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Thyrotoxicosis causes a variety of symptoms and adverse health outcomes. Hyperthyroidism refers to increased thyroid hormone synthesis and secretion, most commonly from Graves' disease or toxic nodular goitre, whereas thyroiditis (typically autoimmune, viral, or drug induced) causes thyrotoxicosis without hyperthyroidism. The diagnosis is based on suppressed serum concentrations of thyroid-stimulating hormone (TSH), accompanied by free thyroxine and total or free tri-iodothyronine concentrations, which are raised (overt hyperthyroidism) or within range (subclinical hyperthyroidism). The underlying cause is determined by clinical assessment, detection of TSH-receptor antibodies and, if necessary, radionuclide thyroid scintigraphy. Treatment options for hyperthyroidism include antithyroid drugs, radioactive iodine, and thyroidectomy, whereas thyroiditis is managed symptomatically or with glucocorticoid therapy. In Graves' disease, first-line treatment is a 12–18-month course of antithyroid drugs, whereas for goitre, radioactive iodine or surgery are preferred for toxic nodules or goitres. Evidence also supports long-term treatment with antithyroid drugs as an option for patients with Graves' disease and toxic nodular goitre.

Abstract Thyroid eye disease (TED) is the most consequential extrathyroidal manifestation or complication of Graves' disease (GD). Treatment of hyperthyroidism in GD complicated by TED is challenging. Antithyroid drugs (ATDs) and thyroidectomy do not change the natural course of TED, while radioactive iodine (RAI) is associated with a small but well-documented risk of TED de novo occurrence or its progression/worsening. In the presence of mild TED, any treatment for hyperthyroidism can be used, but should RAI treatment be selected, steroid prophylaxis (short course of low-dose prednisone) is strongly recommended if TED is of recent onset and/or risk factors for progression exist. In moderate to severe and active TED, ATDs are the preferred treatment, but thyroidectomy is a valid option. RAI ablation is generally avoided; it might be used when the clinical situation calls for it, but with extreme caution, if an aggressive treatment for TED with high-dose glucocorticoids (with or without orbital radiotherapy) is administered concomitantly. In moderate to severe and inactive TED, all 3 treatments for hyperthyroidism are acceptable, and steroid prophylaxis in RAI-treated patients should be given when risk factors for TED progression are identified. Management of sight-threatening TED represents the absolute priority, and hyperthyroidism should be controlled with ATDs until TED has been controlled. Search Strategies Current guidelines, original articles, clinical trials, systematic reviews, and meta-analyses up to June 2024 were searched using the following terms: “Graves' disease,” “management of Graves' disease,” “antithyroid drugs,” “radioactive iodine,” “thyroidectomy,” “thyroid eye disease,” “Graves' orbitopathy or ophthalmopathy.”

Background Hyperthyroidism complicated by liver failure is associated with high mortality, and the optimal treatment strategy remains unclear. We aimed to compare the clinical characteristics of patients who received different treatments for hyperthyroidism and liver failure. Methods This retrospective cohort study included 137 patients diagnosed with hyperthyroidism and Liver failure between January 2013 and December 2022. The patients were treated with methimazole (MMI) plus artificial liver support system (ALSS), radioactive iodine ( 131 I) plus ALSS, or MMI alone for 24 weeks. Liver and thyroid function were monitored to determine treatment efficacy and potential complications. Results After propensity score matching, no significant differences in treatment efficacy were observed between MMI plus ALSS and MMI alone at discharge ( P  = 0.425), 12 weeks ( P  = 0.104), or 24 weeks ( P  = 0.104). There were also no significant differences in treatment efficacy between 131 I plus ALSS and MMI alone. However, hospital stays were shorter in the MMI and 131 I plus ALSS groups than in the MMI alone group ( P  = 0.014 and P  = 0.010, respectively). The incidence of adverse events did not differ significantly between the groups. Conclusions Our results suggest that 131 I plus ALSS, MMI plus ALSS or MMI are effective in treating hyperthyroidism and liver failure, and that the addition of ALSS reduces recovery times. Therefore, clinicians can select any of these treatment options based on specific patient characteristics.

