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Graves' disease is an autoimmune disorder in which the thyroid is activated by antibodies to the thyrotropin receptor. The hyperthyroidism that develops is one of many somatic and psychiatric manifestations of the disease that can affect the quality and length of life. Graves’ disease was first recognized in the 19th century as a syndrome comprising an enlarged and overactive thyroid gland, an accelerated heart rate, and ocular abnormalities (Figure 1). Critical for our current understanding of this disease was the discovery of its autoimmune basis, which results from complex interactions between genetic and environmental factors. 1 , 2 Graves’ disease has adverse effects on quality of life, 3 as a consequence of somatic 4 and psychiatric 5 symptoms and an inability to work, 6 and is associated with an increased risk of death. 7 Activating thyrotropin-receptor antibodies induce thyroid hormone overproduction. Many characteristic signs and symptoms of Graves’ disease . . .

Abstract Context Because subclinical hyperthyroidism increases the risk of osteoporosis and fractures, concerns are growing about the long-term skeletal safety of TSH suppression therapy after total thyroidectomy in patients with differentiated thyroid cancer (DTC). Objective We aimed to determine the effect of TSH suppression therapy on bone mineral density (BMD) in DTC patients. Methods We searched PubMed, Embase, the Cochrane library, and other sources. Eligible observational studies included DTC patients who underwent TSH suppression therapy and BMD measurement. Two independent reviewers extracted data on the studies’ characteristics and outcomes and determined their risk of bias. Data were extracted from each study for postmenopausal/premenopausal women’s and men’s lumbar spine (LS), femoral neck (FN), and total hip (TH) BMD and summed using a random-effects meta-analysis model. The weighted mean differences with 95% CIs are expressed for the differences in outcome measurements between groups. Results Seventeen studies (739 patients and 1085 controls) were included for quantitative analysis. In postmenopausal women, TSH suppression therapy showed a significant decrease in LS BMD (-0.03; -0.05, -0.02), and a similar trend was seen in TH. In premenopausal women, TSH suppression therapy significantly increased LS BMD (0.04; 0.02, 0.06) and FN BMD (0.02; 0.01, 0.04). In men, there was no significant association between TSH suppression therapy and BMD at any site compared with the controls. Conclusion Evidence from observational studies suggests that postmenopausal women treated with TSH suppression therapy are at risk for lower BMD. Attention should be paid to long-term skeletal safety in DTC survivors.

Hyperthyroidism is characterized by overproduction of thyroid hormone in the thyroid gland and affects 1.3% of adults in the United States. Thyrotoxicosis is a state of thyroid hormone excess and may be caused by hyperthyroidism, thyroiditis, or exogenous administration. The most common symptoms of hyperthyroidism are weakness, palpitations, weight loss, and heat intolerance, and the most common signs are a palpable goiter, tachycardia, muscle weakness, and tremor. A low thyroid-stimulating hormone (thyrotropin) level has a high sensitivity and specificity for diagnosing thyrotoxicosis. The most common cause of hyperthyroidism is the autoimmune condition Graves disease, typically diagnosed by the presence of thyroid eye disease, which is pathognomonic, or thyrotropin receptor antibodies. Other causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma, and thyroiditis, which can be differentiated by the pattern of uptake on a radioactive iodine scan. Thionamides (most commonly methimazole) typically induce remission of Graves disease and can control hyperthyroidism caused by multinodular goiter and toxic adenoma. Radioactive iodine resolves hyperthyroidism in more than 90% of patients with Graves disease and toxic multinodular goiter, with hypothyroidism developing in most patients 1 year after treatment. Thyroidectomy is the treatment of choice for patients with compressive symptoms from an obstructive goiter.

