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Objective: The objective of this study is to clarify the clinical features of thyroid dysfunction observed in patients with autoimmune pancreatitis (AIP)., Methods: We repeatedly examined thyroid function in 74 patients with type 1 AIP (58 males, 16 females; average onset age of AIP 67 years). Clinical and serological findings in patients with thyroid dysfunction were analyzed., Results: During follow-up, clinical and subclinical hypothyroidism were observed in 3 and 17 patients, respectively. Clinical and subclinical hyperthyroidism were observed in 5 and 1 patients, respectively. One patient showed clinical hyperthyroidism followed by subclinical hypothyroidism. All patients with clinical and subclinical hypothyroidism were asymptomatic and required no medical treatment, whereas four patients with clinical hyperthyroidism were symptomatic and received treatment with thiamazole., Conclusion: Frequent hypothyroidism in AIP, which was previously reported, was confirmed. Moreover, in this study, the association between hyperthyroidism and AIP was demonstrated. Hyperthyroidism in AIP may be more clinically significant than hypothyroidism because patients frequently require medical treatment., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Thyroid adenoma is commonly associated with surgery and radiometabolic treatment; recently, according to previous successful reports, percutaneous ethanol injection therapy under sonographic guidance, has been introduced as an alternative. This technique has already been favourably used in the treatment of focal lesions, such as liver cancer and hyperparathyroidism. In our experience, we have treated with such therapy 69 patients affected by thyroid adenoma (55 females, 14 males; 28 pretoxic, 41 toxic). Ethanol (0.5-2.8 mL/mL nodular tissue) was injected, under sonographic guidance, in 4-9 sessions (1 weekly). Thyroid hormone profile was assessed during treatment and at 3 and 6 months follow-up. Apart from local transient pain in 21% sessions, two cases of pyrexia (38.5 degrees-1 day) and 3 cases of transient dysphonia, no relevant adverse effects were observed. A slight thyroid hormone increase was seen in both groups immediately following treatment. Six months after therapy a biochemical and clinical remission of hyperthyroidism was observed in 33 out of 41 toxic patients (80%); a significant increase of TSH levels was seen in both groups (p < 0.001). With follow-up, significant volume shrinkage (70-80% volume reduction--p < 0.0001) as well as structural alterations of the nodule, were consistently recorded at sonography, in both groups; a linear relationship (p < 0.0001) between pretreatment volume and volume reduction was found. At scintiscan functional activity of extranodular parenchyma was found in 75% of patients affected by pretoxic adenoma and in 63.1% of patients with toxic adenoma. These data confirm that percutaneous ethanol injection therapy is effective in obtaining functional ablation and in inducing remission of hyperthyroidism, when present; so it represents a valid and safe alternative to standard therapeutic tools of thyroid adenoma.

Responsiveness to synthetic thyrotropin-releasing hormone (TRH), thyroid suppressibility by triiodothyronine (T3) and the outcome of hyperthyroidism following prolonged therapy with thionamides were studied in a group of 35 patients with toxic diffuse goiter. TRH and T3 suppression tests were performed 10 days to 24 months (mean 4 months) after withdrawal of antithyroid drugs. Nineteen patients were euthyroid and had a normal thyrotropin (TSH) response to TRH, while 4 were recovering from mild hypothyroidism due to overtreatment and had an exaggerated response. No response was observed in 12 patients with recurrent hyperthyroidism. Positive T3 suppression tests were found only in 10 of the 30 cases examined. Peak and net 2 h secretion responses of TSH to TRH exhibited a significant inverse correlation with the levels of serum thyroxine and serum triiodothyronine, but were unrelated to the degree of thyroid suppressibility. Relapse or recurrence of thyrotoxicosis occurred in at least 9 of the 23 patients having no evidence of hyperthyroidism at the time of TRH test. Each of them was found to be responsive to TRH, while the T3 suppression test was negative in 8 and had to be discontinued in one because of thyrotoxic symptoms. The present data indicate that during the early period after completion of a prolonged course of antithyroid drug therapy responsiveness to TRH in toxic diffuse goiter is: a) correlated with circulating thyroid hormones, b) unrelated to the degree of thyroid suppressibility by T3 and c) of little value in predicting the long-term results of treatment.

