Pathogenesis

Pathogenesis (how the condition develops)

Vitiligo is thought to be caused by oxidative stress (a mismatch between the existence of poisonous “reactive oxygen species” (ROS) and the body’s ability to detoxify them). According to Dell’Anna and colleagues in Rome, Italy, the production of reactive oxygen species (ROS) by mitochondria within melanocytes and blood cells may be important in the progression of vitiligo (Journal of Cellular Physiology 2010; 223: 187-93).

The change of membrane lipid components in vitiligo cells, according to these investigators, could provide a biochemical basis for mitochondrial dysfunction and subsequent formation of intracellular ROS after mild stress.

Despite the fact that the specific origin of vitiligo is unknown, research suggests that autoimmunity plays a role in the disease’s progression. Tyrosine hydroxylase, which is involved in the synthesis of melanin pigment, had previously been identified as an autoantigen target in vitiligo. Tyrosine hydroxylase is an antibody target in non-segmental vitiligo (antibodies discovered in 23 percent), but not in segmental vitiligo, according to researchers at the University of Sheffield. Antibodies against tyrosine hydroxylase appear to be more common in persons with active vitiligo (see Kemp et al., Experimental Dermatology 2011; 20:

 

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