A perennial task is to prevent the occurrence and/or recurrence of most frequent or life-threatening cardiac arrhythmias such as atrial fibrillation (AF) and ventricular fibrillation (VF). VF may be lethal in cases without an implantable cardioverter defibrillator or with failure of this device. Incidences of AF, even the asymptomatic ones, jeopardize the patient’s life due to its complication, notably the high risk of embolic stroke. Therefore, there has been a growing interest in subclinical AF screening and searching for novel electrophysiological and molecular markers. Considering the worldwide increase in cases of thyroid dysfunction and diseases, including thyroid carcinoma, we aimed to explore the implication of thyroid hormones in pro-arrhythmic signaling in the pathophysiological setting. The present review provides updated information about the impact of altered thyroid status on both the occurrence and recurrence of cardiac arrhythmias, predominantly AF. Moreover, it emphasizes the importance of both thyroid status monitoring and AF screening in the general population, as well as in patients with thyroid dysfunction and malignancies. Real-world data on early AF identification in relation to thyroid function are scarce. Even though symptomatic AF is rare in patients with thyroid malignancies, who are under thyroid suppressive therapy, clinicians should be aware of potential interaction with asymptomatic AF. It may prevent adverse consequences and improve the quality of life. This issue may be challenging for an updated registry of AF in clinical practice. Thyroid hormones should be considered a biomarker for cardiac arrhythmias screening and their tailored management because of their multifaceted cellular actions.

Objective In recent years, the incidence of papillary thyroid carcinoma (PTC) has been rapidly increasing, and thermal ablation techniques are gradually emerging as alternative therapies for PTC. The aim of this study was to comprehensively analyse potential factors leading to hyperthyroidism after thermal ablation treatment for PTC, providing a scientific reference for the prevention of and intervention for hyperthyroidism in such condition in the future. Methods Through the analysis of 22 papillary thyroid carcinoma (PTC) patients who received thermal ablation treatment in four different hospitals and later experienced hyperthyroidism during follow-up, we scrutinised their diagnostic and treatment procedures. This comprehensive analysis, in conjunction with pertinent data and reports, sought to delineate optimal approaches for both prevention and treatment. Results Among the PTC patients included in the study, 3 were males and 19 were females, with an average age of 36.05 ± 1.60 years. Thirteen patients underwent radiofrequency ablation treatment, while 9 patients received microwave ablation treatment. Before undergoing treatment, these 22 PTC patients presented no evident abnormalities in thyroid function and did not experience any hyperthyroidism-related symptoms. Additionally, within one week following thermal ablation treatment, thyroid function normalised. During the follow-up period, they subsequently developed hyperthyroidism, accompanied by decreased TSH, along with elevated FT3 and/or FT4. Some patients also presented with clinical symptoms of hyperthyroidism, such as heat intolerance, sweating, hand tremors, palpitations, and other associated signs. Conclusion In summary, PTC patients who exhibit symptoms of thyroiditis or autoimmune diseases prior to the procedure may be at increased risk of developing hyperthyroidism following thermal ablation treatment.

Originally classified as a variant of silent corticotroph adenoma, silent subtype 3 adenomas are a distinct histologic variant of pituitary adenoma of unknown cytogenesis. We reviewed the clinical, biochemical, radiological, immunohistochemical and ultrastructural features of 31 silent subtype 3 adenomas to clarify their cellular origin. Among 25 with clinical and/or radiological data, all were macroadenomas; there was cavernous sinus invasion in 30% of cases and involvement of the clivus in 17% of cases. Almost 90% of patients were symptomatic; 67% had mass effect symptoms, 37% were hypogonadal and 8% had secondary adrenal insufficiency. Significant hormonal excess in 29% of cases included hyperthyroidism in 17%, acromegaly in 8% and hyperprolactinemia above 150  μ g/l in 4%. Two individuals with hyperprolactinemia who were younger than 30 years had multiple endocrine neoplasia type 1. Immunohistochemically, all 31 tumors were diffusely positive for the pituitary lineage-specific transcription factor Pit-1. Although three only expressed Pit-1, others revealed variable positivity for one or more hormones of Pit-1 cell lineage (growth hormone, prolactin, thyroid-stimulating hormone), as well as alpha-subunit and estrogen receptor. Most tumors exhibited perinuclear reactivity for keratins with the CAM5.2 antibody; scattered fibrous bodies were noted in five (16%) tumors. The mean MIB-1 labeling index was 4% (range, 1–9%). Fourteen cases examined by electron microscopy were composed of a monomorphous population of large polygonal or elongated cells with nuclear spheridia. Sixty-five percent of patients had residual disease after surgery; after a mean follow-up of 48.4 months (median 41.5; range=2–171) disease progression was documented in 53% of those cases. These data identify silent subtype 3 adenomas as aggressive monomorphous plurihormonal adenomas of Pit-1 lineage that may be associated with hyperthyroidism, acromegaly or galactorrhea and amenorrhea. Our findings argue against the use of the nomenclature ‘silent’ for these tumors. To better reflect the characteristics of these tumors, we propose that they be classified as ‘poorly differentiated Pit-1 lineage adenomas’.

