Form Of Hyperthyroidism Research Articles

Reasons for difficulties in the interpretation of thyroid scintigraphy results with 99mTc-pertechnetate in functional autonomy of thyroid nodules and Graves’ disease: a clinical case

Thyrotoxicosis is a condition caused by an excess of thyroid hormones, such as thyroxine (T4) and triiodothyronine (T3), in the body, leading to corresponding clinical manifestations. One of the main challenges in the differential diagnosis of various forms of thyrotoxicosis is the similarity in the clinical presentation of diseases. Therefore, the main tools for accurate diagnosis verification in the wide spectrum of thyrotoxicosis nosologies are the correct sequence of laboratory and instrumental investigations and subsequent interpretation of the obtained results. Only accurately established disease etiology will allow for the selection of the most appropriate and effective treatment for a particular patient, as well as the avoidance of unjustified risks of possible complications. In this article, we will discuss the main difficulties that may arise during the differential diagnosis of various forms of thyrotoxicosis, as well as address some key aspects of proper diagnosis.

Psychological meanings reported by patients with Graves’ Disease in hyperthyroidism but without ophthalmopathy about their quotidian life: A qualitative study conducted in a Brazilian university specialized outpatient service

IntroductionTo handle well clinical treatments, it is crucial to know the expectations of patients who seek help. We need to ask ourselves: how do patients interpret subjectively their diagnosis, treatments, and self-care? Medical Psychology brings us theories for this understanding. Grave’s Disease is an autoimmune disorder, a form of hyperthyroidism with a goitre, affecting also the eyes and the skin, as well as emotional manifestations. Weight loss, sometimes psychologically welcome, although due to a disease, can mean a psychoanalytic secondary gain. So, the medicine that leads to clinical improvement can be taken with ambivalence and bad adherence to treatment. It is important to differentiate between disease, a scientific entity explained by the clinical professional, and illness as a patient’s subjective perception of an un-health.ObjectivesTo understand psychodynamically the fantasies, desires, and views related to Graves’ Disease as reported by patients in hyperthyroidism but without ophthalmopathy interviewed at an endocrinology-specialized outpatient clinic. (in the EPA-2023, it was presented the qualitative results of a sample in hyperthyroidism, with ophthalmopathy, studied at the same service).MethodsClinical-Qualitative Method designed by Turato. Data collected through Semi-Directed Interviews with Open-ended Questions in-Depth; and Field Notes, transcript fully. Treated by the Seven Steps of Clinical-Qualitative Content Analysis of Faria-Schützer, using psychodynamic concepts from Balintian Medical Psychology. Although we have extracted categories that permit us interesting discussions, we intend to close the sample (through the information saturation criterion by Fontanella) when we obtain other categories. The interviewer, a male psychologist, is the first author. The findings are validated by peer-reviewers of the Lab of Clinical Qualitative Research of the State University of Campinas.ResultsThree categories were chosen for this presentation: 1) “An atomic bomb in my life”: How drastic changes of a hormonal disease re-symbolize the patient’s life; 2) “I didn’t think the thyroid did that much”: the disease seen as a metaphor in a psychological blaming language to own disease and to himself as a sick person. 3) “I have so much medicine!”: a mode of referring to treatment that would justify an undisciplined use of medications.ConclusionsOur findings can help clinical professionals to have a better understanding of some psychological meanings which have sense in the patients’ conscience, often not verbalized clearly in the conversation, and so to handle better the patients and relatives. In this way, it can reduce the patient’s resistance to recommended treatment, as well as encourage the clinical team to construct empathy with them.Disclosure of InterestNone Declared

Incidence of hyperthyroidism in patients with bipolar or schizoaffective disorder with or without lithium: 21-year follow-up from the LiSIE retrospective cohort study.

