Protein Tyrosine Phosphatase Non-receptor 22 Gene C1858T Polymorphism in Patients with Coexistent Type 2 Diabetes and Hashimoto’s Thyroiditis

Bulut, Funda; Erol, Deniz; Elyas, Halit; Doğan, Halil; Özdemir, Fethi Ahmet; Keskin, Lezan

doi:10.5152/balkanmedj.2014.9418

Cited by 6 publications

(6 citation statements)

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“… 72 – 74 Several studies have also shown that the SNP C1858T (rs2476601), that leads to the substitution of a tryptophan at position 620 of LYP for an arginine (R620W), is linked with both T1DM and AITD. 46 , 73 – 78 However, some contradictory results show that this SNP in PTPN22 is associated with AITD but not with T1DM. 79 Another report indicated that an SNP (rs2476601) in PTPN22 is not associated with AITD.…”

Section: Genetics and Autoimmunitymentioning

confidence: 99%

“…74 Bottini et al (2004);75 Velaga et al (2004);76 Bulut et al (2014);77 Smyth et al (2004);78 Lee et al (2011);79 Alkhateeb et al (2013);80 Liu et al (2015);81 Ikegami et al (2006); 82 El Fotoh et al (2019); 83 Giza et al (2013); 84 Wasniewska et al (2012); 85 Prezioso et al (2017); 86 Burn et al (2011); 87 Blasetti et al (Ban et al (2007); 94 Inoue et al (2010); 95 Villano et al (2009); 96 Li et al (2015); 97 Bossowski et al(2013); 98 Nakano et al (2007); 99 Korn et al (2009); 100 Li et al (2016); 101 Bjornvold et al (2006); 102 Rubio-Cabezas et al (2009); 103 Zavattari et al (2004); 104 Nakanishi and Shima (2007); 105 Brusko et al (2007); 106 Tritt et al (2008); 107 Brode et al (2006); 108 Tian et al (2009); 109 Jaeckel et al (2005); 110 Peng et al (2004); 111 Wu et al (2012); 112 Zheng et al (2009); 113 Johnson et al (2013) 114 Golden et al (2005); 43 Villano et al (2009); 96 Chen et al (2013); 121 Pastuszak-Lewandoska et al (2012); 122 Douroudis et al (2009); 123 Bednarczuk et al (2003); 124 Hou et al (2015); 125 Vaidya et al (1999); 126 Kavvoura et al (2007); 127 Lee et al (2000); 128 Ikegami et al (2006); 129 Mochizuki et al (2003); 130 Howson et al (2007); 131 Tang et al (2012); 132 Takara et al (2000); 133 Mayans et al (2007); 134 Balic et al (2009); 135 Ban et al (2001); 136 Celmeli et al (2013);137 Chen and Li (2019);138 Wang et al (2017); 139 Kavvoura et al (2005); 140 Liu et al (2013); 141 Dong et al (2014); 142 Fathima et al (2019); 143 Bicek et al (2009); 144 Einarsdottir et al (2003);146 Ban and Tomer (2003);147 Aversa et al148 (2019); Orban et al (2011); 149 Orban et al (2014)150 Abatacept AIRE, autoimmune regulator; AITD, thyroid autoimmune disease; CTLA-4, cytotoxic T lymphocyte-associated antigen-4; FOXP3, forkhead box protein P3; HLA, human leukocyte antigen; LYP, lymphoid protein tyrosine phosphatase; T1DM, type 1 diabetes mellitus.…”

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confidence: 99%

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Autoimmune thyroid disease and type 1 diabetes mellitus: same pathogenesis; new perspective?

Li¹,

Liu

2020

Therapeutic Advances in Endocrinology

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Autoimmune thyroid disease (AITD) and type 1 diabetes mellitus (T1DM) are two common autoimmune diseases that can occur concomitantly. In general, patients with diabetes have a high risk of AITD. It has been proposed that a complex genetic basis together with multiple nongenetic factors make a variable contribution to the pathogenesis of T1DM and AITD. In this paper, we summarize current knowledge in the field regarding potential pathogenic factors of T1DM and AITD, including human leukocyte antigen, autoimmune regulator, lymphoid protein tyrosine phosphatase, forkhead box protein P3, cytotoxic T lymphocyte-associated antigen, infection, vitamin D deficiency, and chemokine (C-X-C motif) ligand. These findings offer an insight into future immunotherapy for autoimmune diseases.

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Section: Genetics and Autoimmunitymentioning

confidence: 99%

mentioning

confidence: 99%

Autoimmune thyroid disease and type 1 diabetes mellitus: same pathogenesis; new perspective?

Li¹,

Liu

2020

Therapeutic Advances in Endocrinology

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“…The polymorphism of C1858T was identified by restriction fragment length polymorphism (RFLP) as described by Bulut et al. [ 21 ]. The PCR product was cut by RsaI enzyme (New England Biolabs, Ipswich, MA) at 37 °C for 4 h and resulted in two fragments, 176 bp and 42 bp that indicated the homozygous CC (wild type), whereas the heterozygous CT had three fragments at 218, 176 and 42 bp (see Figure 1 ).…”

