title: A study of the association between a polymorphism in the CTLA-4 gene and postpartum thyroiditis.
abstract: OBJECTIVE
  Postpartum thyroiditis (PPT) is an autoimmune thyroid disease which shares immunological and clinical features with autoimmune hypothyroidism and Graves' disease, and is believed to be caused by a combination of genetic and environmental factors. Recently, an association has been described between Graves' disease or autoimmune hypothyroidism and a polymorphism in the CTLA-4 gene, which encodes a T cell receptor for the B7 family of ligands, and we wished to test whether a similar association exists with PPT.
  
  
  METHODS
  A population-based case-control study of a CTLA-4 gene microsatellite polymorphism was performed, to look for an association with PPT.
  
  
  METHODS
  Caucasoid women (n = 122) were studied; 58 had thyroid antibodies (against thyroglobulin or thyroid peroxidase) alone during the postpartum period (PPT-) and 64 had thyroid antibodies and some form of postpartum thyroid dysfunction (PPT+).
  
  
  RESULTS
  There was no significant difference between this whole group of women and 161 local Caucasoid thyroid antibody-negative women for the CTLA-4106 base pair (AT)n microsatellite polymorphism (relative risk = 1.3; P = 0.3), nor did the PPT+ group differ from controls when analysed separately (P = 0.2). When the postpartum women were subdivided in groups according to clinical pattern of PPT and the type of thyroid antibodies, there were no associations within the subgroups.
  
  
  CONCLUSIONS
  No significant association exists between postpartum thyroiditis and a polymorphism in the CTLA-4 gene. Furthermore, a natural variation in the prevalence of the polymorphism in healthy UK populations underscores the need to select appropriately matched normal subjects in future case-control studies.
authors.affiliation: Department of Medicine, University of Sheffield Clinical Sciences Centre, Northern General Hospital, UK.
authors.forename: E A
authors.initials: EA
authors.lastname: Waterman
authors.forename: P F
authors.initials: PF
authors.lastname: Watson
authors.forename: J H
authors.initials: JH
authors.lastname: Lazarus
authors.forename: A B
authors.initials: AB
authors.lastname: Parkes
authors.forename: C
authors.initials: C
authors.lastname: Darke
authors.forename: A P
authors.initials: AP
authors.lastname: Weetman
mesh_terms: D000069594:Abatacept; D000328:Adult; D000906:Antibodies / Q000097:blood; D015703:Antigens, CD; D000943:Antigens, Differentiation / Q000235:genetics*; D060908:CTLA-4 Antigen; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D005260:Female; D006801:Humans; D018796:Immunoconjugates; D007453:Iodide Peroxidase / Q000276:immunology; D008297:Male; D018895:Microsatellite Repeats / Q000235:genetics; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011247:Pregnancy; D011644:Puerperal Disorders / Q000235:genetics* / Q000276:immunology; D012306:Risk; D013954:Thyroglobulin / Q000276:immunology; D013967:Thyroiditis, Autoimmune / Q000235:genetics* / Q000276:immunology
chemical_list: D000906:Antibodies; D015703:Antigens, CD; D000943:Antigens, Differentiation; D060908:CTLA-4 Antigen; C556706:CTLA4 protein, human; D018796:Immunoconjugates; D000069594:Abatacept; D013954:Thyroglobulin; D007453:Iodide Peroxidase