Lithium-associated hyperthyroidism is much rarer than lithium-associated hypothyroidism. Yet, it may be of substantial clinical significance for affected individuals. For instance, lithium-associated hyperthyroidism could destabilise mood, mimic manic episodes and impact physical health. Only few studies have explored incidence rates of lithium-associated hyperthyroidism. Even fewer studies have compared incidence rates according to lithium exposure history. To determine the impact of lithium treatment on the incidence rate of hyperthyroidism in patients with bipolar or schizoaffective disorder and assess its aetiology. This study is part of the LiSIE (Lithium - Study into Effects and Side Effects) retrospective cohort study. Between 1997 and 2017, patients in the Swedish region of Norrbotten with a diagnosis of bipolar or schizoaffective disorder were screened for all episodes of overt hyperthyroidism in form of thyrotoxicosis or thyroiditis. Incidence rates of episodes of hyperthyroidism per 1000 person-years (PY) were compared in relation to lithium exposure; concurrent, previous, or no exposure ever (lithium-naïve patients). In 1562 patients, we identified 16 episodes of hyperthyroidism corresponding to an incidence rate of 0.88 episodes per 1000 PY. Ninety-four percent of episodes had occurred in women. Patients who had concurrently been exposed to lithium, had an incidence rate of 1.35 episodes per 1000 PY. Patients who had previously been exposed to lithium had an incidence rate of 0.79 per 1000 PY. Patients who had never been exposed to lithium had an incidence rate of 0.47 per 1000 PY. There were no significant differences in the risk ratios for patients with concurrent or previous exposure compared with lithium-naïve patients, neither for hyperthyroidism overall, thyrotoxicosis, or thyroiditis. Lithium-associated hyperthyroidism seems uncommon. The risk of hyperthyroidism does not seem significantly higher in patients with current or previous lithium exposure than in lithium-naïve patients.

ODP655 Apathetic Hyperthyroidism

Abstract Introduction Apathetic hyperthyroidism is a rare presentation of hyperthyroidism described in the elderly population. It is insidious in onset and symptoms are depression, lethargy, and weight loss. The adrenergic symptoms of hyperthyroidism are often absent. Furthermore, orbital disease associated apathetic hyperthyroidism has not been reported widely in literature. We present a clinical scenario of apathetic hyperthyroidism associated with orbitopathy. A 64-year-old lady presented with acute onset bilateral periorbital swelling that developed over 2 days. About 3 weeks prior, she began experiencing symptoms of brain fog, lethargy, intermittent nausea, anorexia, and headache. She experienced palpitations with exertion. Review of other systems was negative. Clinical exam: HR 70. Thyroid gland was enlarged, symmetric with no nodules and nontender, bilateral periorbital puffiness and mild conjunctival redness was noted. Lab data was significant for TSH at 0. 03 uIU/mL, elevated FT4 2.5ng/dL, total T3 of 222ng/dL, TSI 4.2 and sed rate of 10. Her thyroid ultrasound indicated hypervascular and heterogenous gland. Our patient was diagnosed with apathetic hyperthyroidism and thyroid eye disease. She was started on propranolol 60mg ER one tablet a day and methimazole 10mg a day. CT scan of the orbit indicated symmetric enlargement of extraocular muscles. Evaluation by the ophthalmologist confirmed the presence of thyroid eye disease with a clinical activity score of 6 out of 7 indicating severe thyroid eye disease and she was a candidate for treatment with teprotumumab. Discussion Apathetic hyperthyroidism was first described by Lahey in 1931, as a state of non-activated hyperthyroidism. It is manifested with gradual onset of apathy, depressed mood, lethargy, nausea, lack of appetite, weight loss, proximal muscle weakness, goiter, atrial fibrillation, and congestive heart failure. It lacks the typical presentation of a hyperadrenergic state of hyperthyroidism which include palpitations, anxiety, tremor, heat intolerance, and diaphoresis. Due to the lack of typical presentation of hyperthyroidism, timely diagnosis and treatment may be challenging. Concomitant occurrence of occult malignancy and hyperglycemia have been reported in case reports. Patients can also transition from apathetic state to hyperadrenergic state of hyperthyroidism and vice versa. Lahey emphasized the risk of unexpected death following surgery in apathetic hyperthyroidism. The absence of adrenergic symptoms could be supported by the theory that these patients are in a relative state of catecholamine deficiency or have a state of end organ catecholamine resistance. Significant orbital involvement in apathetic hyperthyroidism is not widely reported in the literature. Blepharoptosis has been mentioned in association with this form of hyperthyroidism. Our patient presented with acute onset eye symptoms which prompted testing of thyroid function. Further review of symptoms led to a diagnosis of apathetic hyperthyroidism with thyroid eye disease.

