Role of UVA1 phototherapy in treatment of scleroderma and scleroderma-like disorders”

Abstract

Treatment of scleroderma and scleroderma-like diseases poses a serious challenge to contemporary dermatology due to the complexity of its pathogenesis, low incidence of the diseases and their heterogenous clinical expression. the manifestation of this autoimmune disease includes an increased production and deposition of collagen fibres types I and III in the skin and connective tissue as well as vascular alterations. Ultraviolet A1 (UVA1) phototherapy affects various stages of a morbid process in scleroderma: it inhibits inflammation and affects the consequences of it, fibrosis. Currently, UVA1 is proposed as a potential treatment and is believed to have a multifold mechanism of action. This includes, inducing apoptosis in T and B lymphocytes, inhibition of proinflammatory cytokine production and ability to induce collagenase production by fibroblasts. UVA1 irradiation may also interact with endothelial cells, promoting angiogenesis. Efficacy of high, moderate, and low doses of UVA1 was documented. Advantages of UVA1 phototherapy include the evident avoidance of systemic side effects of psoralens such as nausea and vomiting or photokeratitis as well as lower risk of phototoxic reactions with deeper penetration of radiation. Its disadvantages include high cost of equipment, thus reducing the accessibility of the treatment to specialized centres. Due to its unique mechanism of action, attempts to useUVA1 phototherapy seem justified in other rare diseases, developing with skin induration.

UVA Irradiation Induced Heme Oxygenase‐1: A Novel Phototherapy for Morphea

“…UVA1‐induced effects occur through oxygen‐dependent mechanisms in which endogenous absorption of energy by lipids and proteins occurs and then the resulting oxidized lipids/proteins are responsible for the UVA effect . The singlet oxygen ( 1 O 2 ) is generated after UVA1 irradiation of T lymphocytes and contributes its efficacy in treating inflammatory disease . In addition, ultraviolet A radiation (UVAR) excites the generated intracellular molecule 1 O 2 , then activates the apoptotic p38 and JNK, thus inducing the MAPK cascades .…”

“…Several mechanisms are involved in UVA1 phototherapy such as apoptosis in various skin cell types (T or B lyphocytes, mast cells), modification of the effects of pro‐inflammatory cytokines, as well as lowering of the number of mast cells and Langerhans cells in the epidermis . It has recently been reported that UVA1 phototherapy may promote angiogenesis, the process of new blood vessel formation, in order to cure the skin diseases . During the phototherapy of vitiligo, psoriasis, and T‐cell lymphoma, the UV irradiation diminishes inflammation, reduces scaling, and consequently, promotes repigmentation at the exposed skin .…”