Hypothyroidism is often observed after radioiodine treatment in Graves' disease, but it is considered a rare complication in single hyperfunctioning thyroid nodule ('hot' nodule). This concept has been recently challenged, but the available data are conflicting. In the present study we therefore assessed the development of permanent hypothyroidism in 126 patients with thyroid hot nodule treated with 131I (180 muCi/g of estimated nodule weight, total dose 5.5-28.9 mCi). Follow-up ranged between 1 to 11 years. Hypothyroidism was observed in 5 (4%) patients, corresponding to a cumulative incidence by life-table analysis of 4.8% ten years after treatment. No relationship was found between the development of hypothyroidism and the size of the nodule or the total amount of administered dose. Fifty-six patients with euthyroid hot nodule at the time of treatment had higher cumulative incidence of hypothyroidism after 10 years (9.7%) than those with toxic adenoma (1.5%) (0.1 greater than P greater than 0.05 by logrank test). When the patients were analyzed according to the presence or absence of serum antithyroglobulin and/or antithyroid microsomal autoantibodies, the prevalence of hypothyroidism after 131I treatment was higher (4/25 = 16%) in patients with significant serum antibody titres (greater than or equal to 1/400 by passive haemagglutination), when compared to that observed in subjects with negative antibody tests (1/101 = 1.0%). Life-table analysis showed in antibody positive patients a cumulative incidence of hypothyroidism after 10 years of 18.0% vs 1.4% in antibody negative patients (P less than 0.001 by logrank test).(ABSTRACT TRUNCATED AT 250 WORDS)

The serum free thyroxine concentration was measured by direct radioimmunoassay in 38 untreated T3-thyrotoxic patients with elevated serum total and free triiodothyronine, normal serum thyroxine and free thyroxine index, no TSH response to TRH, and with clinical evidence of hyperthyroidism. An elevation of circulating free thyroxine values was observed in 58% of the patients, whereas total serum thyroxine concentration was within the normal range. It is suggested, therefore, that T3-thyrotoxicosis should be reserved for patients with elevated serum total T3 and free T3 concentrations and normal serum total T4 and free T4 concentrations. Serum thyroxine-binding globulin concentrations were significantly lower (P less than 0.025) in patients with an elevated serum free thyroxine (18.7 +/- 3.6 micrograms/ml: mean +/- SD) as compared with those in patients with a normal free thyroxine concentration (23.4 +/- 2.6 micrograms/ml). In addition, no daily fluctuations in total and free thyroxine concentration were observed in 6 patients over a 4-8 day period.

Amiodarone associated thyrotoxicosis (AAT) occurs in approximately 10% of patients treated with this iodine rich drug in areas of mild iodine deficiency. The thyroid radioactive iodine uptake (RAIU) is usually undetectable or very low in iodine-induced thyrotoxicosis. In the present study, 35 patients with AAT were evaluated. Twelve patients had no thyroid abnormalities by physical exam and all had 24-hr RAIU less than or equal to 4%. In contrast, nine of 11 patients with AAT and diffuse goiters and eight of 12 patients with AAT and nodular goiters had RAIU values greater than 8%. In patients with AAT and goiter it appears possible that the thyroid fails to adapt normally to the excess iodide load, resulting in an inappropriately high RAIU in the presence of excess plasma iodine.

Thyroid function plays a seminal role in the growth and development of children, and alterations in signaling pathways which interfere with the biosynthesis, transport, and metabolism of thyroid hormones might impact on the skin of such patients: this review explores the relationship between different thyroid disorders and dermatological manifestations with a particular focus on the pediatric population. Common cutaneous conditions associated with thyroid dysfunction may include chronic urticaria, vitiligo, and alopecia, which can be early harbingers of an underlying endocrine disruption. This review also highlights the growing cognizance of a "thyroid–skin axis", with thyroid hormones influencing many physiologic processes within the skin such as keratinocyte proliferation, hair growth, and epidermal differentiation. A precocious recognition of abnormal dermatological signs can be crucial in pediatric patients for a timely diagnosis before any development of complications and for personalized treatments of an underlying thyroid disorder, which can even be symptomless at an initial phase. Despite the lack of standardized guidelines for managing dermatologic manifestations occurring in thyroid diseases, a regular screening to identify endocrine dysfunction is recommended in those children who present chronic urticaria, vitiligo, or alopecia, though further research is needed to decipher mechanisms involved in the thyroid-skin partnership and develop more targeted management approaches. [ABSTRACT FROM AUTHOR]

