Pathogenesis (how the condition develops)

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The pathogenesis of vitiligo is believed to involve oxidative stress (an imbalance between the presence of toxic so-called reactive oxygen species (ROS) and the body’s ability to detoxify them). Based on this, according to Dell’Anna and colleagues in Rome, Italy, the generation of reactive oxygen species (ROS) by the mitochondria within melanocytes and blood cells may be relevant in the development of vitiligo (Journal of Cellular Physiology 2010; 223: 187-93).

These authors suggest that the modification of membrane lipid components in vitiligo cells may be a biochemical basis for the mitochondrial impairment and the subsequent production of intracellular ROS following the exposure to a mild stress.

Although the exact cause of vitiligo remains obscure, evidence suggests that autoimmunity plays a role in the pathogenesis of the disease. Previously, tyrosine hydroxylase (important in the production of melanin pigment) was identified as an autoantigen target in vitiligo. Researchers at the University of Sheffield have found that tyrosine hydroxylase is an antibody target in non-segmental vitiligo (antibodies found in 23%) but not in the segmental type.  Also, tyrosine hydroxylase antibodies appear to be more frequent in people with active vitiligo (see Kemp et al. Experimental Dermatology 2011; 20: 35-40).