BACKGROUND AND OBJECTIVE: Vitiligo is an autoimmune polygenic disorder, characterized by loss of pigmentation due to melanocyte destruction. Multiple genes and environmental triggers are thought to play a role in inducing vitiligo. These genes and environmental factors differ across different populations. In this study, we investigated vitiligo patients in Jordan for patient characteristics and analyzed the association of the 1858C/T (rs2476601, R620W) variant of the PTPN22 gene with vitiligo in our patients. METHODS: Fifty-five patients with generalized vitiligo and 85 matched normal control subjects who did not have vitiligo or any apparent autoimmune disorder were recruited and interviewed for clinical and demographic characteristics. DNA samples were obtained from patients and controls and genotyped by restriction fragment length polymorphism for the 1858C/T variant. Fifty-three percent of our patients (29 of 55 overall) were female, the average age at onset was 19.2 years, 84.3% of patients (43 of 51 reported) had changing size of depigmented patches, 3.8% (2 of 53 reported) had other autoimmune disease, and 19.2% (5 of 26 reported) had a family history of vitiligo. RESULTS: The allelic frequency of 1858T (620W) was 1.9% in patients as opposed to 2.9% in controls (p = 0.5). No PTPN22 1858 TT homozygotes were observed among patients or controls; 3.8% of vitiligo patients were 1858 CT heterozygotes compared with 5.9% of controls (p = 0.7). Consequently, no significant association was observed between the 1858C/T functional variant and vitiligo patients. CONCLUSION: Although the PTPN22 1858C/T variant has been reported to play a role in increasing the risk of vitiligo in Caucasian patients, it does not appear to play a similar role in the Jordanian population, though a larger cohort of patients might be needed to confirm such a conclusion.
BACKGROUND AND OBJECTIVE:Vitiligo is an autoimmune polygenic disorder, characterized by loss of pigmentation due to melanocyte destruction. Multiple genes and environmental triggers are thought to play a role in inducing vitiligo. These genes and environmental factors differ across different populations. In this study, we investigated vitiligopatients in Jordan for patient characteristics and analyzed the association of the 1858C/T (rs2476601, R620W) variant of the PTPN22 gene with vitiligo in our patients. METHODS: Fifty-five patients with generalized vitiligo and 85 matched normal control subjects who did not have vitiligo or any apparent autoimmune disorder were recruited and interviewed for clinical and demographic characteristics. DNA samples were obtained from patients and controls and genotyped by restriction fragment length polymorphism for the 1858C/T variant. Fifty-three percent of our patients (29 of 55 overall) were female, the average age at onset was 19.2 years, 84.3% of patients (43 of 51 reported) had changing size of depigmented patches, 3.8% (2 of 53 reported) had other autoimmune disease, and 19.2% (5 of 26 reported) had a family history of vitiligo. RESULTS: The allelic frequency of 1858T (620W) was 1.9% in patients as opposed to 2.9% in controls (p = 0.5). No PTPN22 1858 TT homozygotes were observed among patients or controls; 3.8% of vitiligopatients were 1858 CT heterozygotes compared with 5.9% of controls (p = 0.7). Consequently, no significant association was observed between the 1858C/T functional variant and vitiligopatients. CONCLUSION: Although the PTPN221858C/T variant has been reported to play a role in increasing the risk of vitiligo in Caucasian patients, it does not appear to play a similar role in the Jordanian population, though a larger cohort of patients might be needed to confirm such a conclusion.
Authors: Matthew Roycroft; Marta Fichna; David McDonald; Kate Owen; Magdalena Zurawek; Maria Gryczyńska; Danuta Januszkiewicz-Lewandowska; Piotr Fichna; Heather Cordell; Peter Donaldson; Jerzy Nowak; Simon Pearce Journal: Clin Endocrinol (Oxf) Date: 2008-08-15 Impact factor: 3.478
Authors: Adrian F Arechiga; Tania Habib; Yantao He; Xian Zhang; Zhong-Yin Zhang; Andrew Funk; Jane H Buckner Journal: J Immunol Date: 2009-03-15 Impact factor: 5.422
Authors: Lindsey A Criswell; Kirsten A Pfeiffer; Raymond F Lum; Bonnie Gonzales; Jill Novitzke; Marlena Kern; Kathy L Moser; Ann B Begovich; Victoria E H Carlton; Wentian Li; Annette T Lee; Ward Ortmann; Timothy W Behrens; Peter K Gregersen Journal: Am J Hum Genet Date: 2005-02-17 Impact factor: 11.025
Authors: J Wesoly; X Hu; M M Thabet; M Chang; H Uh; C F Allaart; R E M Toes; J J Houwing-Duistermaat; A B Begovich; T W J Huizinga Journal: Rheumatology (Oxford) Date: 2006-11-29 Impact factor: 7.580
Authors: Stanca A Birlea; Greggory S Laberge; Lucia M Procopciuc; Pamela R Fain; Richard A Spritz Journal: Pigment Cell Melanoma Res Date: 2009-01-17 Impact factor: 4.693
Authors: Ann B Begovich; Victoria E H Carlton; Lee A Honigberg; Steven J Schrodi; Anand P Chokkalingam; Heather C Alexander; Kristin G Ardlie; Qiqing Huang; Ashley M Smith; Jill M Spoerke; Marion T Conn; Monica Chang; Sheng-Yung P Chang; Randall K Saiki; Joseph J Catanese; Diane U Leong; Veronica E Garcia; Linda B McAllister; Douglas A Jeffery; Annette T Lee; Franak Batliwalla; Elaine Remmers; Lindsey A Criswell; Michael F Seldin; Daniel L Kastner; Christopher I Amos; John J Sninsky; Peter K Gregersen Journal: Am J Hum Genet Date: 2004-06-18 Impact factor: 11.025