Management of Thyrotoxicosis Induced by PD1 or PD-L1 Blockade.

ContextThyrotoxicosis is a common immune-related adverse event in patients treated with programmed cell death protein-1 (PD1) or programmed cell death protein ligand-1 (PD-L1) blockade. A detailed endocrinological assessment, including thyroid ultrasound and scintigraphy, is lacking, as are data on response to treatment and follow-up.ObjectiveThe aim of this study was to better characterize the thyrotoxicosis secondary to immune checkpoint inhibitors, gaining insights into pathogenesis and treatment.MethodsWe conducted a retrospective study of 20 consecutive patients who had normal thyroid function before starting immunotherapy and then experienced thyrotoxicosis on PD1 or PD-L1 blockade. Clinical assessment was combined with thyroid ultrasound, 99mtechnecium scintiscan, and longitudinal thyroid function tests.ResultsFive patients had normal or increased scintigraphic uptake (Sci+), no serum antibodies against the thyrotropin receptor, and remained hyperthyroid throughout follow-up. The other 15 patients had no scintigraphic uptake (Sci–) and experienced destructive thyrotoxicosis followed by hypothyroidism (N = 9) or euthyroidism (N = 6). Hypothyroidism was more readily seen in those with normal thyroid volume than in those with goiter (P = .04). Among Sci– individuals, a larger thyroid volume was associated with a longer time to remission (P < .05). Methimazole (MMI) was effective only in Sci+ individuals (P < .05).ConclusionAdministration of PD1- or PD-L1–blocking antibodies may induce 2 different forms of thyrotoxicosis that appear similar in clinical severity at onset: a type 1 characterized by persistent hyperthyroidism that requires treatment with MMI, and a type 2, characterized by destructive and transient thyrotoxicosis that evolves to hypothyroidism or euthyroidism. Thyroid scintigraphy and ultrasound help in differentiating and managing these 2 forms of iatrogenic thyrotoxicosis.

Management of Thyrotoxicosis Induced by PD1 or PD-L1 Blockade

Context: Thyrotoxicosis is a common immune-related adverse event in patients treated with PD1 or PD-L1 checkpoint inhibitors. A detailed endocrinological assessment, including thyroid ultrasound and scintigraphy is missing, as are data on response to treatment and follow-up. Objectives: To better characterize the thyrotoxicosis secondary to immune checkpoint inhibitors, gaining insights into pathogenesis and informing management. Methods: We conducted a prospective cohort study of 20 consecutive patients who had normal thyroid function before starting immunotherapy and then experienced thyrotoxicosis upon PD1 or PD-L1 blockade. Clinical assessment was combined with thyroid ultrasound, scintigraphy, and longitudinal thyroid function tests. Results: Five patients had normal scintigraphic uptake (Sci+), no serum antibodies against the TSH receptor, and remained hyperthyroid throughout follow-up. The other 15 patients had no scintigraphic uptake (Sci-) and experienced destructive thyrotoxicosis followed by hypothyroidism (N= 9) or euthyroidism (N= 6). Hypothyroidism was more readily seen in those with normal thyroid volume than in those with goiter (P= 0.04). Among Sci- subjects, a larger thyroid volume was associated to a longer time to remission (P<0.05). Methimazole (MMI) was effective only in Sci+ subjects (P<0.05). Conclusions: Administration of PD1 or PD-L1 blocking antibodies may induce two different forms of thyrotoxicosis that appear similar in clinical severity at onset: a type 1 characterized by persistent hyperthyroidism that requires treatment with MMI, and a type 2 characterized by destructive and transient thyrotoxicosis that evolves to hypo- or eu-thyroidism. Thyroid scintigraphy and ultrasound help differentiating and managing these two forms of iatrogenic thyrotoxicosis

Pituitary thyrotoxicosis presenting as abnormal thyroid function testing during pregnancy: a case report