Ten eleven translocation 1 (TET1) is a 5-methylcytosine dioxygenase, and its altered DNA demethylation has been implicated in human diseases. However, its role in regulating thyroid function remains totally unknown. Here we first generated thyroid-specific Tet1 knockout combined with thyroid-specific Braf V600E transgenic mouse model ( Thy-Braf V600E ; Tet1 −/− ) and their control mice ( Thy-Braf V600E ; Tet1 +/+ ). The latter developed severe hypothyroidism and lost reproductive ability owing to structural damages of thyroid gland, while thyroid-specific Tet1 knockout effectively restored thyroid structure and function of Thy-Braf V600E ; Tet1 +/+ mice and their reproductive ability. In addition, we also established thyroid-specific Tet1 knockout mouse model ( Thy-Tet1 −/− ) and demonstrated that these mice could develop hyperthyroidism with systemic hypermetabolic symptoms such as weight loss, increased heart rate and elevated systolic blood pressure, further supporting the inhibitory effect of TET1 on thyroid function. Transcriptomic sequencing revealed that key genes related to metabolism and synthesis of thyroid hormones such as PAX8 , SLC5A5 and TPO were significantly upregulated in Thy-Tet1 −/− mice. Mechanistically, TET1 recruits HDAC1 to reduce the levels of H3K27Ac and H3K9Ac in the PAX8 promoter, thereby inhibiting the expression of itself and its downstream targets NIS and TPO. Further studies showed that elevated miR-29c-3p in serum exosomes enhanced thyroid function by targeting TET1, which may be one of the causes of hyperthyroidism. Thus, this study uncovers a new mechanism by which TET1 suppresses thyroid function, providing a new perspective to explore the pathogenesis of hyperthyroidism. TET1 regulates thyroid function and hyperthyroidism mechanisms Hyperthyroidism is a condition in which the thyroid gland produces too many hormones, leading to symptoms such as weight loss and irritability. Here scientists are exploring the role of a protein called TET1 in thyroid function. TET1 is known for its role in modifying DNA, which can affect how genes are turned on or off. In this study, researchers investigated whether TET1 influences thyroid activity. They used mice that were genetically modified to lack TET1 specifically in their thyroid glands. These mice showed signs of hyperthyroidism such as increased thyroid hormone levels and faster metabolism. The researchers found that TET1 normally helps suppress the activity of certain genes involved in thyroid hormone production by interacting with other proteins that modify DNA structure. This study suggests that TET1 plays a crucial role in regulating thyroid function and that its absence can lead to hyperthyroidism. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Thyroid diseases (TDs) have been widely associated with HIV infection. However, data about TDs prevalence and distribution are controversial, and few published studies are available. The aim of our study was to assess prevalence and risk factors of symptomatic thyroid disturbances, including thyroid cancers, in a large cohort of HIV-infected patients. A retrospective cohort study was performed at the Department of Infectious and Tropical Diseases of the University of Brescia, Italy, in the period 2005–2017. We identified all HIV-positive patients with a diagnosis of symptomatic TD in the electronic database of our Department (HIVeDB); we also operated a record-linkage between our data and the Health Protection Agency database (HPADB) of Brescia Province. Multivariate logistic regression analysis was used to determine risk factors associated with TDs onset; an incidence rate analysis was also performed. During the study period, 6343 HIV-infected patients have been followed at our Department; 123 received a diagnosis of symptomatic TD (1.94% of the entire cohort). In the TDs group, almost half of patients were females (n = 59, 48%), mean age was 47.15 years (SD: 11.56). At TD diagnosis, mean T CD4+ cell count was 491 cell/uL and most patients showed undetectable HIV-RNA (n = 117, 95.12%). Among them, 81 patients were found to have hypothyroidism (63 with Hashimoto’s thyroiditis), 21 hyperthyroidism (17 suffered from Graves’ disease), while 11 subjects were diagnosed with a primitive thyroid cancer. Papillary thyroid cancer was the most frequent histotype (n = 7, 63.63%), followed by medullary (n = 2, 18.18%) and follicular thyroid cancer (n = 1, 9.1%). Male gender was a protective factor for TDs development, especially for hypothyroidism (p < 0.001); age emerged as a variable associated with both hypothyroidism (p = 0.03) and thyroid cancer (p = 0.03), while CD4+ cell nadir <200 cell/mm 3 was associated with symptomatic hyperthyroidism (p = 0.005). To conclude, symptomatic thyroid dysfunctions rate in well-treated HIV-infected patients is low. Age and gender are crucial elements in the onset of thyroid abnormalities, together with T CD4+ cell nadir. Interestingly, medullary thyroid cancer seems to be much more frequent in HIV-infected patients compared to the general population.

