Iodide Metabolism and Effects

2020 ◽  
pp. 25-33
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Dietary Supplement ◽  
Thyroid Function ◽  
Thyroid Stimulating Hormone ◽  
Hormone Synthesis ◽  
Serum Tsh ◽  
Tsh Stimulation ◽  
Sensitive Marker

Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.

Effect of goitrogen administration on the circadian rhythm of serum thyroid stimulating hormone in the rat

1981 ◽  
Vol 98 (3) ◽  
pp. 396-401 ◽  
Author(s):  
B. Stringer ◽  
D. Wynford-Thomas ◽  
B. Jasani ◽  
E. D. Williams
Keyword(s):  
Circadian Rhythm ◽  
Thyroid Hormone ◽  
Circadian Rhythms ◽  
Thyroid Function ◽  
Diurnal Rhythm ◽  
Thyroid Stimulating Hormone ◽  
Male Rats ◽  
Hormone Synthesis ◽  
Serum Tsh

Abstract. Adult male rats were fed a goitrogen, aminotriazole, for 74 days at a dose known to suppress thyroid function completely. At the end of this period, these animals along with matched controls were killed in groups of seven at 3 hourly intervals throughout a 24 hour period, and serum TSH, T3, T4 and albumin assayed. No significant circadian rhythms of T3, T4 or albumin were found in either, but a highly significant rhythm of TSH was demonstrated both in controls and goitrogen treated groups, with a diminished relative amplitude in the latter. The results indicate that a significant diurnal rhythm of serum TSH persists in the rat despite long-term blockade of thyroid hormone synthesis and that the existence of this rhythm is therefore independent of the presence of circulating T3 or T4.

scholarly journals AMIODARON SEBAGAI OBAT ANTI ARITMIA DAN PENGARUHNYA TERHADAP FUNGSI TIROID

2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Starry H. Rampengan
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Function ◽  
Hormone Replacement ◽  
Type I ◽  
Peripheral Tissues ◽  
Hormone Synthesis ◽  
Thyroid Hormone Metabolism ◽  
Serum T4 ◽  
Life Threatening

Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring.     Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian  hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya  disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.

The association of thyroid hormones and blood pressure in euthyroid preadolescents

2016 ◽  
Vol 29 (4) ◽  
Author(s):  
Bo Hyun Park ◽  
Sun Jung Baik ◽  
Hye Ah Lee ◽  
Young Sun Hong ◽  
Hae Soon Kim ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Diastolic Blood Pressure ◽  
Pressure Control ◽  
Thyroid Stimulating Hormone ◽  
University Hospital ◽  
Hypertension Status ◽  
Childhood Hypertension ◽  
Serum Tsh

AbstractHypertension is the leading cause of cardiovascular disease worldwide, and both high and low blood pressures are associated with various chronic diseases. Thyroid hormones have profound effects on cardiovascular function, including on blood pressure. Recent studies have shown that childhood hypertension can lead to adult hypertension. Therefore, adequate blood pressure control is important from early life. Employing a life-course approach, we aimed to investigate the association between thyroid hormones and blood pressure in children.A total of 290 children from the Ewha Woman’s University Hospital birth cohort participated in a preadolescent check-up program. We assessed the levels of serum thyroid-stimulating hormone (TSH) and free thyroxine (FT4) and the blood pressure status in these children. Thyroid hormone concentrations were measured using an electro-chemiluminescence immunoassay (ECLIA), and hypertension was defined according to the guideline of the Korea Centers for Disease Control and Prevention.The sex-, age-, and height-adjusted prevalence of hypertension was 27.0% in the present study. On regression analysis, serum FT4 showed significantly negative association with diastolic blood pressure (DBP; β=–8.24, 95% CI: –14.19–2.28, p=0.007). However, these relationships were not significant after adjustment for sex, age, and current body mass index. The levels of serum TSH showed no relationship with mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) after adjustment. No significant differences in serum TSH and FT4 levels according to hypertension status were found.These findings suggest that thyroid hormone is not independently associated with increased blood pressure in euthyroid preadolescents.

scholarly journals The effect of iodine in patients using povidone-iodine mouth wash on thyroid function

2019 ◽  
Vol 5 (6) ◽  
pp. 1562 ◽  
Author(s):  
Gowri Shankar Murugesan ◽  
Manju Priya Venkat
Keyword(s):  
Thyroid Gland ◽  
Thyroid Function ◽  
Povidone Iodine ◽  
Endocrine System ◽  
Thyroid Stimulating Hormone ◽  
Increased Risk ◽  
Before And After ◽  
Mouth Wash ◽  
Serum Tsh ◽  
Stimulating Hormone

<p class="abstract"><strong>Background:</strong> Thyroid gland is a key part of endocrine system and it performs its functions via two most important thyroid hormones thyroxine (T4) and triiodothyronine (T3). Thyroid gland is mainly regulated by thyroid-stimulating hormone (TSH). Povidone-iodine (polyvinylpyrrolidone-iodine, PVP-I) mouthwash is commonly used to treat infections of the oral cavity and oropharynx and iodine released from PVP-I can interfere with thyroid function. In this study the effect of brief treatment with povidone-iodine mouth wash on thyroid function was assessed. The aim of the present study was to assess whether iodine is absorbed through oral transmucosal route and interfere with TSH in serum.</p><p class="abstract"><strong>Methods:</strong> Fifty one patients with acute and chronic pharyngitis and tonsillitis were recruited and out of which forty-seven patients were treated with 20 ml of PVP-I mouthwash twice daily for 3 weeks and blood was collected from the respective patients before and after treatment with PVP-I. Serum thyroid stimulating hormone concentration was measured from the collected blood samples of the patients.</p><p class="abstract"><strong>Results:</strong> In the present study there was a small increase in serum TSH concentration during the therapy with PVP-I but the concentration determined was within the normal range.</p><p class="abstract"><strong>Conclusions:</strong> Based on the results of this study we conclude that the use of PVP-I for a brief period transiently increase TSH value and prolonged use should be avoided in people with an increased risk of thyroid dysfunction and other autoimmune disorders.</p>

scholarly journals Extrathyroidal thyroid hormone synthesis?