BackgroundCentral hyperthyroidism is a rare form of hyperthyroidism caused by thyrotrope pituitary adenomas. It is characterized by elevated thyroid-stimulating hormone alongside high thyroxine and triiodothyronine. Goiter is the most common symptom of central hyperthyroidism. Surgical resection as well as somatostatin analog therapy typically achieve resolution of hyperthyroid symptoms and restoration of a euthyroid state.Case presentationWe report the case of a 30-year-old primigravida Caucasian/White female who presented with abnormal thyroid function testing results and multinodular goiter during pregnancy. Postpartum, she was found to have multinodular goiter on physical examination as well as persistent elevated thyroid-stimulating hormone with elevated free thyroxine and free triiodothyronine. Magnetic resonance imaging disclosed a large pituitary macroadenoma, and she subsequently underwent resection of the mass. She achieved a sustained euthyroid state postoperatively.ConclusionsThis case shows how central hyperthyroidism can present without the more apparent symptoms of thyrotoxicosis and that successful resolution of central hyperthyroidism may be achieved postoperatively.

Serum thyroglobulin level in newly detected thyrotoxicosis and its role in differential diagnosis of thyrotoxicosis

Background: Elevated serum thyroglobulin (Tg) level is commonly observed in various forms of thyrotoxicosis; the levels vary according to different etiologies. This study aimed at identifying the value of serum Tg level in the differential diagnosis of common etiologies of thyrotoxicosis. Methods: This cross-sectional study was conducted at the endocrine outpatient department of a tertiary hospital in Bangladesh from March 2015 to May 2017. In this study, 200 subjects with newly detected untreated thyrotoxicosis were evaluated. Serum Tg was assayed by chemiluminescent immunometric assay. Results: Serum Tg level was raised in 48% of subjects. Subjects aged ≥40 years, and those having a family history of thyroid disorders had relatively higher thyroglobulin levels. The frequency of subjects with an elevated Tg was highest in subacute thyroiditis (89.5%) followed by toxic nodular goiter (77.3%) and Graves’ disease (32.9%); the difference in the frequencies was statistically significant (p&lt;0.001). Median Tg was highest in the subjects with subacute thyroiditis (132.6 ng/ml) followed by toxic nodular goiter (99.55 ng/ml); those with Graves’ disease had the lowest Tg level (12.5 ng/ml); the differences in median Tg levels across the three groups were also statistically significant (p&lt;0.001). Conclusions: Serum thyroglobulin level may be useful for the etiological diagnosis of thyrotoxicosis.

The Role of Nuclear Medicine in the Clinical Management of Benign Thyroid Disorders, Part 2: Nodular Goiter, Hypothyroidism, and Subacute Thyroiditis.

Part 2 of this series of Continuing Education articles on benign thyroid disorders deals with nodular goiter, hypothyroidism, and subacute thyroiditis. Together with Part 1 (which dealt with various forms of hyperthyroidism), this article is intended to provide relevant information for specialists in nuclear medicine dealing with the clinical management of patients with benign thyroid disorders, the primary audience for this series. Goiter, an enlargement of the thyroid gland, is a common endocrine abnormality. Constitutional factors, genetic abnormalities, or dietary and environmental factors may contribute to the development of nodular goiter. Most patients with nontoxic nodular goiter are asymptomatic or have only mild mechanical symptoms (globus pharyngis). Work-up of these patients includes measurement of thyroid-stimulating hormone, free triiodothyronine, free thyroxine, thyroid autoantibodies, ultrasound imaging, thyroid scintigraphy, and fine-needle aspiration biopsy of nodules with certain ultrasound and scintigraphic features. Treatment for multinodular goiter includes dietary iodine supplementation, surgery, radioiodine therapy (to decrease thyroid size), and minimally invasive ablation techniques. Hypothyroidism ranges from rare cases of myxedema to more common mild forms (subclinical hypothyroidism). Primary hypothyroidism often has an autoimmune etiology. Clinical presentations differ in neonates, children, adults, and elderly patients. Work-up includes thyroid function tests and ultrasound imaging. Nuclear medicine is primarily used to locate ectopic thyroid tissue in congenital hypothyroidism or to detect defects in iodine organification with the perchlorate discharge test. Treatment consists of thyroid replacement therapy with l-thyroxine, adjusting the daily dose to the individual patient's metabolic and hormonal requirements. Subacute thyroiditis is a self-limited inflammatory disorder of the thyroid gland, often associated with painless or painful swelling of the gland and somatic signs or symptoms. Inflammation disrupts thyroid follicles resulting in a rapid release of stored thyroxine and triiodothyronine causing an initial thyrotoxic phase, often followed by transient or permanent hypothyroidism. Although subacute thyroiditis is often related to a viral infection, no infective agent has been identified. Subacute thyroiditis may be caused by a viral infection in genetically predisposed individuals. Work-up includes lab tests, ultrasound imaging, and radionuclide imaging. Thyroid scintigraphy demonstrates different findings depending on the phase of the illness, ranging from very low or absent tracer uptake in the thyroid gland in the hyperthyroid phase to a normal appearance in the late recovery phase. Since subacute thyroiditis is self-limited, treatment is directed toward relief of pain. High-dose nonsteroidal antiinflammatory drugs are usually the first-line treatment. If severe pain persists, a course of corticosteroids may be necessary. Permanent hypothyroidism develops in up to 15% of patients with subacute thyroiditis, even more than 1 y after presentation.

