation of the FAS/FAS ligand system (which activates programmed cell death) and reduction in TGFβ, TNFα, IL-5, -6, -8, -13 and -31 and IFNγ [2
]. Therefore, according to what we observed in our samples, it seems that on one hand, there is a reduction in the excess cellularity due to apoptosis, and on the other hand, there is an activation of the remaining fibroblasts which produces a rupture of the disorganized collagen due to the action of metalloproteinases and a new, denser and better organized collagen. Modulation of endothelial dysfunction induced by UVA-1, with an increase in CD34 expression [4
], may also play a role, as endothelial dysfunction and abnormal blood vessel regulation have been proposed as pathogenic factors in keloid development [5
]. In our samples, we observed an increase in vascular structures after the treatment. Finally, mucin, which is found at increased levels in keloids [6
], was reduced after the UVA-1 sessions. All these mechanisms are responsible for the striking changes observed in the histological images of our case, which correlated with patient-reported outcomes. The aesthetic impairment barely changed, maybe because these changes occur mainly in the dermis instead of the epidermis; however, when the patient was asked, she said she was satisfied with the treatment.
There are various UVA-1 dosage regimen recommendations. Generally, each cycle consists of 15–20 sessions with increasing doses, and no more than two cycles per year are recommended [2
]. In our case, the use of only one cycle of 25 sessions with a low-dosage regimen showed striking histological changes and an improvement in the patient’s symptoms. There have been reports of several skin diseases being successfully treated with UVA-1 phototherapy—for example, sclerotic diseases, such as systemic sclerosis and morphea, inflammatory conditions, such as eczema and prurigo, granulomatous diseases, such as sarcoidosis and annular granuloma, and T cell lymphomas and related disorders, such as pityriasis lichenoides and lymphomatoid papulosis [7
]. To the best of our knowledge, there have only been two cases of keloids treated with UVA-1 laser [8
] and a few cases treated with UVA-1 phototherapy, all with high doses [9
], but no cases treated with a low-dosage regimen have been reported to date. UVA-1 phototherapy has less risk of burns and skin cancer development than other types of phototherapy [9
], and the use of low doses further decreases this risk.