scholarly journals Frequency of Autoimmune thyroid disease and its relation with age and gender

2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Muhammad Jawad
2020 ◽  
Author(s):  
Weiwei He ◽  
Jing Zhao ◽  
Xuerong Liu ◽  
Sheli Li ◽  
Kaida Mu ◽  
...  

Abstract Background/AimsRecent researches suggest that the CD160/HVEM/LIGHT/BTLA signaling pathway may contribute to the pathogeneses of autoimmune diseases, but the relationship between CD160 polymorphisms and autoimmune thyroid disease (AITD) has not been reported yet. This study aimed to evaluate the associations between CD160 polymorphisms and AITD.MethodsA total of 1017 patients with AITD (634 Graves' disease and 383 Hashimoto's thyroiditis) and 856 unrelated healthy controls were recruited into our study. Odds ratios (ORs) with 95% confidence interval (95%CI) were calculated through logistic regression analyses. The CD160 SNPs were detected using Hi-SNP high-throughput genotyping. ResultsThere was a statistically significant difference between Graves' disease patients and the control group with respect to both the genotype distribution (P=0.014) and allele frequency of rs744877 (P=0.034). A significant association of CD160 rs744877 with AITD was observed before adjusted age and gender under a dominant model (OR= 0.79, 95%CI 0.66-0.95; P= 0.013) and an additive model (OR= 0.77, 95%CI 0.64-0.94, P=0.008), and was also observed after adjusted age and gender under a dominant model (OR= 0.78, 95%CI 0.65-0.95; P= 0.011) and an additive model (OR= 0.76, 95%CI 0.63-0.93, P=0.007). A significant association of rs744877 with Graves' disease was observed under an allele model (OR= 0.84, 95%CI 0.71-0.98, P=0.027), a dominant model (OR= 0.74, 95%CI 0.60-0.91; P= 0.005), and an additive model (OR= 0.72, 95%CI 0.58-0.90, P=0.004). Multivariate logistic regression analyses suggested that the association remained significant after adjustment for age and gender. However, rs744877 was not related to Hashimoto's thyroiditis. Furthermore, CD160 rs3766526 was not significantly related to either Graves' disease or Hashimoto's thyroiditis.ConclusionThis is the first identification of the association of CD160 rs744877 with Graves' disease. Our findings add new data to the genetic contribution to Graves' disease susceptibility and support the crucial role of the CD160/HVEM/LIGHT/BTLA pathway in the pathogenesis of Graves' disease.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Weiwei He ◽  
Jing Zhao ◽  
Xuerong Liu ◽  
Sheli Li ◽  
Kaida Mu ◽  
...  

Abstract Background Recent researches suggest that the CD160/HVEM/LIGHT/BTLA signaling pathway may contribute to the pathogeneses of autoimmune diseases, but the relationship between CD160 polymorphisms and autoimmune thyroid disease (AITD) has not been reported yet. This study aimed to evaluate the associations between CD160 polymorphisms and AITD. Methods A total of 1017 patients with AITD (634 Graves’ disease and 383 Hashimoto’s thyroiditis) and 856 unrelated healthy controls were recruited into our study. Odds ratios (ORs) with 95% confidence interval (95%CI) were calculated through logistic regression analyses. The CD160 SNPs were detected using Hi-SNP high-throughput genotyping. Results There was a statistically significant difference between Graves’ disease patients and the control group with respect to both the genotype distribution (P = 0.014) and allele frequency of rs744877 (P = 0.034). A significant association of CD160 rs744877 with AITD was observed before adjusted age and gender under a dominant model (OR = 0.79, 95%CI 0.66–0.95; P = 0.013) and an additive model (OR = 0.77, 95%CI 0.64–0.94, P = 0.008), and was also observed after adjusted age and gender under a dominant model (OR = 0.78, 95%CI 0.65–0.95; P = 0.011) and an additive model (OR = 0.76, 95%CI 0.63–0.93, P = 0.007). A significant association of rs744877 with Graves’ disease was observed under an allele model (OR = 0.84, 95%CI 0.71–0.98, P = 0.027), a dominant model (OR = 0.74, 95%CI 0.60–0.91; P = 0.005), and an additive model (OR = 0.72, 95%CI 0.58–0.90, P = 0.004). Multivariate logistic regression analyses suggested that the association remained significant after adjustment for age and gender. However, rs744877 was not related to Hashimoto’s thyroiditis. Furthermore, CD160 rs3766526 was not significantly related to either Graves’ disease or Hashimoto’s thyroiditis. Conclusion This is the first identification of the association of CD160 rs744877 with Graves’ disease. Our findings add new data to the genetic contribution to Graves’ disease susceptibility and support the crucial role of the CD160/HVEM/LIGHT/BTLA pathway in the pathogenesis of Graves’ disease.


