Thyroid disease: assessment and management

This guideline covers investigating all suspected thyroid disease and managing primary thyroid disease (related to the thyroid rather than the pituitary gland). It does not cover managing thyroid cancer or thyroid disease in pregnancy. It aims to improve quality of life by making recommendations on diagnosis, treatment, long-term care and support.

Isoflavin-ß modifies muscle oxidative stress and prevents a thyrotoxicosis-induced loss of muscle mass in rats.

INTRODUCTION: We sought to verify whether isoflavin-beta (Iso-ß), a mixture of isoflavones with antioxidant properties, could prevent thyrotoxicosis-induced loss of muscle mass and the participation of oxidative stress (OS) in the mechanisms of this prevention. METHODS: Two experimental periods of thyrotoxicosis induction were used in Wistar rats: 3 and 5 days to assess Iso-ß effects before and after thyrotoxicosis-induced muscle wasting. After euthanasia, peritoneal fat and gastrocnemius muscle were collected, weighed, and muscle OS was assessed. RESULTS: Iso-ß prevented the loss of gastrocnemius mass in thyrotoxic rats through the prevention of muscle OS generation during thyrotoxicosis, increasing muscle total antioxidant capacity and decreasing mitochondrial cytochrome c oxidase activity, lipid peroxidation, and protein carbonyl content. CONCLUSION: Iso-ß decreased oxidative modification of proteins, which is known to exert a major role during proteolysis induction and is present in thyrotoxic myopathy, highlighting the potential action of Iso-ß in this complication of the disease. Muscle Nerve 56: 975-981, 2017.

2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis.

BACKGROUND: Thyrotoxicosis has multiple etiologies, manifestations, and potential therapies. Appropriate treatment requires an accurate diagnosis and is influenced by coexisting medical conditions and patient preference. This document describes evidence-based clinical guidelines for the management of thyrotoxicosis that would be useful to generalist and subspecialty physicians and others providing care for patients with this condition. METHODS: The American Thyroid Association (ATA) previously cosponsored guidelines for the management of thyrotoxicosis that were published in 2011. Considerable new literature has been published since then, and the ATA felt updated evidence-based guidelines were needed. The association assembled a task force of expert clinicians who authored this report. They examined relevant literature using a systematic PubMed search supplemented with additional published materials. An evidence-based medicine approach that incorporated the knowledge and experience of the panel was used to update the 2011 text and recommendations. The strength of the recommendations and the quality of evidence supporting them were rated according to the approach recommended by the Grading of Recommendations, Assessment, Development, and Evaluation Group. RESULTS: Clinical topics addressed include the initial evaluation and management of thyrotoxicosis; management of Graves' hyperthyroidism using radioactive iodine, antithyroid drugs, or surgery; management of toxic multinodular goiter or toxic adenoma using radioactive iodine or surgery; Graves' disease in children, adolescents, or pregnant patients; subclinical hyperthyroidism; hyperthyroidism in patients with Graves' orbitopathy; and management of other miscellaneous causes of thyrotoxicosis. New paradigms since publication of the 2011 guidelines are presented for the evaluation of the etiology of thyrotoxicosis, the management of Graves' hyperthyroidism with antithyroid drugs, the management of pregnant hyperthyroid patients, and the preparation of patients for thyroid surgery. The sections on less common causes of thyrotoxicosis have been expanded. CONCLUSIONS: One hundred twenty-four evidence-based recommendations were developed to aid in the care of patients with thyrotoxicosis and to share what the task force believes is current, rational, and optimal medical practice.

Thyroid Hormone Therapy and Risk of Thyrotoxicosis in Community-Resident Older Adults: Findings from the Baltimore Longitudinal Study of Aging.