Background: Thyroid hormones are crucial for growth, brain development, reproduction, and the regulation of energy metabolism. The iodoglycoprotein thyroglobulin (Tg) plays a critical role in allowing the thyroid gland to synthesize the thyroid hormones T3 and T4 in humans. Thyrotoxicosis has a wide range of etiologies, symptoms, and therapeutic options. Therefore, a precise diagnosis is necessary for effective treatment. In addition to a thyroid function test (TFT), evaluation for identifying common causes of thyrotoxicosis also includes a thyroid ultrasound that measures thyroidal blood flow, a radioactive iodine uptake test, a thyrotropin receptor autoantibody (TRAb) test, and a 99mTc pertechnetate scan. We hypothesize that Tg levels may be elevated in hyperthyroidism, which includes Graves' disease (GD) and toxic multinodular goiter (TMNG), as there is an increase in thyroid synthesis and secretion. In thyrotoxic phases of thyroiditis, Tg levels could be normal. Objective: This study aimed to evaluate serum Tg levels in differentiating hyperthyroid and thyrotoxic phases of thyroiditis. Methods: In this study, 30 subjects with newly detected untreated thyrotoxicosis were evaluated. Serum Tg, TFT, TRAb, Anti-TPO, and technetium scan were done. Results: Our study results revealed that the Median Tg was highest in the subjects with toxic nodular goiter (356 ng/ml), followed by GD (150.40 ng/ml); those with subacute thyroiditis had the lowest Tg level (7.42 ng/ml); the differences in median Tg levels across the three groups were also statistically significant (P < 0.01). TRAb was significantly higher in people with GD in comparison to TMNG and thyroiditis. In addition, GD patients with a higher titter value of TRAb have elevated levels of Tg. Conclusion: Serum Tg levels can be utilized as a potent marker to distinguish between different types of thyrotoxicosis. [ABSTRACT FROM AUTHOR]

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Thyroid pathology is characterized by abnormal values of thyroid hormones that can affect the brain and can lead to cognitive impairment (attention, memory, mood), depression and anxiety. The aim of the study is to evaluate the association between the cognitive disorders and thyroid disease and the link between thyroid hormone levels FT4 and TSH in depression and anxiety. We included 130 individuals from Endocrinology Clinic of Craiova, over a period of 6 years (2014-2020), none of whom was taking thyroid medication and antidepressants. The most important symptom found in thyroid pathology is depression, which occurs in those with long-lasting illness. We obtained that 45.38% of the cases were diagnosed with depression and 46.92% with anxiety. Depressive symptoms were assessed with Hamilton scale and anxiety symptoms with the Beck scale. Regarding the impaired cognitive function, we found it in 34.7% of cases of hypothyroidism (loss of memory / lack of concentration) and for the cases with hyperthyroidism, we found changes in 51,42%. [ABSTRACT FROM AUTHOR]

The course and pathogenesis of Graves' disease and Graves' ophthalmopathy are interdependent, influencing each other's therapeutic choices. Multiple factors including geographic location, access to medical services, patient and physician preferences influence the management of these conditions. Graves' disease is classically managed with one of three treatment options - antithyroid drugs, radioactive iodine, and thyroidectomy. In recent years, there has been a shift towards antithyroid drugs, including long term therapy with these agents, given the advantage of avoiding hypothyroidism and the apparent safety of this approach. In addition, new therapies are (slowly) emerging, focusing on immunomodulation. Technological advances are opening doors to non-pharmaceutical interventions that aim to deal with both structural thyroid abnormalities as well as biochemical abnormalities of hyperthyroidism. Graves' ophthalmopathy management is guided by its activity and severity status, with treatment options including smoking cessation, control of hyperthyroidism, local eye measures, glucocorticoids, selenium, orbital radiotherapy, and surgery. In addition to these established treatment choices, new immunotherapy- based approaches are being tested. Some of them (tocilizumab and teprotumumab) are very promising but further evaluation is needed before we can establish their role in clinical care. Agents identified as beneficial in Graves' disease management will likely be tested in Graves' ophthalmopathy as well. In the coming years, our main clinical responsibility will be to find the proper balance between the benefits and potential risks of these incoming therapies, and to identify the subgroups of patients where this ratio is most likely to favor a safe and successful therapeutic outcome. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Copyright of Molecular Imaging & Radionuclide Therapy is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The medical treatment of Graves' orbitopathy (GO) is usually reserved to moderate to severe disease. Steroids have been widely employed and possess anti-inflammatory activity, but about 20-30% of patients are not responsive and about 20% present with disease recurrence. Immunosuppressive therapy alternative to corticosteroids may target the different antigens involved in pathogenic mechanisms of GO. Some have already been employed in clinical studies and showed interesting results, although the lack of randomized and controlled trials suggests caution for their use in clinical practice. Potential targets for therapy in GO are the TSH receptor and the IGF-1 receptor on the fibroblasts, inflammatory cytokines, B and T cells. Most promising results are obtained by interacting with the PIK3/mTORC1 signaling cascades for adipogenesis and the anti-IGF-1R with the monoclonal antibody teprotumumab. A recent open study has shown that tocilizumab, an anti-sIL-6R antibody, inactivates GO. Consistent reports on the efficacy of rituximab have recently been challenged by randomized controlled trials. Clinical practice will greatly benefit from the use of disease modifying agents in GO, as compared to steroids, currently standard treatment for GO. Among these, rituximab may be useful, especially in patients resistant to steroid or with contraindications to steroids. However, larger randomized controlled trials are needed for definitive data on the potential disease-modifying role of rituximab in GO. Direct targeting of the orbital fibroblast via immunosuppression or nonimmunosuppressive drugs is emerging as a promising alternative. [ABSTRACT FROM AUTHOR]