Current approach to surgical management of hyperthyroidism.

Hyperthyroidism is a set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland, which leads to thyrotoxicosis. The most common forms of hyperthyroidism include diffuse toxic goiter (Graves' disease), toxic multinodular goiter (Plummer disease), and a solitary toxic adenoma. The most reliable screening measure of thyroid function is the thyroid-stimulating hormone (TSH) level. Options for treatment of hyperthyroidism include: antithyroid drugs, radioactive iodine therapy (the preferred treatment of hyperthyroidism among US thyroid specialists), or thyroidectomy. Massive thyroid enlargement with compressive symptoms, a suspicious nodule, Graves' orbitopathy, and patient preference are indications for surgical treatment of thyrotoxicosis. This paper reviews the current literature and controversies on the surgical approach to the management of hyperthyroidism.

Frequency of Thyrotoxicosis in Patient with One Sided Exophthalmos

Background: Thyroid associated Opthalmo-pathy is a condition of lid retraction causing a staring appearance. This occurs in any form of thyrotoxicosis as a result of sympathetic overactivity.Exophthalmos is the forward protrusion of eye ball beyond the orbital rim.&#x0D; Material &amp; Methods: This case series was observed in medical department Mufti Mehmood Teaching Hospital DIKhan, Pakistan over a period of eight months from February 2018 to September 2018. Detailed history with reference of duration of illness, mode of onset, progression and associated symptoms like fever, pain, diplopia and loss of vision was taken. Complete examination of orbit, eyelid, anterior and posterior segment was done. Routine Investigations along with special diagnostic tests like TFTs and MRI were performed to aid etiological diagnosis.&#x0D; Results: A total 47 patients were observed during this study period. Out of these 20 (21.27%) were male and 27 (57.44%) were female with male to female ratio 1:1.35 with mean age of 32 years. Out of 47 patients30 (63.82%) patients were having thyrotoxicosis as a cause of exophthalmos, 10(21.27%) were having retrobulbartumour, 5(10.63%) patients were with cavernous sinus thrombosis and 2(4.25%) patients were having idiopathic cause of exophthalmos.&#x0D; Conclusion: Thyrotoxicosis is the common cause of one sided exophthalmos and should be considered in all patients with one sided exophthalmos.

The Role of Nuclear Medicine in the Clinical Management of Benign Thyroid Disorders, Part 1: Hyperthyroidism.