Purpose Therapeutic plasma exchange (TPE) is a treatment option to reduce thyroid hormones in the event of contraindication or unresponsiveness to antithyroid drugs (ATDs). Methods We analyzed 11 patients with hyperthyroidism who received TPE prior to surgery between January 2008 and December 2016 at our center. Results In total, 41 processes were applied to 11 patients with hyperthyroidism. The median age was 40 years, and 90.9% of the patients were female. Seven patients had Graves’ disease, while four had a toxic multinodular goiter. The distribution of TPE indications comprised contraindication to ATDs (64%) and insufficient response to ATDs (36%). An adequate response was not obtained with TPE in two patients, and cholestyramine plus methimazole and Lugol solution were applied. The median number of TPE sessions was 3. During the TPE period, a β-blocker was applied concurrently except in one patient who was contraindicated for the drug. The reduction in FT3 and FT4 hormones and the increase in TSH levels were statistically significant after TPE application (p values of 0.003, 0.033 and 0.008, respectively). Regarding adverse events of TPE application, an allergic reaction was seen in one patient, while prolongation of prothrombin time without any clinical findings was seen in another patient. Ten patients underwent total thyroidectomy, and one patient underwent a gynecological surgery procedure without any major complications. Conclusion The American Society for Apheresis guideline, which is the most referenced guideline, mentions the utilization of TPE before thyroid surgery, only in patients with thyrotoxicosis despite the wider necessity of this treatment choice under the condition of uncontrolled hyperthyroidism prior to any kind of surgery. We concluded that TPE is a reliable and effective application in patients with hyperthyroidism before any surgical procedure, according to our study results.

BackgroundFew studies have evaluated associations between pesticides and hyperthyroidism.ObjectiveWe evaluated associations between specific pesticides and incident hyperthyroidism in private pesticide applicators in the Agricultural Health Study.MethodsWe used Cox proportional hazards models to estimate HRs and 95% CIs for associations between pesticide use at enrolment and hyperthyroidism (n=271) in 35 150 applicators (mostly men), adjusting for potential confounders.ResultsEver use of several pesticides (organophosphate insecticide malathion, fungicide maneb/mancozeb, herbicides dicamba, metolachlor, and atrazine in overall sample and chlorimuron ethyl among those ≤62 years) was associated with reduced hyperthyroidism risk, with HRs ranging from 0.50 (95% CI 0.30 to 0.83) for maneb/mancozeb to 0.77 (95% CI 0.59 to 1.00) for atrazine. Hyperthyroidism risk was lowest among those with higher intensity-weighted lifetime days of using carbofuran and chlorpyrifos (ptrend ≤0.05).ConclusionsObserved associations between pesticides and decreased risk of hyperthyroidism warrant further investigation.