Official websites use. Share sensitive information only on official, secure websites. Irradiation triggers inflammation, fibroblast activation, and extracellular matrix deposition in addition to reactive oxygen species generation, leading to a chronic inflammatory response. Radiation-induced fibrosis RIF is a progressive pathology resulting in skin pigmentation, reduced elasticity, ulceration and dermal thickening, cosmetic deformity, pain, and the need for reconstructive surgery.
Deferoxamine DFO is a U. Food and Drug Administration FDA -approved iron chelator for blood dyscrasia management, which has been found to be proangiogenic, to decrease free radical formation, and reduce cell death. Systemic DFO has a short half-life and is cumbersome to deliver to patients intravenously.
Transdermal DFO delivery is complicated by its high atomic mass and hydrophilicity, preventing stratum corneum penetration. A transdermal drug delivery system was developed to address these challenges, in addition to a strategy for topical administration. DFO has great potential to translate from bench to bedside. Furthermore, after an initial plethora of studies reporting DFO treatment by intravenous and subcutaneous routes, a significant advantage of recent studies is the success of transdermal and topical delivery.
Given the strong foundation of basic scientific research supporting the use of DFO treatment on RIF, clinicians will be closely following the results of the ongoing human studies. Keywords: iron chelation, skin radiation, reactive oxygen species, wound healing, irradiation. Radiation, an indispensable component of cancer therapy, also leads to acute and chronic sequelae, such as fibrosis.
Radiation-induced fibrosis RIF typically occurs 4β12 months after radiation therapy and progresses over several years. Manifestations of RIF occur in the skin and subcutaneous tissue, lungs, gastrointestinal and genitourinary tracts, as well as any other organs in the treatment field. The mechanism of RIF can be likened to chronic wound healing. The initial injury triggers acute inflammation, fibroblast activation, and extracellular matrix deposition.