Abstract Context Children born to mothers with gestational hypothyroidism or hyperthyroidism may have increased risk of adverse neurodevelopmental outcomes. However, the effects of maternal thyroid status on offspring brain development are unclear. Objective This work aimed to establish whether adolescent brain morphology is affected by suboptimal gestational thyroid function (SGTF). Methods The Controlled Antenatal Thyroid Screening (CATS) study randomly assigned mothers with SGTF to levothyroxine or no supplementation from approximately 12 weeks’ gestation. At age 9, children born to mothers who were overtreated with levothyroxine had a higher risk of conduct and hyperactivity traits. For the current CATS III study, children underwent neuroimaging studies, including T1-weighted structural magnetic resonance imaging (MRI). A total of 85 children aged 11 to 16 years had usable T1-weighted MRI data (exposed to untreated SGTF [n = 21], normal GTF [n = 24], or treated SGTF [optimally treated (n = 21), overtreated (n = 20)]). The primary outcome was to examine the association of SGTF and its treatment with global brain volumes. Secondary and exploratory outcomes were to investigate the association of maternal thyrotropin (TSH) and free thyroxine (FT4) levels with global and subregional brain volumes. Results were adjusted for age, sex, and pubertal scores. Results There were no significant differences in global brain volumetric measures between groups, including total gray matter volume (P = .373). Weak positive correlations were found between maternal TSH, but not FT4, levels and several brain volumes, but these did not survive testing for multiple comparisons. Conclusion We found no evidence that SGTF was associated with differences in adolescent brain morphology, and no effect of levothyroxine supplementation.

Purpose To study the effect of adjuvant lithium on serum thyroxine (T4) concentrations in patients treated with radioactive iodine (RAI) therapy in our environment. Methods This was a prospective simple randomized comparative, experimental cohort study of patients with hyperthyroidism referred for RAI ablation therapy in the two main academic hospitals in Johannesburg between February 2014 and September 2015. Results Amongst the 163 participants in the final analysis, 75 received RAI alone and 88 received RAI with lithium. The difference in mean T4 concentrations at 3 months between the RAI-only group (17.67 pmol/l) and the RAI with lithium group (11.55 pmol/l) was significant with a small effect size ( U  = 2328.5, Z  = −2.700, p  = 0.007, r  = 0.01). Significant decreases in T4 concentrations were observed as early as 1 month after RAI ( p  = 0.0001) in the RAI with lithium group, but in the RAI-only group, significant decreases in T4 concentrations were observed only at 3 months after RAI therapy ( p  = 0.000). Women and patients with Graves’ disease who received RAI with adjuvant lithium also showed significant decreases in T4 concentrations at 1 month ( p  = 0.002 and p  = 0.003, respectively). Conclusion Adjuvant lithium leads to an earlier and better response to RAI therapy with lower T4 concentrations that are achieved earlier. This earlier response and decrease in T4 concentrations were noted in patients with Graves’ disease and nodular goitre, and in women with hyperthyroidism who received adjuvant lithium therapy.

Hyperthyroidism is characterised by increased thyroid hormone synthesis and secretion from the thyroid gland, whereas thyrotoxicosis refers to the clinical syndrome of excess circulating thyroid hormones, irrespective of the source. The most common cause of hyperthyroidism is Graves' disease, followed by toxic nodular goitre. Other important causes of thyrotoxicosis include thyroiditis, iodine-induced and drug-induced thyroid dysfunction, and factitious ingestion of excess thyroid hormones. Treatment options for Graves' disease include antithyroid drugs, radioactive iodine therapy, and surgery, whereas antithyroid drugs are not generally used long term in toxic nodular goitre, because of the high relapse rate of thyrotoxicosis after discontinuation. β blockers are used in symptomatic thyrotoxicosis, and might be the only treatment needed for thyrotoxicosis not caused by excessive production and release of the thyroid hormones. Thyroid storm and hyperthyroidism in pregnancy and during the post-partum period are special circumstances that need careful assessment and treatment.

