Graves’ Disease

Viard, Jean‐Paul; Gilquin, Jacques

doi:10.1056/nejmc1614624

Cited by 38 publications

(22 citation statements)

References 7 publications

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“…Большинство иммунометрических исследований в настоящее время используют принцип конкурентного связывания, в связи с чем определяемые антитела обозначаются как иммуноглобулины, подавляющие связывание рецептора ТТГ (TBII). Такие исследования выявляют факт наличия или отсутствия АТ-рТТГ, а также их концентрацию в сыворотке, но не позволяют оценить их биологическую активность [23,24]. Метаанализ 21 исследования показал, что диагностическая чувствительность и специфичность определения TBII методами второго и третьего поколения составили соответственно 97% и 98% [25].…”

Section: научный обзор 6 |unclassified

Review of European Thyroid Association Guideline (2018) for the Manage-ment of Graves’ Hyperthyroidism

Фадеев

2020

Clin Exp Thyroid

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Болезнь Грейвса (БГ)-системное аутоиммунное заболевание, характеризующееся инфильтрацией тканей, экспрессирующих рецептор тиреотропного гормона (ТТГ), а также Т-лимфоцитами, специфичными к антигенам щитовидной железы (ЩЖ). При БГ стимулирующие антитела (АТ) активируют рецептор к ТТГ (рТТГ), что приводит к гиперплазии ЩЖ и нерегулируемой гиперпродукции и гиперсекреции тиреоидных гормонов. Диагностика БГ базируется на лабораторном подтверждении тиреотоксикоза, повышении уровня АТ-рТТГ, обнаружении гиперваскуляризации и гипоэхогенности ЩЖ при УЗИ в сочетании с эндокринной орбитопатией (ЭОП). Определение уровня АТ-рТТГ необходимо для дифференциальной диагностики, прогнозирования риска рецидива тиреотоксикоза и при беременности. Тиреотоксикоз при БГ купируется назначением тиреостатиков, которые подавляют синтез тиреоидных гормонов; радикальное лечение подразумевает разрушение ткани ЩЖ при помощи радиоактивного йода (131 I) или ее хирургическое удаление (тиреоидэктомию). Пациентам с впервые выявленной БГ в большинстве случаев назначается терапия тиамазолом (ТМЗ), который рассматривается как препарат первого выбора, сроком 12-18 месяцев. Детям с БГ традиционно рекомендуется более длительный курс терапии ТМЗ-обычно на 24-36 месяцев. Если у пациента сохраняется повышение уровня АТ-рТТГ спустя 12-18 месяцев тиреостатической терапии, она, в части случаев, может быть продолжена с повторным определением АТ-рТТГ еще через 12 месяцев; альтернативой является 131 I или тиреоидэктомия. Женщин, получающих терапию ТМЗ, при планировании беременности или в ее I триместре, рекомендуется перевести на пропилтиоурацил (ПТУ). В случае развития рецидива или сохранения тиреотоксикоза после окончания курса тиреостатической терапии пациенту показано радикальное лечение. Тем не менее в отдельных случаях тиреостатическая терапия может проводиться длительно. Тиреоидэктомию следует доверять специализированным эндокринным хирургам, имеющим достаточный опыт проведения этой операции. Терапия 131 I противопоказана пациентам с тяжелой активной орбитопатией (ЭОП) и должна проводиться на фоне профилактического назначения глюкокортикоидов (ГК) при умеренно активной ЭОП.

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Section: научный обзор 6 |unclassified

Review of European Thyroid Association Guideline (2018) for the Manage-ment of Graves’ Hyperthyroidism

Фадеев

2020

Clin Exp Thyroid

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“…Hashimoto's thyroiditis (HT) is an organ-specific autoimmune disease susceptible to women with genetic susceptibility, mainly causing hypothyroidism (Viard and Gilquin, 2017). HT is characterized by lymphocytic infiltration of the thyroid tissue accompanied by the production of specific antibodies, among which, thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TgAb) are the most important pathogenic antibodies (Antonelli et al, 2015;Wang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Metformin Reverses Hashimoto’s Thyroiditis by Regulating Key Immune Events

Jia

Zhai

et al. 2021

Front. Cell Dev. Biol.

