Immunogenetics of Graves’ Ophthalmopathy

Weetman, Anthony P.; So, Alex; Warner, Catherine A.; Foroni, Letizia; Fells, P; Shine, Brian

doi:10.1111/j.1365-2265.1988.tb00236.x

Cited by 15 publications

(16 citation statements)

References 29 publications

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“…Similar data have been reported for DR3 [16,68,84], while other studies have denied such associations [2]. Some authors report a positive association with DR3 or B8 DR7 [54] and with blood group P and a negative association with B17 [39]; others, report no association [105]. Some authors report a positive association with DR3 or B8 DR7 [54] and with blood group P and a negative association with B17 [39]; others, report no association [105].…”

Section: Disease Heterogeneitysupporting

confidence: 64%

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Genetics of autoimmune endocrine diseases

Bach

Caillat‐Zucman

1993

Springer Semin Immunopathol

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Section: Disease Heterogeneitysupporting

confidence: 64%

“…Such polymorphism has been studied in both GD and IDDM with contradictory results. Conversely, other authors have not confirmed these findings either in GD [105] or IDDM [22,44,88]. These associations appear to be HLA dependent.…”

Section: V D and C Tcr Genesmentioning

confidence: 76%

Genetics of autoimmune endocrine diseases

Bach

Caillat‐Zucman

1993

Springer Semin Immunopathol

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“…Balazs et al (39) observed that 36 of 38 Hungarian patients with Graves' ophthalmopathy were smokers, whereas only 10 of 45 patients without ocular manifestations smoked. In disagreement with others (40,41), these authors also observed a strong association between eye disease and HLA-DR3 and/or B8 (39). Tellez et al (42) reported that cigarette smoking produced a risk for developing ophthalmo¬ pathy that was 2.4 times higher than that observed in patients who never smoked.…”

Section: Thyroid Autoimmune Diseasementioning

confidence: 69%

Cigarette smoking and the thyroid

Bartalena

Bogazzi

Tanda

et al. 1995

European Journal of Endocrinology

107

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The effects of smoking on the function of endocrine glands have been investigated extensively but still are to be elucidated fully. It is widely recognized that the most important component of the smoke produced from the burning of tobacco, in terms of endocrine effects, is nicotine. Nicotine acts through the interaction with acetylcholine receptors, but it seems likely that others among the numerous smoke products may somehow influence endocrine homeostasis.The present paper will focus on the relationship between smoking and variations in thyroid economy or the occurrence of thyroid dysfunction. Thyroid functionSeveral studies have been carried out to ascertain whether smoking is associated with variations in thyroid economy. The rationale for these investigations was dictated by the observation that smoking is associated with a decrease in body mass, and, conversely, refrain from smoking is often accompanied by an increase in body mass (1). These changes might be mediated by variations in appetite and food intake but might also be linked to smoking-induced alterations in thyroid function. Melander et al. reported that cessation of smoking was associated with a small decrease in serum T4, reverse T3 (rT3) and a small increase in serum TSH levels, while serum T3 concentration was not altered significantly (2). These data were interpreted as being suggestive of the fact that cigarette smoking might stimulate thyroid function, which would be readjusted following smoking with¬ drawal. The fact that serum T3 levels were unchanged was interpreted as indicative of a selective stimulation of T4 secretion or, alternatively, of an increased T3 clearance caused by smoking.Results obtained in subsequent studies are far from unequivocal, because T3 has been reported to be increased (3-5), unchanged (6-8) or slightly decreased (9, 10). Likewise, serum T4 has been found to be increased (6), normal (3-5, 7) or decreased (9, 10). Serum TSH concentrations in most cases were unchanged (3-5, 8) but also decreased values have been found (6, 7, 10). Interestingly, Sepkovic et al. observed that changes in T3, T4 and TSH concentra¬ tions were more pronounced in heavy smokers than in light-to-moderate smokers, while plasma thiocyanate levels progressively increased with the degree of smoking, implying a relationship between the increased absorption of cigarette smoke thiocyanate and the changes occurring in thyroid economy (9). The conflicting results in the different series are not readily explainable. Several factors may have affected the results, including enrolment of heavy vs moderate smokers, the evaluation of short-term vs long-term effects and differences in age and body mass. In addition, differences might be related to the relative contribution of opposite mechanisms. If sympathetic nervous stimulation is prevailing, this might lead to stimulation of thyroid hormone secretion (11) and, in turn, to a decreased TSH release. On the other hand, the presence of substances in cigarette smoke that stimulate drug metabolism (12) might...

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“…Some papers have confirmed an association between HLADRB1*03 and GO [48]–[49]. However, other authors have not found differences in the distribution of the HLADRB1*03 allele in GD patients with or without GO [10], [27], [50]–[51]. There is no sufficient evidence to support a correlation between the C(1858)T polymorphism in the PTPN22 gene and GO [29], [42].…”

Section: Discussionmentioning

confidence: 99%

Association between Polymorphisms in the TSHR Gene and Graves' Orbitopathy

et al. 2014

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BackgroundGraves' orbitopathy (GO) as well as Graves' disease (GD) hyperthyroidism originate from an autoimmune reaction against the common auto-antigen, thyroid-stimulating hormone receptor (TSHR). GO phenotype is associated with environmental risk factors, mainly nicotinism, as well as genetic risk factors which initiate an immunologic reaction. In some patients GO is observed before diagnosis of GD hyperthyroidism, while it can also be observed far after diagnosis. The intensity of GO symptoms varies greatly in these patients. Thus, the pathogenesis of GD and GO may correlate with different genetic backgrounds, which has been confirmed by studies of correlations between GO and polymorphisms in cytokines involved in orbit inflammation. The aim of our analysis was to assess genetic predisposition to GO in young patients (age of diagnosis ≤30 years of age), for whom environmental effects had less time to influence outcomes than in adults.Methods768 GD patients were included in the study. 359 of them had clinically evident orbitopathy (NOSPECS ≥2). Patients were stratified by age at diagnosis. Association analyses were performed for genes with a known influence on development of GD - TSHR, HLA-DRB1, cytotoxic T-lymphocyte antigen 4 (CTLA4) and lymphoid protein tyrosine phosphatase (PTPN22).ResultsThe rs179247 TSHR polymorphism was associated with GO in young patients only. In young GO-free patients, allele A was statistically more frequent and homozygous carriers had a considerable lower risk of disease incidence than patients with AG or GG genotypes. Those differences were not found in either elderly patients or the group analyzed as a whole.ConclusionsAllele A of the rs179247 polymorphism in the TSHR gene is associated with lower risk of GO in young GD patients.

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Immunogenetics of Graves’ Ophthalmopathy

Cited by 15 publications

References 29 publications

Genetics of autoimmune endocrine diseases

Genetics of autoimmune endocrine diseases

Cigarette smoking and the thyroid

Association between Polymorphisms in the TSHR Gene and Graves' Orbitopathy

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