Abstract Context Invited update on the management of systemic autoimmune Graves disease (GD) and associated Graves orbitopathy (GO). Evidence acquisition Guidelines, pertinent original articles, systemic reviews, and meta-analyses. Evidence synthesis Thyrotropin receptor antibodies (TSH-R-Abs), foremost the stimulatory TSH-R-Abs, are a specific biomarker for GD. Their measurement assists in the differential diagnosis of hyperthyroidism and offers accurate and rapid diagnosis of GD. Thyroid ultrasound is a sensitive imaging tool for GD. Worldwide, thionamides are the favored treatment (12-18 months) of newly diagnosed GD, with methimazole (MMI) as the preferred drug. Patients with persistently high TSH-R-Abs and/or persistent hyperthyroidism at 18 months, or with a relapse after completing a course of MMI, can opt for a definitive therapy with radioactive iodine (RAI) or total thyroidectomy (TX). Continued long-term, low-dose MMI administration is a valuable and safe alternative. Patient choice, both at initial presentation of GD and at recurrence, should be emphasized. Propylthiouracil is preferred to MMI during the first trimester of pregnancy. TX is best performed by a high-volume thyroid surgeon. RAI should be avoided in GD patients with active GO, especially in smokers. Recently, a promising therapy with an anti-insulin-like growth factor-1 monoclonal antibody for patients with active/severe GO was approved by the Food and Drug Administration. COVID-19 infection is a risk factor for poorly controlled hyperthyroidism, which contributes to the infection–related mortality risk. If GO is not severe, systemic steroid treatment should be postponed during COVID-19 while local treatment and preventive measures are offered. Conclusions A clear trend towards serological diagnosis and medical treatment of GD has emerged.

Thyroid disorders are prevalent in pregnant women. Furthermore, thyroid hormone has a critical role in fetal development and thyroid dysfunction can adversely affect obstetric outcomes. Thus, the appropriate management of hyperthyroidism, most commonly caused by Graves disease, and hypothyroidism, which in iodine sufficient regions is most commonly caused by Hashimoto thyroiditis, in pregnancy is important for the health of both pregnant women and their offspring. Gestational transient thyrotoxicosis can also occur during pregnancy and should be differentiated from Graves disease. Effects of thyroid autoimmunity and subclinical hypothyroidism in pregnancy remain controversial. Iodine deficiency is the leading cause of hypothyroidism worldwide. Despite global efforts to eradicate iodine deficiency disorders, pregnant women remain at risk of iodine deficiency due to increased iodine requirements during gestation. The incidence of thyroid cancer is increasing worldwide, including in young adults. As such, the diagnosis of thyroid nodules or thyroid cancer during pregnancy is becoming more frequent. The evaluation and management of thyroid nodules and thyroid cancer in pregnancy pose a particular challenge. Postpartum thyroiditis can occur up to 1 year after delivery and must be differentiated from other forms of thyroid dysfunction, as treatment differs. This Review provides current evidence and recommendations for the evaluation and management of thyroid disorders in pregnancy and in the postpartum period.Thyroid hormone is important during pregnancy, as it facilitates appropriate fetal development. Furthermore, thyroid dysfunction during pregnancy can negatively affect obstetric outcomes and maternal health. This Review discusses the evaluation and management of thyroid disorders in pregnancy and in the postpartum period.