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BackgroundHashimoto’s thyroiditis (HT) is a common autoimmune disease characterized by high levels of thyroid peroxidase antibody (TPOAb) and thyroid globulin antibody (TgAb) as well as infiltration of lymphocytes in thyroid. In recent years, metformin has been proven to be effective in a variety of autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis.MethodsThis study systematically explored the therapeutic effect of metformin on HT and its underlying mechanism by comprehensively utilizing methods including animal model, in vitro cell culture and differentiation, mRNA sequencing and 16S rRNA sequencing.FindingsWe found that metformin indeed had a therapeutic effect on mice with HT mainly by reducing TgAb and lymphocyte infiltration in thyroid tissue. In addition, metformin also significantly suppressed the number and function of Th17 cells and M1 macrophages polarization in HT mice. Furthermore, metformin can inhibit the differentiation and function of Th17 in vitro. The results of mRNA sequencing of thyroid tissue illustrated that the therapeutic effect of metformin on HT was mainly achieved by regulating immune pathways. 16S RNA sequencing of the intestinal flora found that the intestinal flora of HT mice differs significantly from that of the normal mice and also were altered by metformin treatment.InterpretationThese experiments provided a preliminary theoretical basis for the clinical application of metformin in the treatment of HT.

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“…Autoimmune thyroid diseases (AITDs) are not a disease but a group of diseases; the main damage is not only the thyroid gland but also the other parts of the body. AITDs mainly include two types of Graves' disease (GD) and Hashimoto's thyroiditis (HT) [ 1 ]. GD is characterized by an abnormal increase in thyroid-stimulating hormone (TSH) receptor antibody (TRAb), which competitively binds to the TSH receptor (TSHR) on thyroid follicular cells with TSH, resulting in increased synthesis and secretion of thyroid hormones [ 1 , 2 ].…”

Section: Introductionmentioning

confidence: 99%

“…AITDs mainly include two types of Graves' disease (GD) and Hashimoto's thyroiditis (HT) [ 1 ]. GD is characterized by an abnormal increase in thyroid-stimulating hormone (TSH) receptor antibody (TRAb), which competitively binds to the TSH receptor (TSHR) on thyroid follicular cells with TSH, resulting in increased synthesis and secretion of thyroid hormones [ 1 , 2 ]. The main feature of HT is the abnormal increase in thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb).…”

Section: Introductionmentioning

confidence: 99%

“…Epidemiological surveys show that the prevalence of GD in China is about 0.8%, and the prevalence of HT is as high as 10% or more; the global prevalence of AITD is approximately 5%, with about 10 million GD patients and more than 130 million HT patients [ 6 – 8 ]. Patients with AITD increase in cardiovascular and tumor risks, increase the likelihood of adverse pregnancy such as miscarriage and premature birth, and seriously endanger public health [ 1 , 9 ]. However, the current treatment methods are very limited, especially the treatment methods for the etiology are lacking.…”

Section: Introductionmentioning

confidence: 99%

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Associations between NLRC4 Gene Polymorphisms and Autoimmune Thyroid Disease

Liu

Bai

Zhao

et al. 2020

BioMed Research International

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Background. Many studies have shown that NLRC4 inflammasome polymorphisms are associated with a variety of autoimmune diseases, but the associations between NLRC4 polymorphisms and autoimmune thyroid diseases (AITDs) are unclear. Our research was aimed at identifying the correlations between NLRC4 polymorphisms and AITDs. Methods. Hi-SNP high-throughput genotyping technology was used for detecting four single-nucleotide polymorphisms (SNPs) of NLRC4 in 1005 AITDs patients (including 629 Graves’ disease and 376 Hashimoto’s thyroiditis) and 781 healthy controls. Results. Compared with healthy controls, the allele frequencies and genotype distribution of rs385076 were statistically related to AITDs (P=0.016 and P=0.048, respectively) and Hashimoto’s thyroiditis (P=0.022 and P=0.046, respectively). Before adjusting for age and gender, rs385076 and AITDs had a significant association in three models of allele model, dominant model, and homozygous model. After adjusting for age and gender, in the above three models, there is still a clear relationship between them. Before adjusting for age and gender, there were prominent discrepancy between rs385076 and Hashimoto’s thyroiditis in the allele model (OR=0.81, 95% CI 0.67-0.97; P=0.021) and the dominant model (OR=0.73, 95% CI 0.57-0.94; P=0.014), after adjusting for age and gender, rs385076 and Hashimoto’s thyroiditis were significantly related to allele model, dominant model, and homozygous model. However, rs455060, rs212704, and rs675712 were not related to AITDs in our study. Conclusion. NLRC4 rs385076 was found to have a significant association with Hashimoto’s thyroiditis for the first time. It laid a foundation for the disclosure of the pathogenesis of AITDs, and provided a possible treatment prospect for HT.

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Graves’ Disease

Cited by 38 publications

References 7 publications

Review of European Thyroid Association Guideline (2018) for the Manage-ment of Graves’ Hyperthyroidism

Review of European Thyroid Association Guideline (2018) for the Manage-ment of Graves’ Hyperthyroidism

Metformin Reverses Hashimoto’s Thyroiditis by Regulating Key Immune Events

Associations between NLRC4 Gene Polymorphisms and Autoimmune Thyroid Disease

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