2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Hussam H. Alhawari ◽  
Yousef S. Khader ◽  
Hussein H. Alhawari ◽  
Amal F. Alomari ◽  
Hiba N. Abbasi ◽  
...  

Purpose.The association between autoimmune diseases and keratoconus (KC) has been proposed based on previous retrospective studies and case reports. The aim of our study is to investigate whether KC is associated with autoimmune thyroid disease. Methods.A comparative study was conducted on 131 adult subjects from September 2015 to May 2017 at Jordan University Hospital, Amman, Jordan. Subjects were classified into 2 groups: subjects with autoimmune thyroid disease, including Graves’ disease and Hashimoto’s thyroiditis (n=68), and a healthy group for comparison (n=63). Subjects with any other conditions known to be associated with KC were excluded. The diagnosis of KC was based on clinical and corneal topographic findings utilizing the Oculus-Pentacam machine. In addition, TSH and total T4 levels as well as thyroid peroxidase antibodies were measured in all study participants. Antithyroglobulin antibodies, thyroid stimulating immunoglobulin, thyroid ultrasound, and thyroid uptake and scan were also selectively performed in some participants.Results.This study included a total of 131 participants (101 females and 30 males), including patients and controls. In the multivariate analysis, autoimmune disease was not significantly associated with keratoconus (OR = 1.1; 95% confidence interval: 0.3, 3.8;pvalue = 0.353) after adjusting for age and gender.Conclusion.This study did not show a statistically significant association between autoimmune thyroid disease and KC.


Praxis ◽  
2002 ◽  
Vol 91 (27) ◽  
pp. 1151-1160
Author(s):  
Fajfr ◽  
Müller

Les maladies thyroïdiennes auto-immunes ou immunes (autoimmune thyroid disease, AITD) sont relativement fréquentes. Le terme de AITD comprend les thyréodites euthyroidiennes ou hypothyroïdiennes de Hashimoto avec ou sans goitre, les hyperthyroïdies classiques de Basedow et leurs variantes nettement plus rares euthyroïdiennes ou hypothyroïdiennes. Aucune des nombreuses classifications des AITD n'a pu s'imposer sur le plan international. La pathogénèse de toutes les formes d'AITD comprend une perturbation de la tolérance immune chez les individus prédisposés génétiquement (séquence HLA-DQAI*0501 sur le bras court du chromosome 6) qui provoque un processus auto-immun contre la glande thyroïdienne. Ces processus sont soit destructeurs ou inhibiteurs, soit stimulateurs, ce qui permet d'expliquer les formes très différentes de AITD. Dans de cas rares, ces processus peuvent se contrebalancer («balance hypotheseis»). Les anticorps anti-récepteurs TPO et TSH (TRAK) ont une place particulière dans le diagnostic des AITD. Les dosages de routine utilisent pour la mesure des TRAK des récepteurs qui ne peuvent pas différencier entre les anticorps stimulants ou bloquants contre les récepteurs TSH. C'est, entre autre pour ces raisons, que les résultats d'anticorps positifs ne sont utilisables qu'en connaissance de la clinique et / ou des paramètres de la fonction thyroïdienne. Ce travail présente quatre patients avec des formes plus complexes d'AITD et résume les connaissances actuelles.


Pneumologie ◽  
2012 ◽  
Vol 66 (11) ◽  
Author(s):  
C Ravaglia ◽  
C Gurioli ◽  
M Romagnoli ◽  
G Casoni ◽  
S Tomassetti ◽  
...  

2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
M Meilinger ◽  
N Schweighofer ◽  
A Forjanics ◽  
H Dobnig ◽  
A Fahrleitner-Pammer ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document