Abstract Context Hyperthyroidism is associated with low levels of cholesterol and triglycerides, and hypothyroidism is associated with hypercholesterolemia and hypertriglyceridemia. Objective The aim of this systematic review was to investigate the impact of therapy for overt and subclinical hyper- and hypothyroidism on serum lipids. Data Sources We searched MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, the Cochrane Database of Systematic Reviews, and Scopus from 1970 through April 5, 2018. Study Selection Pairs of independent reviewers selected randomized and observational studies evaluating lipid parameters in patients undergoing treatment for hyper- or hypothyroidism. Data Extraction Pairs of independent reviewers extracted data and appraised studies. Data Synthesis Treatment of overt hyperthyroidism showed a significant increase in total cholesterol (TC) by 44.50 mg/dL (95% confidence interval [CI]: 37.99, 51.02), low-density lipoprotein cholesterol (LDL-C) by 31.13 mg/dL (95% CI: 24.33, 37.93), high-density lipoprotein cholesterol (HDL-C) by 5.52 mg/dL (95% CI: 1.48, 9.56), apolipoprotein A (Apo A) by 15.6 mg/dL (95% CI: 10.38, 20.81), apolipoprotein B (apo B) by 26.12 mg/dL (95% CI: 22.67, 29.57), and lipoprotein (Lp[a]) by 4.18 mg/dL (95% CI: 1.65, 6.71). There was no significant change in triglyceride (TG) levels. Treatment of subclinical hyperthyroidism did not change any lipid parameters significantly. Levothyroxine therapy in overt hypothyroidism showed a statistically significant decrease in TC by -58.4 mg/dL (95% CI: -64.70, -52.09), LDL-C by -41.11 mg/dL (95% CI: -46.53, -35.69), HDL-C by -4.14 mg/dL (95% CI: -5.67, -2.61), TGs by -7.25 mg/dL (95% CI: -36.63, 17.87), apo A by -12.59 mg/dL (95% CI: -17.98, -7.19), apo B by -33.96 mg/dL (95% CI: 41.14, -26.77), and Lp(a) by -5.6 mg/dL (95% CI: -9.06, -2.14). Levothyroxine therapy in subclinical hypothyroidism showed similar changes but with a smaller magnitude. The studies contained varied population characteristics, severity of thyroid dysfunction, and follow-up duration. Conclusions Treatment of overt but not subclinical hyperthyroidism is associated with worsening of the lipid profile. Levothyroxine therapy in both overt and subclinical hypothyroidism leads to improvement in the lipid profile, with a smaller magnitude of improvement in subclinical hypothyroidism.

ContextSupplemental selenium (Se) may affect the clinical course of Graves disease (GD).ObjectiveEvaluate efficacy of add-on Se on medical treatment in GD.DesignDouble-blind, placebo-controlled, randomized supplementation trial.SettingAcademic endocrine outpatient clinic.PatientsSeventy untreated hyperthyroid patients with GD.InterventionAdditionally to methimazole (MMI), patients received for 24 weeks either sodium selenite 300 µg/d po or placebo. MMI was discontinued at 24 weeks in euthyroid patients.Main Outcome MeasuresResponse rate (week 24), recurrence rate (week 36), and safety.ResultsA response was registered in 25 of 31 patients (80%) and in 27 of 33 (82%) at week 24 [odds ratio (OR) 0.93; 95% confidence interval (CI), 0.26 to 3.25; P = 0.904] in the Se (+MMI) and placebo (+MMI) groups, respectively. During a 12-week follow-up, 11 of 23 (48%) and 12 of 27 (44%) relapsed (OR 1.13; 95% CI, 0.29 to 2.66; P = 0.81) in the Se and placebo groups, respectively. Serum concentrations of Se and selenoprotein P were unrelated to response or recurrence rates. At week 36, 12 of 29 (41%) and 15 of 33 (45%) were responders and still in remission in the Se and placebo groups, respectively (OR 0.85; 95% CI, 0.31 to 2.32; P = 0.80). Serum levels of free triiodothyronine/free tetraiodothyronine, thyroid-stimulating hormone receptor antibody, prevalence of moderate to severe Graves orbitopathy, thyroid volume, and MMI starting dose were significantly lower in responders than in nonresponders. A total of 56 and 63 adverse events occurred in the Se and placebo groups, respectively (P = 0.164), whereas only one drug-related side effect (2.9%) was noted in 35 patients on placebo + MMI.ConclusionsSupplemental Se did not affect response or recurrence rates in GD.This double-blind, placebo-controlled supplementation trial demonstrated no effect of an add-on relevant daily dose of selenium on hyperthyroid patients with Graves disease.