BACKGROUND: Both endogenous and exogenous thyrotoxicosis has been associated with atrial fibrillation and low bone mineral density. Therefore, this study investigated the risk factors associated with prevalent and incident thyrotoxicosis and the initiation of thyroid hormone therapy in a healthy, aging cohort. METHODS: A total of 1450 ambulatory community volunteer participants in the Baltimore Longitudinal Study of Aging examined at the NIA Clinical Research Unit in Baltimore, MD, have undergone longitudinal monitoring of serum thyrotropin (TSH) and thyroid hormone (free thyroxine and free triiodothryonine) levels as well as medication use every one to four years, depending on age, between 2003 and 2014. RESULTS: The prevalence of low TSH was 9.6% for participants on thyroid hormone and 0.8% for nontreated individuals (p < 0.001). New cases occurred at a rate of 17.7/1000 person-years of exposure to thyroid hormone therapy [CI 9-32/1000] and 1.5/1000 person-years in the unexposed population [CI 0.7-2.9/1000]. Women were more likely to be treated and more often overtreated than men were. The adjusted hazard ratio (HR) for thyrotoxicosis between treated and untreated women was 27.5 ([CI 7.2-105.4]; p < 0.001) and 3.8 for men ([CI 1.2-6.3]; p < 0.01). White race/ethnicity and older age were risk factors for thyroid hormone therapy but not overtreatment. Body mass index was not associated with starting therapy (HR = 1.0). Thyroid hormone initiation was highest among women older than 80 years of age (3/100 person-years). For one-third of treated participants with follow-up data, overtreatment persisted at least two years. CONCLUSIONS: Iatrogenic thyrotoxicosis accounts for approximately half of both prevalent and incident low TSH events in this community-based cohort, with the highest rates among older women, who are vulnerable to atrial fibrillation and osteoporosis. Physicians should be particularly cautious in treating subclinical hypothyroidism in elderly women in light of recent studies demonstrating no increased risk of cardiovascular morbidity or death for individuals with elevated TSH levels <10 mIU/L.

Tiroiditis posparto. Revisión / Postpartum thyroiditis. A review

La tiroiditis posparto (TPP) es una disfunción tiroidea transitoria de etiología autoinmune que se presenta de forma típica en el primer año tras el parto en mujeres sin enfermedad tiroidea conocida antes del embarazo. Puede cursar con síntomas de tirotoxicosis seguida de hipotiroidismo y recuperación posterior de la función tiroidea, o como tirotoxicosis o hipotiroidismo aislados. Un gran porcentaje de las pacientes que presentan TPP reproducirán esta enfermedad tras los siguientes embarazos. Una gran proporción de mujeres desarrollará hipotiroidismo permanente durante los 3-10 años siguientes a un episodio de TPP. Es importante para el médico de familia estar familiarizado con esta enfermedad, por su gran prevalencia, y para un correcto diagnóstico e intervención terapéutica. Es fundamental también su papel en el seguimiento de estas pacientes, dadas las implicaciones negativas que el hipotiroidismo establecido tiene sobre la reproducción, en una población en edad genésica. En este artículo se revisan las características principales de la TPP, así como su abordaje diagnóstico y terapéutico (AU)

Postpartum thyroiditis (PPT) is a transient thyroid dysfunction of autoimmune origin that can occur in the first year postpartum in women who have not been previously diagnosed with thyroid disease. It may start with clinical thyrotoxicosis followed by hypothyroidism and the subsequent recovery of thyroid function, or may just appear as isolated thyrotoxicosis or hypothyroidism. PPT recurs in high percentage of patients after subsequent pregnancies. Many women develop permanent hypothyroidism sometime during the 3 to 10 year period after an episode of PPT. It is important for family physicians to be familiar with this disease, due to its high prevalence in order to make a correct diagnosis and therapeutic intervention. Family doctors also play a crucial role in the monitoring of these patients, given the negative implications of established hypothyroidism on reproduction in the female population during their reproductive years. This article reviews the principle characteristics of PPT along with its diagnosis and treatment (AU)

[Thyroid disorders during pregnancy]. / Schilddrüsenerkrankungen in der Schwangerschaft.

Thyroid disorders may not only be the cause infertility but also increases the incidence of miscarriages and the morbidity of the pregnancies. During pregnancy the demand of thyroid hormones increases to about 30 - 50 % and the thyroid has to cope with this increase. In Germany the iodine intake has improved significantly during the last 20 years, but still is borderline low with an mean intake of about 120 microg iodide per day. Therefore it is still recommended that pregnant women are supplemented with about 100 - 150 microg of iodide during pregnancy and the time of breast-feeding, to avoid hypothyroidism of the foetus with concomitant delay of the brain development. Not only women with subclinical hypothyroidism, but only elevated TPO antibodies have a significant increase in early miscarriage and preterm delivery. An early supplementation with Levothyroxin despite euthyroidism might reduce these risks. Those women also more frequently develop postpartum thyroiditis. This risk can be reduced by a supplementation with selenium during and after pregnancy. Graves' disease is a rare disorder and only about 0,1 - 0,4 pregnancies are affected. The course of the disease is biphasic, with an exacerbation within the first trimester and an improvement thereafter, but a recurrence after delivery. Overt thyrotoxicosis has to be treated with propylthiouracil, to maintain euthyroidism during pregnancy. The TSH receptor antibodies are transferred to the foetus with the risk of thyrotoxicosis. Special care of the foetus is therefore necessary. Transient mild hyperthyroidism may occur in women with very high HCG levels during the first three months of pregnancy. This often is associated with hyperemesis gravidarum. Subclinical hypothyroidism of the mother will disturb the normal development of the foetus and therefore has to be treated even when TSH is within the upper normal level. Special care is necessary in women with elevated TPO antibodies, because these more often develop postpartum thyroiditis.

