Analysis of diabetes-associated autoantibodies in children and adolescents with autoimmune thyroid diseases

2019 ◽  
Vol 32 (4) ◽  
pp. 355-361 ◽  
Author(s):  
Marta Rydzewska ◽  
Justyna Michalak ◽  
Anna Bossowska ◽  
Shu Chen ◽  
Sarah Black ◽  
...  

Abstract Background Zinc transporter 8 autoantibodies (ZnT8Abs) together with glutamic acid decarboxylase autoantibodies (GADAbs), insulinoma antigen 2 autoantibodies (IA-2Abs) and insulin autoantibodies (IAbs) are markers of type 1 diabetes mellitus (T1DM). We studied the prevalence of ZnT8Ab in children with autoimmune thyroid diseases (AITDs) to assess the association of AITDs and T1DM at the serological level. Methods The study groups consisted of 44 children with Graves’ disease (GD), 65 children with Hashimoto’s thyroiditis (HT), 199 children with T1DM with or without AITDs and 58 control children. ZnT8Ab, GADAb, IA-2Ab, IAb, 21-hydroxylase autoantibodies (21-OHAbs) and acetylcholine receptor autoantibodies (AChRAbs) were measured. Results ZnT8Abs were found in 4/44 (9.1%) patients with GD, and 4/44 (9.1%) patients with GD were positive for GADAb. Of the 65 HT patients, six (9.2%) were positive for ZnT8Ab, while four (6.2%) were positive for GADAb. In the T1DM group, 128/199 (64%) of the patients were positive for ZnT8Ab, 133/199 (67%) for GADAb and 109/199 (55%) for IA-2Ab. One GD patient and one HT patient were positive for all the four diabetes-associated autoantibodies. Two HT patients were positive for three diabetes autoantibodies. Two GD (4.5%) and five HT (7.7%) patients were positive for 21-OHAb only. None of the patients had AChRAb. In the control group, 2/58 (3.4%) were positive for GADAb and 2/58 (3.4%) were positive for ZnT8Ab. Conclusions Diabetes-associated autoantibodies including ZnT8Ab were found in children and adolescents with GD and HT.

2014 ◽  
Author(s):  
Artur Bossowski ◽  
Hanna Borysewicz-Sanczyk ◽  
Natalia Wawrusiewicz-Kurylonek ◽  
Mieczyslaw Szalecki ◽  
Beata Wikiera ◽  
...  

2018 ◽  
Vol 45 (5) ◽  
pp. 1787-1796 ◽  
Author(s):  
Ling Li ◽  
Xiaolian Ding ◽  
Xuan Wang ◽  
Qiuming Yao ◽  
Xiaoqing Shao ◽  
...  

Background/Aims: The IKZF3 gene encodes a zinc-finger protein that plays an important role in the proliferation and differentiation of B lymphocytes. Autoimmune thyroid diseases (AITDs), mainly include Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), are probably caused by the aberrant proliferation of B cells. The objective of this study was to explore the association between IKZF3 polymorphisms and AITDs. Methods: We examined 915 AITD patients (604 GD and 311 HT) and 814 healthy controls. IKZF3 variants (rs2941522, rs907091, rs1453559, rs12150079 and rs2872507) were tested by PCR-ligase detection reaction. Results: It was manifested that that the minor alleles of the five loci increased susceptibility to GD (p<0.05 for rs2941522, and p<0.01 for rs907091, rs1453559, rs12150079 and rs2872507) but in HT patients, these loci showed no significant difference compared with controls. Similarly, the genotype distributions of GD patients manifested obvious differences in all these loci compared with the control group, whereas no statistical differences were observed between HT patients and controls. Furthermore, bioinformatics tools were used to analyze rs1453559, rs12150079 and rs907091. These variants were believed to be the transcription regulator. Conclusion: It is the first time we reported the association between the IKZF3 polymorphisms and GD, indicating that IKZF3 gene tends to bean important risk factor for the development of GD.


2016 ◽  
Vol 40 (1-2) ◽  
pp. 245-252 ◽  
Author(s):  
Cui Li ◽  
Jianghong Yuan ◽  
Yuan-feng Zhu ◽  
Xiang-ju Yang ◽  
Qiong Wang ◽  
...  