Benign thyroid disorders, especially hyper- and hypothyroidism, are the most prevalent endocrine disorders. The most common etiologies of hyperthyroidism are autoimmune hyperthyroidism (Graves disease, GD), toxic multinodular goiter (TMNG), and toxic thyroid adenoma (TA). Less common etiologies include destructive thyroiditis (e.g., amiodarone-induced thyroid dysfunction) and factitious hyperthyroidism. GD is caused by autoantibodies against the thyroid-stimulating hormone (TSH) receptor. TMNG and TA are caused by a somatic activating gain-of-function mutation. Typical laboratory findings in patients with hyperthyroidism are low TSH, elevated free-thyroxine and free-triiodothyronine levels, and TSH-receptor autoantibodies in patients with GD. Ultrasound imaging is used to determine the size and vascularity of the thyroid gland and the location, size, number, and characteristics of thyroid nodules. Combined with lab tests, these features constitute the first-line diagnostic approach to distinguishing different forms of hyperthyroidism. Thyroid scintigraphy with either radioiodine or 99mTc-pertechnetate is useful to characterize different forms of hyperthyroidism and provides information for planning radioiodine therapy. There are specific scintigraphic patterns for GD, TMNG, TA, and destructive thyroiditis. Scintigraphy with 99mTc-sestamibi allows differentiation of type 1 from type 2 amiodarone-induced hyperthyroidism. The radioiodine uptake test provides information for planning radioiodine therapy of hyperthyroidism. Hyperthyroidism can be treated with oral antithyroid drugs, surgical thyroidectomy, or 131I-iodide. Radioiodine therapy is generally considered after failure of treatment with antithyroid drugs, or when surgery is contraindicated or refused by the patient. In patients with TA or TMNG, the goal of radioiodine therapy is to achieve euthyroid status. In GD, the goal of radioiodine therapy is to induce hypothyroidism, a status that is readily treatable with oral thyroid hormone replacement therapy. Dosimetric estimates based on the thyroid volume to be treated and on radioiodine uptake should guide selection of the 131I-activity to be administered. Early side effects of radioiodine therapy (typically mild pain in the thyroid) can be handled by nonsteroidal antiinflammatory drugs. Delayed side effects after radioiodine therapy for hyperthyroidism are hypothyroidism and a minimal risk of radiation-induced malignancies.

Thyrotoxicosis. Clinical guidelines for diagnosis and treatment. Part ІІ

Background. Recently they have reported an increased rate of thyrotoxicosis, which is characterized by polyetiology, a variety of clinical manifestations and potential treatment. Appropriate treatment requires an accurate diagnosis and depends on the comorbidities and preferences of the patient.&#x0D; Purpose. To highlight the key points of clinical guidelines for diagnosis and treatment of thyrotpxicosis provided by the American Thyroid Association and the American Association of Clinical Endocrinologists, US Endocrine Society dealing with diagnosis and treatment of thyroid diseases as well as the local clinical protocols of SO «Grigoriev Institute for Medical Radiology and Oncology of the National Academy of Medical Sciences of Ukraine».&#x0D; Materials and methods. Based on the search of contributions in the electronic databases over the last 5 years, which are included in the Cochrane Library, PUBMED and MEDLINE databases. Clinical guidelines are based on expert consensus and assessing the significance according to the international guidelines for thyrotoxicosis.&#x0D; Results and discussion. The paper deals with up-to-date guidelines on diagnosis, management and treatment of patients with different forms of thyrotoxicosis. It presents a detailed strategy for those patients depending on etiology of the disease. The therapeutic approaches to treating Graves’ disease, autoimmune ophthalmopathy, thyrotoxic crisis, gravidae as well as the peculiarities of treating patients with subclinical hyperthyroidism and iodine-induced thyrotoxicosis have been substantiated.&#x0D; Conclusions. The treatment of thyrotoxicosis remains a challenging issue of modern internal medicine. Despite the existing numerous clinically proven protocols for the treatment of this pathology, the comorbid background of patients complicates following them. The implementation of the provided protocol elements will make it possible to introduce the principles of a customized approach in thyrotoxicosis patients.

Thyroid dysfunction among chronic hepatitis C patients and its relation to Interferon therapy