Background: Ectopic TSH-secreting pituitary adenoma (TSH-oma) is a very unusual disorder. To date, there are only four cases reported. It is difficult to distinguish ectopic cases from both regular TSH-omas and resistance to thyroid hormone (RTH). Case presentation: A newly identified case of ectopic TSH-oma arising from the nasal pharynx was described, and reports of four prior cases were reviewed. The patient was a 41-year-old male who developed what appeared to be typical hyperthyroidism and atrial fibrillation in 2009. Thyroid function tests showed elevated basal levels of free T3 (FT3, 24.08 pmol/L), free T4 (FT4, 75.73 pmol/L), and serum TSH (7.26 μIU/ml). Both TSH-oma and resistance to thyroid hormone syndrome were considered. TRH stimulating test was negative, whereas octreotide inhibition test showed a reduction in TSH by 30.8%. Furthermore, a large space-occupying lesion located at the nasopharynx was found by computed tomography and magnetic resonance imaging (MRI). A normal pituitary was visualized. Ectopic TSH-oma was preliminarily established. Using an endoscopic endonasal approach, the tumor was resected. Histological features and immunophenotypes were consistent with those of TSH-secreting tumor. The levels of both free thyroxine and TSH returned to normal ranges the day after surgery and remained within normal range for 48 months. Conclusions: Although exceedingly rare, ectopic TSH-oma should be considered for patients with inappropriate secretion of TSH with hyperthyroidism and pituitary tumor undetectable by computed tomography and MRI. To our knowledge, this is the first case followed up more than 4 years. The characteristics and successful interventions summarized in this report provide a guideline for clinicians. [ABSTRACT FROM AUTHOR]

Introduction: The presentation, diagnosis, clinical course and treatment of a man with hyperthyroidism secondary to autoimmune thyroiditis in the setting of type 1 diabetes mellitus has not previously been described.Case Presentation: A 32-year-old European-American man with an eight-year history of type 1 diabetes mellitus presented with an unintentional 22-pound weight loss but an otherwise normal physical examination. Laboratory studies revealed a suppressed thyroid-stimulating hormone concentration and an elevated thyroxine level, which are consistent with hyperthyroidism. His anti-thyroid peroxidase antibodies were positive, and his thyroid-stimulating immunoglobulin test was negative. Uptake of radioactive iodine by scanning was 0.5% at 24 hours. The patient was diagnosed with autoimmune thyroiditis. Six weeks following his initial presentation he became clinically and biochemically hypothyroid and was treated with thyroxine.Conclusion: This report demonstrates that autoimmune thyroiditis presenting as hyperthyroidism can occur in a man with type 1 diabetes mellitus. Autoimmune thyroiditis may be an isolated manifestation of autoimmunity or may be part of an autoimmune polyglandular syndrome. Among patients with type 1 diabetes mellitus who present with hyperthyroidism, Graves' disease and other forms of hyperthyroidism need to be excluded as autoimmune thyroiditis can progress quickly to hypothyroidism, requiring thyroid hormone replacement therapy. [ABSTRACT FROM AUTHOR]

The article discusses research on the differential diagnosis and therapies of amiodarone-induced thyrotoxicosis (AIT) in children and adolescent. The study stated that identifying the types of AIT could help determine the appropriate medical treatment. It was found that AIT is common in countries where there is low intake of iodine.

