HLA-A2 Phenotype may be Protective Against Graves' Disease but not Against Hashimoto's Thyroiditis in Caucasians

被引:19
作者
Bernecker, C. [1 ]
Ostapczuk, M. [2 ]
Vordenbaeumen, S. [1 ]
Ehlers, M. [1 ]
Thiel, A. [1 ]
Schinner, S. [1 ]
Willenberg, H. [1 ]
Scherbaum, W. A. [1 ]
Schott, M. [1 ]
机构
[1] Univ Hosp Duesseldorf, Div Endocrinol Diabet & Rheumatol, D-40225 Dusseldorf, Germany
[2] Univ Dusseldorf, Inst Expt Psychol, D-40225 Dusseldorf, Germany
关键词
autoimmune thyroiditis; Graves' disease; Hashimoto's thyroiditis; major histocompatibility complex (MHC); autoimmunity; thyroid epidemiology; CLASS-II ALLELES; JAPANESE PATIENTS; TSH-RECEPTOR; ASSOCIATION; GENE; SUSCEPTIBILITY; ANTIBODIES; RELEVANCE; THYROGLOBULIN; EPIDEMIOLOGY;
D O I
10.1055/s-0032-1323704
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Graves' disease (GD) and Hashimoto's thyroiditis (HT) are the most common autoimmune thyroid diseases (AITDs) affecting up to 5 % of the general population. In Caucasians HT has a prevalence of up to 4.60 % and GD a prevalence of 1-2 %. The aim of this study was to investigate the association between HLA-A2 and the AITDs GD and HT among Caucasians. HLA alleles of 33 patients with GD and 75 patients with HT were determined by serological typing. The frequency of HLA A2 was significantly reduced in GD (p = 0.033) but not in HT (p = n.s.) as compared to control samples. In individuals positive for HLA-A2 odds ratio for protection from GD was found to be 2.8. This study supports the hypothesis that genetic predisposition to GD is not restricted to MHC class II molecules. The significant negative association between HLA A2 and GD supports the hypothesis that MHC class I genes may be relevant for the protection from GD. In contrast the nonsignificant results for HT indicate that this association may not apply to AITDs in general.
引用
收藏
页码:74 / 77
页数:4
相关论文
共 42 条
[21]   Thyroid Function in Japanese Adults as Assessed by a General Health Checkup System in Relation with Thyroid-Related Antibodies and Other Clinical Parameters [J].
Kasagi, Kanji ;
Takahashi, Norihiro ;
Inoue, Gen ;
Honda, Toyohiko ;
Kawachi, Yasunori ;
Izumi, Yoichiro .
THYROID, 2009, 19 (09) :937-944
[22]   HLA CLASS-II ALLELES IN JAPANESE PATIENTS WITH GRAVES-DISEASE - WEAK ASSOCIATIONS OF HLA-DR AND HLA-DQ [J].
KATSUREN, E ;
AWATA, T ;
MATSUMOTO, C ;
YAMAMOTO, K .
ENDOCRINE JOURNAL, 1994, 41 (06) :599-603
[23]   HLA-BW35 AND B5 IN JAPANESE PATIENTS WITH GRAVES-DISEASE [J].
KAWA, A ;
NAKAMURA, S ;
NAKAZAWA, M ;
SAKAGUCHI, S ;
KAWABATA, T ;
MAEDA, Y ;
KANEHISA, T .
ACTA ENDOCRINOLOGICA, 1977, 86 (04) :754-757
[24]   GENETIC-FACTORS IN AUTOIMMUNE THYROID-DISEASE ANALYZED BY RESTRICTION-FRAGMENT-LENGTH-POLYMORPHISMS OF CANDIDATE GENES [J].
MANGKLABRUKS, A ;
COX, N ;
DEGROOT, LJ .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1991, 73 (02) :236-244
[25]   Two HLA DRB 1 alleles confer independent genetic susceptibility to Graves disease: Relevance of cross-population studies [J].
Marga, M ;
Denisova, A ;
Sochnev, A ;
Pirags, V ;
Farid, NR .
AMERICAN JOURNAL OF MEDICAL GENETICS, 2001, 102 (02) :188-191
[26]   Human leukocyte antigens associated with hyperthyroid Graves ophthalmopathy in Japanese patients [J].
Ohtsuka, K ;
Nakamura, Y .
AMERICAN JOURNAL OF OPHTHALMOLOGY, 1998, 126 (06) :805-810
[27]   ASSOCIATION OF HLA-DPB1-ASTERISK-0501 WITH EARLY-ONSET GRAVES-DISEASE IN JAPANESE [J].
ONUMA, H ;
OTA, M ;
SUGENOYA, A ;
INOKO, H .
HUMAN IMMUNOLOGY, 1994, 39 (03) :195-201
[28]   Current concepts: Thyroiditis [J].
Pearce, EN ;
Farwell, AP ;
Braverman, LE .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (26) :2646-2655
[29]   Association of DRB1*04-DQB1*0301 haplotype and lack of association of two polymorphic sites at CTLA-4 gene with hashimoto's thyroiditis in an Italian population [J].
Petrone, A ;
Giorgi, G ;
Mesturino, CA ;
Capizzi, M ;
Cascino, I ;
Nistico, L ;
Osborn, J ;
Di Mario, U ;
Buzzetti, R .
THYROID, 2001, 11 (02) :171-175
[30]   The environment and autoimmune thyroid diseases [J].
Prummel, MF ;
Strieder, T ;
Wiersinga, WM .
EUROPEAN JOURNAL OF ENDOCRINOLOGY, 2004, 150 (05) :605-618