Index of contents
Introduction
Vitiligo is a chronic disorder acquired pigmentary characterized by progressive loss of skin melanocytes and normal function abnormality, It is resulting in hypopigmented areas of skin that become progressively amelanotic. This disease is generated in most cases the child.
Different studies highlight how half of vitiligo patients develop the disease before the age of 20 and how about 25% of them develop the disease before age 8.
In the pediatric ageVitiligo can represent profound psychological trauma for both patients and their parents, and leads to a poor quality of life. Even if treatment of the disease is the goal of dermatologists by mail, a better understanding of vitiligo can be helpful for better patient management.
Etiology
As is well known, vitiligo is inherited in a non-Mendelian, multifactorial, and polygenic pattern.
A part of the molecules that encode genes relevant for normal melanogenesis (for example, TYR that encodes tyrosinase), recent studies show a strong association of vitiligo with particular HLA haplotypes (HLAs-A2, -DR4, -DR7 and -DQB1 * 0303) and other genes that are involved in cellular and humoral immunity. Due to the possible associated with different autoimmune diseases, in the future, recognition of the genetic background should be useful to recognize eventual comorbidities and a personalized focused treatment.
Environmental factors
Much data supports the profound impact of environmental factors on the development of vitiligo. Firstly, there is evidence of a variable prevalence of the disease in different countries, ranging from 0.1 to 2.0%.
Then there are the data on the incidence of the disease among familiarities. It has been estimated that the majority of vitiligo cases are sporadic and up to 20% of the patients report an affected relative. Furthermore, the incidence of vitiligo concordance in monozygotic twins is only 23%.
Different environmental factors can trigger the disease: its recognition would be essential to limit the incidence and progression of skin disease.
Comorbidities
The highest risk of developing autoimmune diseases in patients with vitiligo is a well-known fact.
| • Atopic dermatitis |
| • autoimmune hemolytic anemia |
| • autoimmune thyroid disease |
| • Mellitus diabetes |
| • inflammatory bowel disease |
| • Morphea |
| • Multiple sclerosis |
| • Pemphigus vulgaris |
| • Pernicious anemia |
| • psoriasis |
| • Rheumatoid arthritis |
| • Systemic lupus erythematosus |
| • Others |
Pathobiology
Today the exact pathobiology of vitiligo is still unclear. Even if multiple theories have been put forward, recent data supports that vitiligo is a T-cell mediated autoimmune disease, triggered by oxidative stress. In melanocytes, the progressive accumulation of reactive oxygen species (ROS) causes DNA damage, lipid and protein peroxidation.
Many are the altered proteins, which show a partial or complete loss of their functionality. In particular, tyrosinase is found to be inhibited by high concentrations of hydrogen peroxide. Keratinocytes are also significantly altered by oxidative stress, leading to a deficiency of their trophic support for melanocytes.