Background Thyroglobulin (TG) deficiency is an autosomal-recessive disorder that results in thyroid dyshormonogenesis. A number of distinct mutations have been identified as causing human hypothyroid goitre. Objectives The purpose of this study was to identify and characterize new mutations in the TG gene in an attempt to increase the understanding of the genetic mechanism responsible for this disorder. A total of six patients from four nonconsanguineous families with marked impairment of TG synthesis were studied. Methods Single-strand conformation polymorphism (SSCP) analysis, sequencing of DNA, genotyping, expression of chimeric minigenes and bioinformatic analysis were performed. Results Four different inactivating TG mutations were identified: one novel mutation (c.7006C>T [p.R2317X]) and three previously reported (c.886C>T [p.R277X], c.6701C>A [p.A2215D] and c.6725G>A [p.R2223H]). Consequently, one patient carried a compound heterozygous for p.R2223H/p.R2317X mutations; two brothers showed a homozygous p.A2215D substitution and the remaining three patients, from two families with typical phenotype, had a single p.R277X mutated allele. We also showed functional evidences that premature stop codons inserted at different positions in exon 7, which disrupt exonic splicing enhancer (ESE) sequences, do not interfere with exon definition and processing. Conclusions In this study, we have identified a novel nonsense mutation p.R2317X in the acetylcholinesterase homology domain of TG. We have also observed that nonsense mutations do not interfere with the pre-mRNA splicing of exon 7. The results are in accordance with previous observations confirming the genetic heterogeneity of TG defects. [ABSTRACT FROM AUTHOR]

Thyroid dysfunction has been implicated as a cause of reversible cognitive impairment and as such, the thyroid stimulating hormone has long been part of the screening laboratory test for dementia. Recently, several population-based studies demonstrated an association between hypo- or hyperthyroidism and Alzheimer's disease. This review discusses the role of thyroid hormone in the normal development and regulation of central nervous system functions and summarizes the studies that have linked thyroid function and dementia risk. Finally, it explores possible biological mechanisms to explain this association, including the direct effects of thyroid hormone on cerebral amyloid processing, neurodegeneration and thyrotropin-mediated mechanisms and vascular mediated enhancement of Alzheimer's disease risk. [ABSTRACT FROM AUTHOR]

Objective To investigate how North American thyroidologists assess and treat amiodarone-induced thyrotoxicosis (AIT) and to compare the results with those of the same questionnaire-based survey previously carried out among European thyroidologists. Design Members of the American Thyroid Association (ATA) with clinical interests were sent by e-mail a questionnaire on the diagnosis and management of AIT, 115 responses were received from the United States and Canada, representing about one-third of ATA members with clinical interests. Results The majority of respondents (91% vs. 68% in Europe, P < 0·05) see < 10 new cases of AIT per year, and AIT seems less frequent than amiodarone-induced hypothyroidism (AIH) in North America (34% and 66% of amiodarone-induced thyroid dysfunction, respectively, vs. 75% and 25%, respectively, in Europe, P < 0·001). When AIT is suspected, in North America hormonal assessment is mostly based on serum free T4 (FT4) and TSH measurements, while serum free T3 (FT3) determination is requested less frequently than in Europe; thyroid autoimmunity is included in the initial assessment less than in Europe. Most commonly used additional diagnostic procedures include, as in Europe, thyroid colour-flow Doppler sonography, and to a lesser extent, thyroid radioactive iodine uptake and scan, but Europeans tend to request multiple tests more than North Americans. Withdrawal of amiodarone is more often considered unnecessary by North American thyroidologists (21% vs. 10% in Europe in type 1 AIT, P < 0·05, 34% vs. 20% in type 2 AIT, P < 0·05). In type 1 AIT thionamides represent the treatment of choice for North Americans as well as for Europeans, but the former use them as monotherapy in 65% vs. 51% of Europeans ( P < 0·05) who more often consider potassium perchlorate as an useful addition (31% vs. 15% of North Americans, P < 0·01). Glucocorticoids are the selected treatment for type 2 AIT, alone (62% vs. 46% in Europe, P < 0·05) or in association with thionamides (16% vs. 25% in Europe, P = NS). After restoration of euthyroidism, thyroid ablation in the absence of recurrent thyrotoxicosis is recommended in type 1 AIT less frequently by North Americans. If amiodarone therapy needs to be reinstituted, prophylactic thyroid ablation is advised by 76% in type 1 AIT, while a ‘wait-and-see’ strategy is adopted by 61% in type 2 AIT, similar to behaviour of European thyroidologists. Conclusion Similarities and differences exist between expert North American and European thyroidologists concerning the diagnosis and management of AIT. While differences reflect the frequent uncertainty of the underlying mechanism leading to AIT, similarities may represent the basis to refine the diagnostic criteria and to improve the therapeutic outcomes of this challenging clinical situation. [ABSTRACT FROM AUTHOR]

