Study Status: Recruiting
Recruit Status: Recruiting
Study Type: Interventional
Official Title: A Split Body Study of the Effects of Combined Therapy With Narrow-Band Ultraviolet B Phototherapy and Apremilast for the Treatment of Vitiligo
Brief Summary: Vitiligo is a common acquired disorder of pigmentation affecting 0.5% to 1% of the world population. Sharply demarcated patches of depigmentation, which can affect all ethnicities, and can lead to cosmetic disfiguration and psychosocial distress, characterize the disease. The etiology of vitiligo remains unknown. Various mechanisms have been proposed, such as autoimmunity, self-destruction, biochemical, genetic, neural, oxidative stress, and an imbalance of epidermal cytokines leading to inflammation and selective loss of epidermal melanocytes. Currently, the most popular theory is autoimmunity. Previous studies noted that around 25-30% of patients have at least one other autoimmune disease, such as autoimmune thyroid disease, Addison's disease, pernicious anemia, and alopecia areata. Currently, NB-UVB phototherapy is the most widely used therapeutic option for vitiligo affecting more than 10-20% of the skin surface, as it is generally considered to be a safe initial treatment. Potential side effects include phototoxic reaction, thickening of the skin and koebnerization. NB-UVB is a band of UV radiation with a wavelength of 311-313 nm. UVB induces mitogenesis and migration in melanocytes mediated by several factors such as IL-1, TNF alpha, and leukotriene C4. UV radiation produces increased number and activity of melanocytes, increased melanin density, elongation and branching of dendrites, with increased transfer of more heavily melanized melanosomes to keratinocytes, seen clinically as increased pigmentation. Apremilast is an oral small molecule phosphodiesterase-4 (PDE4) inhibitor that has been shown to regulate inflammatory mediators. Apremilast enters cells by passive diffusion and, once intracellular, binds PDE4. PDE-4, the dominant phosphodiesterase expressed in immune cells, degrades cyclic AMP (cAMP) into AMP. PDE4 inhibition thereby elevates intracellular cAMP, which can down-regulate the inflammatory responses such as TNF-α, IFN-γ, interleukins