IFNalpha-induced recurrence of Graves' disease ten years after thyroidectomy in chronic viral hepatitis C. Case report.

In contrast to chronic or subacute thyroiditis, Graves' disease rarely complicates IFN-alpha therapy for chronic viral C hepatitis. We report the case of a 51-year-old man in whom IFN-alpha treatment was followed by recurrence of Graves' disease 10 years after thyroidectomy was performed and the patient was declared cured. Despite severe thyrotoxicosis, combined IFN-alpha and ribavirin therapy was continued and radioiodine treatment was considered for Graves' disease.

[Suggestions for prevention of adverse reactions after intravasal administration of iodinated contrast media]. / Empfehlungen zur Prophylaxe der Nebenwirkungen bei intravasaler Applikation jodhaltiger Kontrastmittel. Suggestions for prevention of adverse reactions after intravasal administration of iodinated contrast media.

Iodinated contrast media are widely used in computed tomography and angiography. Adverse reactions such as contrast-medium induced nephropathy (CIN), anaphylactoid reactions and iodine-induced thyrotoxicosis are associated with intravasal administration of contrast agents. Iodinated contrast agents are generally considered to be safe, but in rare cases they can cause severe life threatening situations. In this review we present an overview about the incidence, pathways, and risk factors of adverse reactions. Simple schemes including hydration protocols for prevention of CIN, medication for prophylaxis of iodine-induced thyrotoxicosis with thyreostatics and anaphylactoid reactions with histamine antagonists and corticosteroids are suggested.

[Development of neonatal Graves' disease--prediction, prevention and treatment].

It is well known that neonatal hyperthyroidism or neonatal Graves' disease is caused by trans-placental transfer of TSH receptor antibodies. The antibodies stimulate the thyroid gland in the fetal and neonatal stages, which induces hyperfunction of the thyroid gland and increased thyroid hormone production. In this paper, I would like to focus on four clinically interesting issues related neonatal hyperthyroidism. 1. High risk of mothers whose infants develop neonatal Graves' disease. 2. How to predict for development of neonatal Graves' disease. 3. How to prevent for development of neonatal Graves' disease. 4. How to treat the infants with Graves' disease. I also mention on the neonatal thyrotoxicosis and fetal hyperthyroidism.

[Incidence and predictors of thyroid dysfunction caused by long-term intake of amiodaron].

AIM: To analyze occurrence of thyroid dysfunction due to regular long-term intake of amiodaron (for one year), to search for predictors of amiodaron-induced hypothyroidism and thyrotoxicosis. MATERIAL AND METHODS: Sixty two patients with different types of arrhythmia have undergone examination including tests for TTH (once in three months), free T3 and T4 (once in 6 months), ultrasound thyroid investigation, general clinical and physical check-up, resting ECG in 12 leads, echocardiography, chest x-ray, biochemical blood tests, blood count, urinalysis. RESULTS: Amiodaron intake for 1 year was associated with amiodaron-induced thyroid dysfunction in 25% patients: 19.2% developed hypothyroidism, 5.8%--thyrotoxicosis. Organic pathology of cardiovascular system, cardiac failure, left ventricular aneurysms, low global myocardial contractility, organic thyroid pathology, elevated levels of antithyroid antibodies predicted hypothyroidism. Thyrotoxicosis was associated with a young age and male sex. CONCLUSION: Amiodaron may cause thyroid dysfunction in patients with arrhythmia.

Amiodarone-induced thyrotoxicosis due to destructive thyroiditis: therapeutic recommendations.