Context:When the liver function tests are aggravated after starting antithyroid drugs (ATDs) in Graves'' hyperthyroidism, discontinuation of ATDs is generally considered. However, a question arises whether such aggravation constitutes an adverse effect of the drugs or not.Objective:The aim of this study was to clarify the influence of thyrotoxicosis on liver function tests, comparing the results with those in thyrotoxicosis induced by painless thyroiditis.Design:We prospectively studied liver biochemical tests in 30 patients with Graves'' disease and in 27 patients with painless thyroiditis.Main outcomes:Twenty-three (76.7) untreated Graves'' disease patients and 14 (51.9) untreated painless thyroiditis patients were found to have at least one liver function test abnormality. One month after starting ATD therapy in patients with Graves'' disease, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) elevations from initial values were observed in 16 (53.3). Similar elevations of AST and ALT from initial values at 1 month were observed in 10 (37.0) and 7 (25.9) patients with painless thyroiditis, respectively. Alkaline phosphatase (ALP) increased gradually after starting ATD therapy and maintained an elevated value for 35 months in Graves'' disease. In painless thyroiditis, ALP also increased gradually, similarly to that in Graves'' disease, but changes were mild. Elevation of ALT after 1 month of ATD therapy in Graves'' disease was significantly higher in patients whose estimated disease duration was 6 months or more compared to those with duration of less than 6 months. Elevated AST and ALT at 1 month after ATD therapy decreased to normal ranges, even though patients were receiving the same ATDs in Graves'' disease.Conclusion:Similar serial changes in liver function tests in both Graves'' disease and painless thyroiditis strongly suggest that increases of AST and ALT after starting ATD therapy may not be due to ATD side effects but may be induced by changes in thyroid function. [ABSTRACT FROM AUTHOR]

Context Two main forms of amiodarone-induced thyrotoxicosis (AIT) exist. Type 1 AIT is a form of iodine-induced hyperthyroidism. Its management is complex and includes thionamides, potassium perchlorate and, occasionally, thyroidectomy. Type 2 AIT is a destructive thyroiditis, responds to glucocorticoids, and usually does not require further thyroid treatment once euthyroidism has been restored. Objective To assess retrospectively the prevalence and relative proportion of type 1 and type 2 AIT over a 27-year period at a tertiary referral centre in Italy. Patients Consecutive AIT patients ( n = 215) seen at the department of endocrinology of the University of Pisa between 1980 and 2006. Results Type 1 AIT constituted the most frequent AIT form (60%) during the first years covered by this study. The annual mean number of type 1 AIT patients was 3·6 at the beginning of the study period, and 2·5 during the later years. In contrast, the mean annual number of new cases of type 2 AIT progressively increased from 2·4 to 12·5. Likewise, the proportion of type 2 AIT increased in a significant linear manner ( P < 0·0001), currently accounting for 89% of AIT cases. Type 2 AIT patients showed a male preponderance, higher serum FT4/FT3 ratio ( P < 0·002), lower 3-h and 24-h thyroidal radioactive iodine uptake values ( P < 0·0001), and received a higher cumulative dose of amiodarone ( P < 0·0001) than type 1 AIT patients. Conclusions Over a 27-year period, the epidemiology of AIT changed, as the prevalence of type 2 AIT progressively increased and that of type 1 remained constant. Thus, under most circumstances, endocrinologists nowadays deal with type 2 AIT, which is a destructive thyroiditis, generally treated successfully with glucocorticoids. Although no additional treatment is usually required after the destructive process subsides, periodic assessment of thyroid function is warranted, because of the occurrence of hypothyroidism (up to 17%) during long-term follow-up of these patients. [ABSTRACT FROM AUTHOR]