Aims: To clarify the imbalance of Th17/Treg in different subtypes of autoimmune thyroid diseases (AITDs) including Graves' disease(GD), Hashimoto's thyroiditis(HT) and Graves' ophthalmopathy (GO). Methods: 47 patients with AITD (including 16 GD, 15 HT, and 16 GO) and 12 healthy controls were enrolled in this study. The percentages of Th17 and Treg cells, the ratio of Th17/Treg, as well as their related transcription factors RORγt and Foxp3 mRNA in peripheral blood mononuclear cells (PBMCs) were measured by flow cytometry and real-time quantitative PCR Results: Compared with those in control group, the percentage of CD4+IL-17+T cell(Th17) and the mRNA expression of its transcription factor RORγt were higher in PBMCs of AITDs (P<0.05), particularly in HT subgroup (P<0.01). The percentage of CD4+Foxp3+T (Treg) cells and its transcription factor Foxp3 mRNA were significantly decreased in PBMCs of GD (P<0.05). In addition, the ratio of Th17/Treg was elevated in AITD group and GO subgroup (P<0.01). In GO subgroup, the patients with clinical activity score (CAS) above 4.5 had higher percentages of Th17 than those with CAS ranging from 3 to 4.5 (P<0.05). Conclusion: Increased Th17 lymphocytes may play a more important role in the pathogenesis of HT and GO while decreased Treg may be greatly involved in GD.


2018 ◽  
Vol 47 (5) ◽  
pp. 534-542 ◽  
Author(s):  
Naoya Inoue ◽  
Mikio Watanabe ◽  
Yuka Katsumata ◽  
Naoko Ishido ◽  
Yoh Hidaka ◽  
...  

2011 ◽  
Vol 14 (2) ◽  
pp. 23-31 ◽  
Author(s):  
Ekaterina Alexandrovna Repina

This review generalizes current data on the genes responsible for combined susceptibility to type 1 diabetes and autoimmune thyroid diseases. Analysisof the role of common genetic markers facilitates understanding their contribution to the development of each of the two or several concomitantautoimmune diseases affecting a single patient


2019 ◽  
Vol 92 (1) ◽  
pp. 52-55 ◽  
Author(s):  
Valeria Calcaterra ◽  
Corrado Regalbuto ◽  
Giulia Dobbiani ◽  
Chiara Montalbano ◽  
Federica Vinci ◽  
...  

2020 ◽  
Vol 8 ◽  
Author(s):  
Hanna Borysewicz-Sańczyk ◽  
Beata Sawicka ◽  
Natalia Wawrusiewicz-Kurylonek ◽  
Barbara Głowińska-Olszewska ◽  
Anna Kadłubiska ◽  
...  

2014 ◽  
Vol 60 (3) ◽  
pp. 43-52 ◽  
Author(s):  
A A Larina ◽  
E A Troshina ◽  
O N Ivanova

At present, four main types of autoimmune polyglandular syndromes (APS) are distinguished. Type 1 APS is associated with candidiasis, primary hypoparathyroidism, and primary adrenal insufficiency developing in the childhood as a result of mutations in the AIRE gene. Type 2 APS involves primary adrenal insufficiency in combination with autoimmune thyroid diseases and/or type 1 diabetes mellitus. Type 3 APS is characterized by the combination of autoimmune thyroid diseases with other endocrine and non-endocrine autoimmune pathologies in the absence of adrenal cortical dysfunction and hypoparathyriodism. Type 4 APS is presented by the combinations of autoimmune diseases other than the aforementioned ones. The above syndromes usually manifest themselves at the age between 20 and 60 years; they are of the polygenic type and associated with the genetic markers, such as HLAII-complex haplotypes, CTLA-4, PTPN22, FOXP3 genes, etc. In addition, the latent forms of APS have been described that occur in the populations much more frequently than the manifest disorders. These latent diseases can exert strong influence on the compensation and risk of complications of the underlying pathology. Of great importance in this context is the timely identification of the groups of patients at risk of developing clinical forms of APS among the subjects presenting with a single endocrine pathology.


Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2316
Author(s):  
Moschoula Passali ◽  
Knud Josefsen ◽  
Jette Lautrup Frederiksen ◽  
Julie Christine Antvorskov

In this review, we summarize the clinical data addressing a potential role for gluten in multiple sclerosis (MS), psoriasis, type 1 diabetes (T1D) and autoimmune thyroid diseases (ATDs). Furthermore, data on the prevalence of celiac disease (CD) and gluten-related antibodies in the above patient groups are presented. Adequately powered and properly controlled intervention trials investigating the effects of a gluten-free diet (GFD) in non-celiac patients with MS, psoriasis, T1D or ATDs are lacking. Only one clinical trial has studied the effects of a GFD among patients with MS. The trial found significant results, but it is subject to major methodological limitations. A few publications have found beneficial effects of a GFD in a subgroup of patients with psoriasis that were seropositive for anti-gliadin or deamidated gliadin antibodies, but no effects were seen among seronegative patients. Studies on the role of gluten in T1D are contradictive, however, it seems likely that a GFD may contribute to normalizing metabolic control without affecting levels of islet autoantibodies. Lastly, the effects of a GFD in non-celiac patients with ATDs have not been studied yet, but some publications report that thyroid-related antibodies respond to a GFD in patients with concomitant CD and ATDs. Overall, there is currently not enough evidence to recommend a GFD to non-celiac patients with MS, psoriasis, ATDs or T1D.


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