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At least 19 recordsLinked to original sources
PubMed2024

Epigenome-wide Association Study Shows Differential DNA Methylation of MDC1, KLF9, and CUTA in Autoimmune Thyroid Disease.

CONTEXT: Autoimmune thyroid disease (AITD) includes Graves disease (GD) and Hashimoto disease (HD), which often run in the same family. AITD etiology is incompletely understood: Genetic factors may account for up to 75% of phenotypic variance, whereas epigenetic effects (including DNA methylation [DNAm]) may contribute to the remaining variance (eg, why some individuals develop GD and others HD). OBJECTIVE: This work aimed to identify differentially methylated positions (DMPs) and differentially methylated regions (DMRs) comparing GD to HD. METHODS: Whole-blood DNAm was measured across the genome using the Infinium MethylationEPIC array in 32 Australian patients with GD and 30 with HD (discovery cohort) and 32 Danish patients with GD and 32 with HD (replication cohort). Linear mixed models were used to test for differences in quantile-normalized &#x3b2; values of DNAm between GD and HD and data were later meta-analyzed. Comb-p software was used to identify DMRs. RESULTS: We identified epigenome-wide significant differences (P < 9E-8) and replicated (P < .05) 2 DMPs between GD and HD (cg06315208 within MDC1 and cg00049440 within KLF9). We identified and replicated a DMR within CUTA (5 CpGs at 6p21.32). We also identified 64 DMPs and 137 DMRs in the meta-analysis. CONCLUSION: Our study reveals differences in DNAm between GD and HD, which may help explain why some people develop GD and others HD and provide a link to environmental risk factors. Additional research is needed to advance understanding of the role of DNAm in AITD and investigate its prognostic and therapeutic potential.

Humans↗
PubMed1978

UCLA conference. Autoimmune thyroid diseases--Graves' and Hashimoto's.

Thyroid-related autoimmune diseases (Graves' thyroid disease, Graves' ophthalmopathy, and Hashimoto's thyroiditis) may occur alone or in any association. The diagnosis of Hashimoto's thyroiditis requires multiple criteria; pathologic changes in the thyroid are not due to antibodies but may result from cytotoxic lymphocytes or a deficiency of suppressive T cells. In Graves' and Hashimoto's diseases the increased prevalence of HLA-B8 may not be significant, but that of HLA-AW30 in Hashimoto's disease is. In 48 first-degree relatives of patients with Graves' disease, thyroid abnormalities were frequent but not correlated with HLA type. Elevated serum thyroglobulin levels in all patients with hyperthyroidism fell to normal after surgical resection or radioiodine therapy. Patients whose illness recurred after antithyroid drug treatment was stopped had higher pretreatment thyroglobulin levels and no fall during treatment; those whose illness remitted had lower initial levels and a significant fall during treatment. Sodium ipodate lowered serum triiodothyronine and thyroxine levels in hyperthyroid patients and may be useful in the treatment of hyperthyroidism.

Animals↗
PubMedDate not supplied

Clinical evaluation of a hemagglutination method for microsomal and thyroglobulin antibodies in autoimmune thyroid disease.

A simple and reproducible hemagglutination technique for detecting microsomal and thyroglobulin antibodies has been evaluated in normal subjects and in patients with thyroid disease. Microsomal antibodies were detected in 89 percent of all patients with autoimmune thyroid disease and in 97 percent of patients with biopsy proven Hashimoto's thyroiditis. In contrast, thyroglobulin antibodies were present in only 55 percent of patients with biopsy proven Hashimoto's thyroiditis and in 44 percent of all patients with suspected autoimmune thyroid disease. It is suggested, therefore, that measurement of microsomal antibodies by a simple hemagglutination techniques be carried out in all patients with suspected thyroid disorders.

Antibodies↗
PubMed1976

Measurement of circulating thyroid microsomal antibodies by the tanned red cell haemagglutination technique: its usefulness in the diagnosis of autoimmune thyroid diseases.