Perchlorate is a competitive inhibitor of the sodium/iodine symporter, decreasing the active transport of iodine into the thyroid. It was used as an antithyroid drug in the treatment of hyperthyroidism in the 1950s and 1960s but was discontinued because of the occasional occurrence of aplastic anemia. More recently, lower doses of perchlorate have been used successfully in the treatment of iodine-induced hyperthyroidism. There has been concern that naturally occurring perchlorate and industrial contamination of water supplies with perchlorate might pose a health hazard by inducing or aggravating underlying thyroid dysfunction. In a series of studies in normal volunteers, administration of perchlorate from 2 weeks to 6 months and in perchlorate production workers exposed intermittently to high levels of perchlorate for years, no abnormalities of circulating thyroid hormones, thyroid-stimulating hormone, thyroglobulin, or ultrasound evaluation of thyroid structure were observed even though the thyroid 123I uptake was decreased in some studies. Further studies of the effects of perchlorate on thyroid function in normal volunteers will now be difficult to carry out due to the adverse publicity that perchlorate and the studies on its effect have received. [ABSTRACT FROM AUTHOR]

Background: Amiodarone-induced thyrotoxicosis (AIT) may be caused by excessive thyroidal hormone synthesis and release (type 1) or by a destructive process (type 2). This differentiation is considered essential for therapeutic choice. Purpose: To evaluate the utility of color-flow Doppler sonography (CFDS) in the differential diagnosis and management of AIT. Material and Methods: The clinical and laboratory data, thyroid sonography (grayscale sonography [GSS], CFDS), thyroid radioiodine uptake (RAIU) and thyroid scintigraphy, treatment, and clinical outcome were retrospectively reviewed in 21 AIT patients. The CFDS pattern of thyroid nodules was separately described from that of the perinodular parenchyma, and AIT was classified as type 1 (increased blood flow) or type 2 (low/no blood flow). Type 1 AIT patients were treated with methimazole (alone or associated with potassium perchlorate), while type 2 patients were treated with prednisone or amiodarone withdrawal alone. Results: Eleven patients with increased blood flow were considered as type 1, and 10 with low/no blood flow as type 2. Ten of the 11 patients in the first group showed a hypervascular nodular pattern, while one showed a hypervascular parenchymal pattern. Clinical diagnoses were toxic nodular goiter and Graves' disease, respectively. Of the 10 patients with low/no blood flow, six had normal thyroid volume, three small diffuse goiter, and one small multinodular goiter. The clinical outcome showed that 20 of the 21 patients were treatment responsive. Conclusion: CFDS is a useful tool in the differential diagnosis of AIT. This differentiation appeared to be of clinical relevance as regards therapeutic choice. Separate evaluation of parenchymal blood flow from that of nodules may prove beneficial in the diagnosis of underlying thyroid diseases in patients with type 1 AIT. [ABSTRACT FROM AUTHOR]

The clinical and laboratory findings are described in three patients who ingested large amounts of l-thyroxine (two cases) and l-thyroxine together with l-triiodothyronine and who were treated with propranolol. Serum concentrations of thyroxine (maximum values 75 µg/dl, 64 µg/dl, and 20 µg/dl, respectively; normal range 4-12 µg/dl), triiodothyronine (maximum values 837 ng/dl, 453 ng/dl, and 566 ng/dl, resp.; normal range 80-180 ng/dl), reverse triiodothyronine (maximum values 235 ng/dl, 190 ng/dl, and 65 ng/dl, resp.; normal range 10-40 ng/dl) as well as free thyroxine equivalent and free triiodothyronine equivalent were monitored daily until they reached the normal range. Statistical analysis of the kinetics of these parameters indicated that the extreme thyroxine conversion was directed toward reverse triiodothyronine, partly due to the treatment with the β-adrenergic blocker propranolol. The striking discrepancy between the high concentrations of the active hormones and the moderate clinical symptoms was most likely caused by peripheral effects of propranolol. [ABSTRACT FROM AUTHOR]

Percutaneous ethanol injection (PEI) is an effective treatment for autonomously functioning thyroid nodules (AFTNs). The aims of this study were to assess: (1) the ultrasound (US) and colour-coded duplex sonography (CCDS) baseline and post-therapy patterns of AFTN, and (2) the contribution of CCDS in determining the efficacy and optimum duration of PEI. Forty AFTNs were evaluated by US and CCDS before, during and 6 and 12 months after PEI. Four grades of increasing vascularity were arbitrarily identified at CCDS (0-1-2-3). These data were compared with thyroid scintiscan and hormonal findings. All nodules showed a striking volume decrease. After treatment a hypoechoic pattern and blurred outlines on US were associated with a higher percentage volume reduction. Soon after PEI a reduction in the vascularity score was noticed in 29 of 40 of AFTNs. Pre- and post-treatment vascular score distributions were significantly different. It is concluded that a vascular score decrease to grade 0-1 at the end of PEI is an index of successful treatment. [ABSTRACT FROM AUTHOR]