BACKGROUND: Amiodarone-induced thyrotoxicosis (AIT) type 1 occurs in subjects with an underlying thyroid disease, whereas type 2 AIT is a form of destructive thyroiditis. Our hypothesis was that the common practice of thyroid testing before prescription of amiodarone would reduce the incidence of pure type 1 AIT, though a stringent classification may be difficult (mixed type AIT). MATERIALS AND METHODS: Thyroid testing before and after treatment of AIT (n = 12) and the response to combined antithyroid and glucocorticoid treatment (n = 11) were recorded in a consecutive series of patients seen at a university hospital. RESULTS: Some criteria for type 1 AIT were fulfilled in 3 patients, but the diagnosis of a mixed form AIT was more likely in 2 of these. Type 2 AIT was diagnosed in the other 9 patients, while 6 patients had diffuse hypoechoic goitre. The median time to euthyroidism (defined as normal fT3 concentration) under thionamide and prednisolone (starting dose 20 to 75 mg/d) was 2 months (interquartile range 1 to 2.7 months). Thionamide treatment was stopped after a median duration of 5.7 months (interquartile range 4.2 to 8.7 months) and glucocorticoids were completely withdrawn after 6.7 months (5.5 to 8.7 months). CONCLUSIONS: Nowadays, isolated type 1 AIT is rarely found and destructive thyroiditis (as type 2 AIT or mixed form) is the predominant cause of AIT. To accelerate recovery, we prescribed thionamide and glucocorticoids simultaneously as first-line therapy once contraindications for the use of steroids had been ruled out.

Scintigraphy for risk stratification of iodine-induced thyrotoxicosis in patients receiving contrast agent for coronary angiography: a prospective study of patients with low thyrotropin.

The risk of iodine-induced thyrotoxicosis in euthyroid patients receiving iodine-containing contrast agents is known to be low, but data on this risk in patients with latent hyperthyroidism are scarce. We investigated the role of thyroid scintigraphy using Tc-99m preceding the application of iodine-containing contrast material to estimate the risk of iodine-induced thyrotoxicosis in patients with low levels of TSH. In a prospective study on 91 patients, thyroid scintigraphy was performed before coronary angiography (CA). In patients with technetium thyroid uptake (TCTU) less than 1%, CA was done without prophylactic drugs (n = 56). Patients with TCTU greater than 1% were treated either with 900 mg of perchlorate or, depending on the autonomous volume, combined with 20 to 60 mg thiamazole. In the 56 patients with TCTU less than 1%, no case of iodine-induced hyperthyroidism occurred within 4 wk after CA. In the patients who received prophylactic drugs, two cases of mild thyrotoxicosis were observed. Our data suggest that in patients with low levels of TSH, the risk of hyperthyroidism after application of iodine-containing contrast media is negligible if TCTU is less than 1%. In these patients, CA can be performed without administration of prophylactic drugs.

Iodine repletion, thyrotoxicosis and atrial fibrillation in Isfahan, Iran.

BACKGROUND: Iodized salt was reintroduced in Iran in 1989. Just before distribution of iodized salt, thyrotoxicosis was observed in 3.7% of the patients with atrial fibrillation (AF) in university teaching hospitals in Isfahan, a centrally located city in Iran. As repletion of iodine may increase the rate of autoimmune thyroid diseases and toxic multinodular goiter, this study was designed to evaluate the rate of thyrotoxicosis in patients with AF in the same hospitals after about a decade of iodized salt consumption. METHODS: In a case-control study with convenience sampling, 100 patients with AF and an equal number of age- and sex-matched subjects taking the same medications were selected as case and control groups, respectively, in university hospitals in 1997. RESULTS: Eight percent of patients with atrial fibrillation had overt thyrotoxicosis versus one percent in the control group (odds ratio=8.6, 95% CI = 6.5 to 10.7, P<0.02). Thyrotoxicosis in patients with AF was 8 times higher than in the control group without AF. In comparison with the period before use of iodized salt, AF more than doubled (8% vs. 3.7%). CONCLUSION: Thyroid function should be evaluated in all patients older than 40 years of age with AF. The benefits of iodine supplementation are great, but more attention should be paid to the complications of iodine repletion, including thyrotoxicosis and its frequent accompaniment, AF.

Radioiodine ablation of the thyroid to prevent recurrence of amiodarone-induced thyrotoxicosis in patients with resistant tachyarrhythmias.

