Vitiligo in Graves' Disease

A single-nucleotide polymorphism in the gene encoding lymphoid protein tyrosine phosphatase (PTPN22) confers susceptibility to generalised vitiligo

“…The frequent association of vitiligo with autoimmune disorders and the demonstration of autoantibodies to melanosomal proteins in the serum of patients with the disease support this theory. [2][3][4][5][6] In addition, autoreactive CTLs, which specifically recognise melanocyte differentiation antigens, have been detected in both the peripheral blood and perilesional skin of individuals with vitiligo. [7][8][9] Melanocyte-specific CTLs have also been identified in patients with melanoma where vitiligo has occurred during immunotherapy and the adoptive transfer of melanoma antigen-specific CTLs may be associated with the regression of melanoma metastases and the appearance of vitiligo.…”

“…1 Support for this theory arises from the frequent association of vitiligo with autoimmune disorders and the demonstration of autoantibodies to melanosomal proteins in the serum of patients with the disease. [2][3][4][5][6] More recently, autoreactive cytotoxic T lymphocytes (CTLs), which specifically recognise melanocyte differentiation antigens, have been detected in both the peripheral blood and perilesional skin of individuals with vitiligo. [7][8][9] Furthermore, several genes that have a role in regulating immunity have been associated with susceptibility to vitiligo including: polymorphic markers in the cytotoxic T lymphocyte antigen-4 (CTLA-4) gene, the autoimmune susceptibility loci AIS1, AIS2, AIS3 and SLEV1 and certain human leukocyte antigen specificities of the major histocompatibility complex.…”

Treatment of Vitiligo with Oral Corticosteroids

“…There is evidence suggesting that vitiligo is an autoimmune disease: (1) high frequency of the association with other autoimmune diseases, such as thyroid diseases, pernicious anemia and diabetes mellitus [1,4,5,9,15]; (2) high incidence of various autoantibodies in sera [2][3][4]; (3) the presence of antimelanin antibodies in the sera [14].…”

Treatment of vitiligo with a chimeric monoclonal antibody to CD20: a pilot study

“…Antibodies to several antigens in melanocytes are present in the serum of the vast majority of patients, and recent findings reported by ourselves indicate that such antibodies might play a crucial physiopathological role by triggering apoptosis of melanocytes [19]. Although vitiligo is not, in itself, a life-threatening disease, the cosmetic, social, psychological and emotional consequences of this common condition prompt for a reasonable and reliable treatment; so far, immunosuppressant therapy has proved useful not only to delay the disease progression, but to recover pigmentation to a certain extent [5][6][7][8][9][10][11][12][13][14][15][16]. Rituximab, sold under the trade names Rituxan® and MabThera®, is a chimeric (murine/ human) monoclonal antibody against the human CD20 protein, which is expressed primarily on the surface of B cells.…”

“…Although several theories have been forwarded to explain the cause of vitiligo, the autoimmune origin of the disease is the most plausible [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. Antibodies to several antigens in melanocytes are present in the serum of the vast majority of patients, and recent findings reported by ourselves indicate that such antibodies might play a crucial physiopathological role by triggering apoptosis of melanocytes [19].…”