Thyroid-microsomal antibodies were quantitated by a new technique utilizing tanned sheep red blood cells coated with human thyroid microsomal antigens. This haemagglutination assay (MCHA) correlated with the immunofluorescent antibody (FAB) but not with the thyroglobulin haemagglutination antibodies (TGHA) assay. Of forty-one patients with Hasmimoto's thyroiditis, thirty-nine (95%) were MCHA but only twenty-four (59%) TGHA positive. Titres were similar for the hypothyroid and euthyroid patients. Patients less than 20 years of age had either negative (50%) or low titre (less than 1:160) TGHA but 100% positive MCHA at titres greater than 1:1280. Of twenty-one patients with Graves' disease eighteen (86%) were MCHA and six (29%) TGHA positive. Of thirty-two patients without thyroid disease eleven (34%) were MCHA and/or TGHA positive. On the basis of family history and associated abnormalities, in eight of eleven, positive antibodies may have been due to subclinical Hashimoto's thyroiditis. Fourteen subjects of a control group (10%) were MCHA positive. Seven of ten examined had goitres. MCHA is a simple and quantitative test, useful in the diagnosis of autoimmune thyroid diseases.

Autoantibodies↗
PubMed1978

Changes of serum anti-thyroid antibodies during and after pregnancy in autoimmune thyroid diseases.

Changes of serum anti-thyroglobulin haemagglutination antibodies (TGHA) and anti-thyroid microsomal haemagglutination antibodies (MCHA) were observed during pregnancy and after delivery in Graves' disease and autoimmune thyroiditis. Both TGHA and MCHA decreased as pregnancy progressed, and sometimes they became negative in late pregnancy. Transient increases of TGHA and MCHA were observed after delivery and the antibody titres reached peaks about 3-4 months post-partum in more than halft the patients. In some patients, antibodies developed after delivery. Similar transient increases of antibodies were observed after spontaneous and therapeutic abortion. These changes seem to be induced by physiological and immunological changes occurring during pregnancy and after delivery.

Abortion, Spontaneous↗
PubMed1978

Autoimmune thyroid disease and the polymyalgia rheumatica-giant cell arteritis syndrome.

In a study of 250 patients with autoimmune thyroid disease, seven (2.8%) were found to have polymyalgia rheumatica or giant cell arteritis. All cases occurred in female patients over the age of 60 years, a prevalence in this group of 9.3%. No cases of either disorder were seen in a control population of 150 female patients over the age of 50 years attending a cardiac clinic at the same hospital. Awareness of this association may allow earlier diagnosis and treatment of this syndrome in elderly patients with thyroid disease.

Aged↗
PubMed1977

The role of autoimmunity in hypoendocrine and hyperendocrine function: with special emphasis on autoimmune thyroid disease.

There is considerable evidence to suggest that the organspecific autoimmune endocrinopathies are primary disorders of the lympoid system. Although proof is not complete, the basic genetic defect in each condition may be one of immune surveillance, that is, a defect in suppressor "T" lymphocytes. Combinations of two or more of these conditions may be due to the concurrence of two or more specific defects in immune control, as well as the random appearance of the appropriate self-directed "forbidden" clones of lymphocytes. In this concept, there is no need for antigenic alteration (only antigenic availability) to initiate these disorders. Both cell-mediated and humoral immunity seem essential, with roles for immune complexes and "killer" cells as well. Antireceptor antibodies are of particular interest in Graves' disease, where they are stimulatory: other antireceptor antibodies have been found that are blocking antibodies, and others may merely bind without either stimulating or blocking.

Addison Disease↗
PubMed2026

Thyroid-stimulating hormone receptor mediates peripheral-central neuroimmune crosstalk in autoimmune thyroid diseases.