UNLABELLED: Amiodarone-induced thyrotoxicosis (AIT) is a common complication of amiodarone therapy. Although permanent withdrawal of amiodarone is recommended due notably to the risk of worsening of tachyarrhythmias, some patients may require the reintroduction of amiodarone several months after normalizing their thyroid function. We, retrospectively, assessed the effects of (131)I therapy to prevent recurrence of AIT in euthyroid patients requiring reintroduction of amiodarone. SUBJECTS AND METHODS: Amiodarone was required in 10 cases of recurrent symptomatic paroxysmal atrial fibrillation (AF) and in 5 cases of ventricular tachycardia (VT) (M = 12, F = 3, mean age: 63 +/- 14). The underlying heart disease was dilated cardiomyopathy (n = 4), ischaemic heart disease (n = 4), hypertensive heart disease (n = 2), arrhythmogenic right ventricular dysplasia (n = 27) and valvulopathy (n = 1). Two patients had idiopathic paroxysmal AF. RESULTS: A mean (131)I dose of 579 +/- 183 MBq was administered 34 +/- 37 after the episode of AIT. Amiodarone was reintroduced in 14 of 15 patients after a mean interval of 103 +/- 261 d. Fourteen patients developed definite hypothyroidism necessitating l-thyroxine but we observed no late recurrence of AIT. After a mean follow-up of 22 +/- 16 months, tachyarrhythmias were controlled in 12 of 14 patients. CONCLUSION: (131)I therapy appears to be an effective and safe approach to prevent the recurrence of AIT in a patient requiring the reintroduction of amiodarone for tachyarrhythmias.

Effect of iodinated contrast media on thyroid function in adults.

Excess free iodide in the blood (ingested or injected) may cause thyrotoxicosis in patients at risk. Iodinated contrast medium solutions contain small amounts of free iodide and may be of significance for patients at risk. The free iodide may also interfere with nuclear medicine diagnostic studies and treatment. Therefore the Contrast Media Safety Committee of the European Society of Urogenital Radiology reviewed the literature on this subject in order to prepare guidelines. A report and guidelines were prepared based on an extensive Medline search. The report was discussed with the participants attending the Tenth European Symposium on Urogenital Radiology, Uppsala, Sweden, September 2003. Contrast medium induced thyrotoxicosis is rare. Contrast medium injection does not affect thyroid function tests (e.g., T3, T4, TSH) in patients with a normal thyroid. Routine monitoring of thyroid function tests before contrast medium injection in patients with a normal thyroid is not indicated even in areas where there is dietary iodine deficiency. Patients at risk of developing thyrotoxicosis after contrast medium injection are patients with Graves' disease and patients with multinodular goiter with thyroid autonomy, especially elderly patients and patients living in areas of iodine deficiency. Patients at high-risk should be carefully monitored by endocrinologists after contrast medium examinations. Prophylaxis in these groups is not generally recommended, although it may offer some protection in selected high-risk individuals. The free iodide load of contrast media injections interferes with iodide uptake in the thyroid and therefore compromises diagnostic thyroid scintigraphy and radio-iodine treatment of thyroid malignancies for 2 months after administration of contrast media. Simple guidelines on the subject are proposed.

[Assessment of early immunosuppressive therapy in the prevention of complications of Graves' disease]. / Ocena wczesnego zastosowania leczenia immunosupresyjnego w zapobieganiu powiklaniom choroby Graves-Basedowa.

UNLABELLED: Regardless the autoimmune origin of Graves' disease, the preferred method of its treatment remains antithyroid drug administration. Use of immunosuppressive agents (mostly steroids) is still limited to the therapy of disease complications, such as proliferative ophthalmopathy. The aim of the study was to assess the influence of early immunosuppressive treatment of autoimmune thyrotoxicosis with azathioprine on the course of the disease and the incidence of its complications. The study comprised 64 patients (47 females and 17 males aged 20-43 years) for the first time diagnosed with Graves' disease. The subjects were randomised into two groups. Group I consisted of 28 patients treated only with antithyroid drugs, the remaining 36 subjects additionally receiving azathioprine were included into group II. The dose of both drugs was adjusted during the treatment according to metabolic status of each patients. The treatment was continued for 8-14 months, the follow-up duration after therapy withdrawal was 5 years. Euthyreosis was achieved in all patients 2-8 weeks after treatment initiation. No drug intolerance symptoms were observed in group I. In four patients additionally treated with azathioprine, gastrointestinal side effects or leucopenia were present. The disease relapse was observed during the follow-up period in 15 (53.5%) patients of group I and in 3 (8.3%) of group II, the difference was statistically significant (p<0.01). Only one patient receiving additionally azathioprine presented ophthalmic symptoms compared with seven subjects (25%) treated only with antithyroid drugs (p<0.001). The patients of group I were also more frequently referred to surgical treatment due to rapid goitre growth (accordingly 5 (17.8%) and 1 (2.7%) patients, p=0.07), the difference between both groups not being statistically significant. CONCLUSIONS: Additional early immunosuppressive treatment significantly decreased frequency of Graves' disease complications and thyrotoxicosis recurrence. The use of azathioprine may be advised in patients with contraindications to the radical Graves' disease treatment and in prophylaxis of its complications.