Section: Methodsmentioning

confidence: 99%

The association between PTPN22 C1858T gene polymorphism and type 1 diabetes mellitus: an Indonesian study

et al. 2023

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Background Type 1 diabetes mellitus (T1DM) is disease caused by the destruction of β pancreatic cells. The activation of T-lymphocyte and proliferation inhibitor are induced by protein tyrosine phosphatase non-receptor type 22 ( PTPN22 ). However, the link between PTPN22 C1858T gene polymorphism and T1DM is still controversy. This study aimed to analyse the C1858T gene polymorphism in Indonesian children with T1DM. Materials and methods This case-control study was conducted from March 2021 to May 2022 in the Endocrinology Outpatient Clinic at Dr. Soetomo Hospital and Tropical Disease Center Universitas Airlangga. Patients with controlled T1DM during the study period were included. The PTPN22 analysis used polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. Results Sixty-two children voluntarily participated in this study, and were equally divided into the T1DM and control groups. Most of the patients (94%, 58/62) are Javanese. This study revealed a more frequent CC genotype (9.4%) and allele-C (54.6%) polymorphism in the T1DM group, while more frequent CT genotype (100%) and allele-T (50%) polymorphism were in the control group. The C- and T-allele frequency was 54.6% and 45.4% in the T1DM group, respectively. The T1DM and control groups did not significantly differ ( p = .2381). Conclusions PTPN22 homozygous genotype-CC and allele-C polymorphisms are more frequent in patients with T1DM. However, the PTPN22 C1858T gene polymorphism did not significantly correlate to T1DM children in this study. Key Messages: The PTPN22 C1858T gene polymorphism does not significantly affect the susceptibility of T1DM in Indonesian children. PTPN22 homozygous genotype-CC polymorphism was more observed in the T1DM group; thus, this genotype may play as a risk factor for T1DM children in the Indonesian population.

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“…Выявлены гены, позволяющие объяснить связь между СД 2-го типа и аутоиммунными заболеваниями щитовидной железы. В настоящее время идентифицировано по меньшей мере четыре общих гена, включая HLA [16], CTLA-4 [17], PTPN22 [18] и FOXP3 [19]. У пациентов с диабетом ночной ТТГпик «затуплен» и отмечено, что характерное «низкое состояние Т3» может быть обусловлено замедлением превращения Т4 в Т3 в периферических тканях, которое нормализуется с улучшением показателей гликемического контроля.…”

Section: факторы риска формирования сосудистых и нейропатических осло...unclassified

Risk factors of the development of vascular and neuropathic complications in patients with type 2 diabetes mellitus and autoimmune thyroiditis

Мелешкевич

Kurnikova

Митичкин³

et al. 2021

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Issues of the formation and progression of late complications of diabetes mellitus remain interesting and foreground today, especially in cases of type 2 diabetes mellitus (dm) combined with other endocrine diseases. The pathogenetic relation between the mechanisms leading to blood vessels and nerves damage against the background of diabetes mellitus, and, for example, mechanisms of autoimmune thyroid abnormality (ait), is far from being unambiguous, but the very fact of its existence cannot be denied.Purpose: to determine the predominant type of comorbidity (trans-syndromal, trans-nosological or chronological) and the level of comorbidity according to the disease rating scale (cirs) in patients with type 2 diabetes and ait, to study the structure of later complications of diabetes mellitus in this group of patients and to assess the contribution of certain factors to increased risk of complications.Methods. 428 patients were examined in a specialized endocrinology department, and two groups were formed: an observation group — 213 people with diagnosed type 2 diabetes and ait, and a comparison group — 215 people with a diagnosis of type 2 diabetes. These groups were comparable in age, the duration of diabetes, body mass index, correction of the disease. The analysis included clinical and laboratory parameters, the results of hormones level studies (tsh, free t4, insulin, c-peptide) and antibodies (at-tpo), thyroid ultrasonography, calculation of the insulin resistance index (homa) and the comorbidity index (cirs — cumulative illness rating scale) followed by a correlation-regression analysis of statistical data. The state of the peripheral nervous system was evaluated with the use of electromyography in patients of both groups, and the severity of diabetic neuropathy was evaluated with the use of the neuropathy disability score and vas (visual analogue scale) scales. The state of the vascular system was studied according to the data of ultrasound examination of the vessels of the lower extremities, echocardiography, and ophthalmoscopy.Results. The obtained data made it possible to determine the factors infl uencing the risk of type 2 diabetes complications developement, and to establish that neuropathic complications begin and progress faster in patients with comorbid endocrine pathology, however, there is no such dependence for vascular complications. According to the linear regression equation of the dependence of total complications on the duration of the disease, it was revealed that the development of vascular complications in patients with combined endocrinopathy occurs even more slowly than in patients with diabetes. The contribution of diabetes compensation and identifi ed risk factors to the progression of diabetic complications was less important for patients with endocrinopathies. As for evaluating the contribution of individual parameters, the most signifi cant were the duration of diabetes mellitus, albuminuria, atherosclerosis of the vessels of the lower extremities.Conclusion. In addition to the known risk factors for the development and progression of vascular complications, in patients with overlapping endocrinopathy, the preservation of residual insulin secretion and renal function (chronic kidney disease, proteinuria) were important. the prevalence of “total” Complications in the group of patients with combined endocrine pathology was lower, however, neuropathic complications in the same group were observed more often,т which indicates the primary eff ect of thyroid dysfunction on the structure of the nervous tissue.

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Protein Tyrosine Phosphatase Non-receptor 22 Gene C1858T Polymorphism in Patients with Coexistent Type 2 Diabetes and Hashimoto’s Thyroiditis

Cited by 6 publications

References 28 publications

Autoimmune thyroid disease and type 1 diabetes mellitus: same pathogenesis; new perspective?

Autoimmune thyroid disease and type 1 diabetes mellitus: same pathogenesis; new perspective?

The association between PTPN22 C1858T gene polymorphism and type 1 diabetes mellitus: an Indonesian study

Risk factors of the development of vascular and neuropathic complications in patients with type 2 diabetes mellitus and autoimmune thyroiditis

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