BACKGROUND: Organ-specific autoimmune diseases, particularly Graves' disease (GD) and its extrathyroidal manifestation, Graves' orbitopathy (GO), are characterized by systemic autoimmunity that may extend its impact to the central nervous system (CNS). While thyroid-stimulating hormone receptor (TSHR) is the primary driver of pathological remodeling in the thyroid and orbital tissues, emerging evidence suggests it is also expressed in the brain and may participate in neuroimmune signaling. However, the molecular mechanisms linking peripheral TSHR-driven autoimmunity to these extended systemic features remain unclear. Thus, GD and GO provide a unique window to investigate how peripheral autoantibodies influence CNS involvement as part of its broader pathological spectrum. METHODS: Genome-wide association studies (GWAS) and post-GWAS analyses were integrated with bulk RNA sequencing, single-cell and spatial transcriptomics, and brain imaging phenotypes to comprehensively characterize peripheral and central alterations in GD and GO. Mendelian randomization was applied to test causal relationships between genetic variants and brain signatures. Structural biology analyses were further conducted including protein-protein docking, small-molecule docking, and normal mode dynamics to identify prospective modulators of TSHR. Immunofluorescence staining was performed in a GO mouse model to validate the colocalization of potential interacted proteins in the specific brain region. RESULTS: Brain imaging-derived phenotypes (IDPs) alterations in GO and GO were systematically analyzed to identify neuroanatomical and functional alterations. TSHR was further identified as a shared genetic driver across peripheral and central compartments. TSHR was expressed in spiny projection neurons, microglia, and peripheral T cells, with cell-cell communication analyses highlighting TSHR-mediated interactions among neurons, endothelial cells, and microglia. Immunofluorescence staining in a GO mouse model confirmed the colocalization of TSHR with FN1 and GNAS in the basal ganglia, providing tissue-level validation of the computationally predicted ligand-receptor interactions. Immune profiling further showed immune alterations in GD and GO. Structural modeling supported plausible physical interfaces between TSHR and interacting proteins, and small-molecule screening identified three repurposable compounds - venetoclax, irinotecan, and dutasteride - with predicted favorable docking scores and stable binding poses in our simulations. CONCLUSIONS: These findings demonstrate that TSHR acts as a molecular hub mediating peripheral-central neuroimmune crosstalk in GD and GO. The results support a broader "disease-molecule axis" framework that links genetic susceptibility with multi-level immune and neural mechanisms. This work provides mechanistic insights relevant to the development of TSHR-targeted therapies, with implications for both peripheral immune modulation and central regulation. However, the limited sample size, lack of longitudinal follow-up, and absence of in vivo validation warrant cautious interpretation and further investigation.

Receptors, Thyrotropin↗
PubMed1977

Gm phenotypes in autoimmune thyroid disease.

The Gm phenotype Gm f,b or Gm f,n,b was found in all forty patients with Graves' disease studied, contrasted with thirty-five out of forty controls and twenty out of thirty-one patients with thyroiditis. The difference between the two groups with autoimmune thyroid disease was significant. These results suggest that thyroid stimulating antibodies may be allotypically restricted.

Alleles↗
PubMed2026

Cushing's disease and autoimmune thyroid disorders in women: Impacts on fertility, pregnancy, and menopause.

Cushing's disease (CD) and autoimmune thyroid diseases (AITDs) are two distinct but interconnected endocrinopathies affecting predominantly women. A primary cause of CD is excess adrenocorticotropic hormone (ACTH) secretion, which leads to hypercortisolism and profound hormonal and immune changes. As with AITDs, Hashimoto's thyroiditis and Graves' disease are caused by a loss of immune tolerance and frequently coexist with female reproductive dysfunction. Emerging evidence suggests that chronic hypercortisolism in CD suppresses immunity as well as alters hypothalamic-pituitary-thyroid (HPT) axis activity, which may mask or exacerbate thyroid autoimmunity after disease remission. Coexisting CD and AITD has significant effects on women's reproductive health, pregnancy outcomes, and menopausal transitions, as thyroid and adrenal hormones play a crucial role in regulating ovulatory cycles, placental development, bone formation, and cardiovascular health. In this review, shared pathophysiological pathways are explored, clinical and therapeutic challenges are highlighted, and integrated management strategies are discussed. To improve early diagnosis, tailor treatment approaches, and guide future endocrine research, it is essential to understand the compounded risks of dual endocrinopathy.

Humans↗
PubMed1978

HLA antigens in autoimmune thyroid diseases.

HLA antigens were determined in 85 unrelated Japanese patients with Graves' disease and 56 patients with Hashimoto's thyroiditis, with the use of the microcytotoxicity test. HLA-Bw35 was found in 36.4% of 85 patients with Graves' disease compared with 13.3% of 150 normal control subjects. This difference in antigen frequency is significant at the level of P less than .0005. The association with HLA-Bw35 in Japanese patients with Graves' diseases is different from that with HLA-B8 in white patients. In patients with Hashimoto's thyroiditis, HLA-Bw35 was also increased (28.5% of 56 patients) but not at a level of statistical significance (P less than .05).

Adult↗