Background:Thyroid dysfunction (TD) represents an extrahepatic manifestation of chronic hepatitis C (CHC). Moreover, the currently approved treatment of CHC is often associated with TD. However, it remains debatable if TD is mainly virus or treatment related. The aim of this study was to assess the incidence of TD and to identify its predictors in treated and untreated CHC-infected patients.Patients and methods:A total of 1290 patients with CHC were evaluated for TD for 48 weeks: 200 were untreated (control group) and 1090 were treated with pegylated interferon α (PEG-IFN-α) plus ribavirin (treatment group).Results:The incidence of TD was more evident by the end of treatment (week 48); it was found to be 15.5%, mostly in the form of hypothyroidism (8.4%), whereas the least incidence was detected by week 12 (9.1%), mostly in the form of hyperthyroidism (5.2%). Generally, hyperthyroidism was higher than hypothyroidism in multiple folds, but in the end, hypothyroid cases became more dominant. Males were more affected, but the prevalence of hypothyroidism was more in females (10.1%) than males (8.0%). TD was not related to sex, age, BMI, pretreatment viral load, pretreatment laboratory characteristics, post-treatment biochemical tests, treatment duration, severity of hepatic inflammation and fibrosis, type of biopsy used, or virological outcome, but PEG-IFN formulation was related, particularly IFN-α-2a. TD did not lead to dose reduction or therapy withdrawal.Conclusion:Both hepatitis C virus and IFN-α therapy have been found to be inducing thyroid disorders in patients with CHC virus infection. Antiviral therapy of CHC possibly induces de novo or exacerbates pre-existing silent TD especially subclinical hypothyroidism. The role of CHC per se in TD remains to be determined.

Tiroidna kriza posle traume grudnog koša

Thyroid storm is an acute and severe complication of thyrotoxicosis. It is characterized by high fever, sweating, tachycardia, and often heart failure too. The objectives of the paper is to present the case of a patient with thyroid storm developed after the trauma of the chest at previously apparently healthy individuals, diagnosed on the basis of clinical preview and based on the diagnostic criteria according to Burch and Wartofsky. The most common complication is Mb. Graves - Basedow, but often associated with multi-nodose goiter. Thyroid storm is the most severe form of thyrotoxicosis with a mortality rate of 8 to 25 %. Case report. We present an interesting case from our practice: thyroid storm caused after chest trauma in apparently healthy people, but with unrecognized hyperthyroidism and thyroid gland nodule. Conclusion. The objectives of this presentation were to raise awareness of the association between signs and symptoms of thyroid storm that dominate the clinical picture and complicate the initial presentation and the evolution of the situation caused by trauma. The treatment of hyperthyroidism resulted in conversion in sinus rhythm, withdrawal of symptoms and signs heart failure, and normalization of artery pressure.

Hypothyroidism and Thyrotoxicosis

Thyroid disorders are the most common endocrine conditions encountered in clinical practice and can range from clinically obvious to clinically silent. This review provides the definition and epidemiology of the conditions of hypothyroidism and hyperthyroidism. Hypothyroidism can be congenital or acquired, and its pathogenesis, diagnosis, and management are presented. The three most common disorders of thyrotoxicosis (diffuse toxic goiter [Graves disease], toxic nodular goiter, and iatrogenic thyrotoxicosis in thyroid hormone–treated patients are addressed, as well as the many diseases in each of these categories. This review also discusses thyroiditis, goiter, thyroid nodules, and thyroid cancer. Tables list the causes of elevated serum thyroid-stimulating hormone (TSH) levels, the etiologic classification of thyrotoxicosis, characteristic features of thyroiditis, and causes of elevated serum total thyroxine levels. Figures show the prevalence of abnormalities in thyroid function tests in different populations, certain forms of hyperthyroidism that result from pathophysiologic activation of the TSH receptor, and inflammation of thyroid tissue in acute thyroiditis. This review contains 3 figures, 12 tables, and 61 references. Key Words: Hypothyroidism, Thyrotoxicosis, Thyrotropin, celiac disease, vitiligo, pernicious anemia, Sjögren syndrome, Graves disease, Munchausen syndrome

