title: Autoantibodies against tyrosine hydroxylase in patients with non-segmental (generalised) vitiligo.
abstract: Vitiligo is an acquired idiopathic hypomelanotic skin disorder characterised by depigmented macules because of loss of cutaneous melanocytes. Although the exact cause of vitiligo remains obscure, evidence suggests that autoimmunity plays a role in the pathogenesis of the disease. Previously, tyrosine hydroxylase (TH) was identified as a putative autoantigen in vitiligo using phage-display technology. In this study, the prevalence of TH antibodies in patients with vitiligo was investigated. A radioimmunoassay (RIA) was used to detect TH antibodies in sera from patients with either non-segmental vitiligo (n=79), segmental vitiligo (n=8) or other autoimmune diseases without concomitant vitiligo (n=91). Sera from healthy individuals (n=28) were also tested. Patients with segmental vitiligo, healthy controls and patients with other autoimmune diseases without concomitant vitiligo were all negative for TH antibody reactivity. Of 79 patients with non-segmental vitiligo, 18 (23%) were positive for TH antibodies in the RIA, and a significant increase in the prevalence of TH antibodies in patients with non-segmental vitiligo was evident when compared with controls (P=0.003). TH antibody prevalence was also significantly elevated in patients with active vitiligo compared to those with stable disease (P=0.009). Overall, the results indicate that TH is an antibody target in non-segmental but not in segmental vitiligo and that TH antibodies appear to be more frequent in patients with active vitiligo.
authors.affiliation: Department of Human Metabolism, School of Medicine, University of Sheffield, Sheffield, UK. e.h.kemp@sheffield.ac.uk
authors.forename: E Helen
authors.initials: EH
authors.lastname: Kemp
authors.forename: Sherif
authors.initials: S
authors.lastname: Emhemad
authors.forename: Samia
authors.initials: S
authors.lastname: Akhtar
authors.forename: Philip F
authors.initials: PF
authors.lastname: Watson
authors.forename: David J
authors.initials: DJ
authors.lastname: Gawkrodger
authors.forename: Anthony P
authors.initials: AP
authors.lastname: Weetman
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D001324:Autoantigens / Q000235:genetics; D001483:Base Sequence; D016022:Case-Control Studies; D002648:Child; D017931:DNA Primers / Q000235:genetics; D005260:Female; D057809:HEK293 Cells; D006801:Humans; D008297:Male; D008875:Middle Aged; D014442:Monophenol Monooxygenase / Q000276:immunology; D011863:Radioimmunoassay; D017481:Receptors, Somatostatin / Q000276:immunology; D011994:Recombinant Proteins / Q000235:genetics / Q000276:immunology; D014446:Tyrosine 3-Monooxygenase / Q000235:genetics / Q000276:immunology*; D014820:Vitiligo / Q000201:enzymology* / Q000276:immunology* / Q000473:pathology; D055815:Young Adult
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D017931:DNA Primers; C103263:MCHR1 protein, human; D017481:Receptors, Somatostatin; D011994:Recombinant Proteins; D014446:Tyrosine 3-Monooxygenase; D014442:Monophenol Monooxygenase