Introduction: Amiodarone is associated with thyroid dysfunction and life-threatening thyrotoxicosis. In medically refractory cases, or where medical therapy is contraindicated, thyroidectomy may be required. To decrease perioperative thyroid storm and to reduce overall surgical risk, apheresis may be considered preoperatively to restore euthyroidism. Case Description: We report a 46-year-old female with a history of cardiac arrhythmia and tachycardia-induced cardiomyopathy for which she received amiodarone. Months after discontinuation of amiodarone, the patient presented with wide complex tachycardia and symptoms of thyrotoxicosis. Laboratory testing confirmed severe thyrotoxicosis which was subsequently refractory to medical therapy. Total thyroidectomy was required. Following a total of 10 apheresis treatments, thyroid hormone levels were reduced to near normal levels and the patient's symptoms improved. Thyroidectomy was performed without intraoperative or postoperative complication. Discussion: In the setting of life-threatening, medically refractory amiodarone-induced thyrotoxicosis, therapeutic apheresis can effectively reduce thyroid hormone levels and restore a state of clinical and biochemical euthyroidism. J. Clin. Apheresis 29:168-170, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Numerous drugs have been associated with destructive thyroiditis (subacute thyroiditis). Sunitinib, a tyrosine kinase inhibitor employed in renal cell carcinoma and gastrointestinal stromal tumors, has recently been linked to destructive thyroiditis with resultant hypothyroidism. We report a patient with transient overt thyrotoxicosis followed by hypothyroidism, apparently related to sunitinib therapy. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to determine whether or not the titre of thyroid-stimulating hormone receptor antibody with stimulating (TRAb-S) activity changes in patients with Graves' disease (GD) or toxic multinodular goitres (TMNG) 3 months after treatment with sodium iodide ((131)I).Subjects and Methods: Serum specimens were obtained from 21 hyperthyroid patients (15 with GD and 6 with TMNG) at a median 0.5 months before and 3 months after (131)I treatment using a standard ablative dose of 555 MBq. TRAb-S activity was measured in a sensitive and specific luminescent bioassay employing the lulu cell line and expressed as a stimulation index (SI; normal Results: The mean TRAb-S in the GD patients was 2.72 SI (95% CI: 1.51-4.03) 0.5 months before administration of (131)I and 3.98 SI (95% CI: 1.20-6.76) 3 months after administration of (131)I. The difference was not statistically significant at p LT; 0.8. It was not elevated in the TMNG patients before (0.57 SI; 95% CI: 0.41- 0.73) and after (1.00 SI; 95% CI: 0.74-1.26) treatment either.Conclusions: Radioiodine therapy for GD or TMNG did not induce a significant change in TRAb-S activity at 3 months after treatment with (131)I, probably due to effective antithyroid therapy or the timing of samples. [ABSTRACT FROM AUTHOR]

RECURRENT EPISODES OF SPONTANEOUSLY RESOLVING HYPERTHYROIDISM may be caused by release of preformed hormone from the thyroid gland after it has been damaged by inflammation (recurrent silent thyroiditis) or by exogenous administration of thyroid hormone, which might be intentional or surreptitious (thyrotoxicosis factitia). Community-wide outbreaks of "hamburger thyrotoxicosis" resulting from inadvertent consumption of beef contaminated with bovine thyroid gland have been previously reported. Here we describe a single patient who experienced recurrent episodes of this phenomenon over an 11-year period and present an approach to systematically evaluating patients with recurrent hyperthyroidism. [ABSTRACT FROM AUTHOR]

Here the case of a subject who developed changes in forced expiratory volume that were significant when examined from day to day but were not significant when values up to 7 or 8 hours after ending challenge is considered. A 44 years old cap painter developed work-related respiratory symptoms approximately 1 year before being examined. He underwent specific inhalation challenges 3 months after leaving work. It is interesting to note that discontinuation of exposure to the causal agent for almost 1 week resulted in the documentation of an hourly pattern.

The occurrence of levothyroxine-induced hyperthyroidism is rare but possible. Levothyroxine (LT) has been used for the treatment of hypothyroidism and for the suppression of thyroid-stimulating hormone levels in patients with thyroid nodules or thyroid gland enlargement. Allergic or idisyncratic reactions are extremely rare with the synthetic LT. There was a report of hypersensitivity caused by synthetic thyroid hormone in a hypothyroid patient with autoimmune Hashimoto's thyroiditis. Therefore, these adverse effects of the drug are of critical importance in the clinical management of patients.