Hypothyroidism and Thyrotoxicosis

Thyroid disorders are the most common endocrine conditions encountered in clinical practice and can range from clinically obvious to clinically silent. This review provides the definition and epidemiology of the conditions of hypothyroidism and hyperthyroidism. Hypothyroidism can be congenital or acquired, and its pathogenesis, diagnosis, and management are presented. The three most common disorders of thyrotoxicosis (diffuse toxic goiter [Graves disease], toxic nodular goiter, and iatrogenic thyrotoxicosis in thyroid hormone–treated patients are addressed, as well as the many diseases in each of these categories. This review also discusses thyroiditis, goiter, thyroid nodules, and thyroid cancer. Tables list the causes of elevated serum thyroid-stimulating hormone (TSH) levels, the etiologic classification of thyrotoxicosis, characteristic features of thyroiditis, and causes of elevated serum total thyroxine levels. Figures show the prevalence of abnormalities in thyroid function tests in different populations, certain forms of hyperthyroidism that result from pathophysiologic activation of the TSH receptor, and inflammation of thyroid tissue in acute thyroiditis. This review contains 3 figures, 12 tables, and 61 references. Key Words: Hypothyroidism, Thyrotoxicosis, Thyrotropin, celiac disease, vitiligo, pernicious anemia, Sjögren syndrome, Graves disease, Munchausen syndrome

Thyroid Uptake Exceeding 100%: How Is That Possible?

Measurement of thyroid uptake is perhaps one of the most basic procedures performed in nuclear medicine today. The uptake procedure assesses iodide trapping and organification within the gland ([1][1]). It is most commonly performed to differentiate thyroiditis from other forms of thyrotoxicosis and

Cardiothyreosis: Prevalence and risk factors

Cardiothyreosis (CT) or thyrotoxic heart disease is associated with higher morbidity and mortality than the other forms of hyperthyroidism. Its risk factors have been analyzed in a limited number of studies. The aims of our study were to investigate the prevalence of CT and its risk factors in patients with hyperthyroidism. MethodsWe identified 538 patients with a hospital discharge diagnosis of hyperthyroidism from January 2000 to December 2015. Among them, 35 patients were diagnosed as having CT. Their demographic, clinical and biological characteristics were studied and compared with those of 72 controls (patients admitted for hyperthyroidism without CT) randomly selected using univariate and multivariate analysis. ResultsThe prevalence of CT in patients hospitalized with overt hyperthyroidism was 6.5%. The cardiac complications seen were atrial fibrillation (AF) in 33 cases (6.1%) and cardiac heart failure (CHF) in 11 cases (2%). The risk factors of CT were age greater than 50 years (OR=13.1; 95% CI [4.9–34.4]), low socioeconomic status (OR=2.8; 95% CI [1.2–6.7]), low educational level (OR=3.1; 95% CI [1.2–8.3]), personal history of hypertension (OR=3.5; 95% CI [1.1–11.2]) and a multinodular toxic goiter as the etiology of hyperthyroidism (OR=4.6; 95% CI [1.6–13.9]). After multivariate analysis, age greater than 50 years was the only independent risk factor of CT (adjusted OR=11.6; 95% CI [2.7–49.5]). Severe biological hyperthyroidism (FT4 >3 times normal) was associated with a lower risk of CT (adjusted OR=0.2; 95% CI [0.1–0.9]). ConclusionsThe prevalence of CT in patients with overt hyperthyroidism was relatively low. Cardiac complications were AF and CHF with a clear predominance of AF. Advanced age was the only independent risk factor of CT. Cardiac complications may be seen even if hyperthyroidism is not biologically severe.

Antithyroid Drugs.

The thionamide drugs, i.e. carbimazole and its metabolite methimazole (MMI), and propylthiouracil (PTU) have extensively been used in the management of various forms of hyperthyroidism over the past eight decades. This review aims to summarize different aspects of these outstanding medications. Thionamides have shown their own acceptable efficacy and even safety profiles in treatment of hyperthyroidism, especially GD in both children and adults and also during pregnancy and lactation. Of the antithyroid drugs (ATDs) available, MMI is the preferred choice in most situations taking into account its better efficacy and less adverse effects accompanied by once-daily dose prescription because of a long half-life and similar cost. Considering the more severe teratogenic effects of MMI, PTU would be the selected ATD for treatment of hyperthyroidism during pre-pregnancy months and the first 16 weeks of gestation. Recent studies have confirmed the efficacy and safety of long-term MMI therapy with low maintenance doses for GD and toxic multinodular goiter. Despite the long-term history of ATD use, there is still ongoing debate regarding their pharmacology and diverse mechanisms of action, viz. their immunomodulatory effects, and mechanisms and susceptibility factors to their adverse reactions.