2011 ◽  
Vol 210 (1) ◽  
pp. 3-4 ◽  
Author(s):  
Marian Ludgate
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis

A paper published in this issue of the Journal of Endocrinology has revisited the hypothesis that thyroid hormones may be generated by tissues outside the thyroid gland in higher organisms including mammals. This commentary appraises the strengths and weaknesses of the study, the alternative explanations for the findings and possible future measures to investigate further. The concept of extrathyroidal thyroxine and triiodothyronine synthesis has previously been proposed; by assuming that Nagao et al. and earlier authors are correct, the plausibility and possible mechanisms underlying the hypothesis are discussed.

scholarly journals Combined effects of cadmium and decabrominated diphenyl ether on thyroid hormones in rats

2012 ◽  
Vol 63 (3) ◽  
pp. 255-262 ◽  
Author(s):  
Marijana Ćurčić ◽  
Saša Janković ◽  
Vesna Jaćević ◽  
Sanja Stanković ◽  
Slavica Vučinić ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Wistar Rats ◽  
Diphenyl Ether ◽  
Thyroid Stimulating Hormone ◽  
Combined Effects ◽  
Single Substance ◽  
Hormone Homeostasis ◽  
Stimulating Hormone

The aim of this study was to see how a mixture of cadmium (Cd) and decabrominated diphenyl ether (BDE209) affect thyroid function, namely thyroid-stimulating hormone (TSH), thyroxin (T4), free thyroxin (FT4), triiodothyronin (T3), and free triiodothyronin (FT3) in Wistar rats (eight per group) receiving either a single substance or their combination by gavage for 28 days. Three groups were receiving Cd alone in the doses of 2.5 mg kg-1, 7.5 mg kg-1, or 15 mg kg-1 b. w. a day, three groups were receiving BDE209 in the doses of 1000 mg kg-1, 2000 mg kg-1, or 4000 mg kg-1 b. w. a day, while nine groups were receiving different mixtures of Cd and BDE209 in these doses (3x3 design). The results have indicated that the Cd+BDE209 mixtures more potently disrupt thyroid hormone homeostasis than would be expected from these chemicals alone.

scholarly journals Modern concepts of primary thyroid gland failure

1996 ◽  
Vol 42 (1) ◽  
pp. 179-182 ◽  
Author(s):  
E C Ridgway
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Hormone Deficiency ◽  
Clinical Effects ◽  
Normal Range ◽  
Medical Disorder ◽  
Clinical Detection ◽  
Key Genes ◽  
Serum Tsh

Abstract Primary thyroid gland failure is a common medical disorder occurring in mild or severe forms in 10% to 15% of our population. Symptoms may be classical and easy to recognize or very subtle, escaping clinical detection. This disorder is more common in females and increases with advancing age. The most important diagnostic test is measurement of the serum thyrotropin (TSH) concentration, which will increase above the normal range in both mild and severe cases. Most clinical effects of thyroid hormone deficiency can be explained by the "nuclear thyroid hormone hypothesis," which states that thyroid hormones act predominantly by effecting the transcription of key genes in affected tissues. Therapy of hypothyroidism is easy, inexpensive, and precise, involving pure L-thyroxine and measuring dose requirements and efficacy by monitoring serum TSH concentrations.

scholarly journals Applicability of thyroxine measurements and ultrasound imaging in evaluations of thyroid function in turtles

2019 ◽  
Vol 63 (2) ◽  
pp. 267-273
Author(s):  
Joanna Pajdak-Czaus ◽  
Elżbieta Terech-Majewska ◽  
Dagmara Będzłowicz ◽  
Martyn Mączyński ◽  
Wioletta Krystkiewicz ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Ultrasound Imaging ◽  
Ultrasound Examination ◽  
Plasma Concentrations ◽  
Physiological Homeostasis ◽  
Low Levels ◽  
And Function

AbstractIntroduction: The thyroid and parathyroid glands play a major role in maintaining physiological homeostasis in all vertebrates. Reptiles have plasma concentrations of thyroid hormones far lower than mammals. Low levels of these hormones in reptiles impede thyroid hormone detection with assays designed for the higher levels of mammals. The aim of this study was to explore teaming this with ultrasound imaging of the thyroid to appraise glandular function. Material and Methods: Thyroid function of four pond sliders was evaluated based on the results of T4 analyses and ultrasound. Results: The concentrations of T4 varied considerably between the examined animals from <9 nmol/L to >167.3 nmol/L. Ultrasound examination revealed uniform echogenicity and a smooth outline of the thyroid gland in all animals. Conclusion: Monitoring of thyroid function based on T4 and electrolyte concentrations is helpful in assessing the health and living conditions of reptiles, which is important in veterinary practice but problematic. Ultrasound examinations are useful in diagnosing changes in gland structure, such as tumours and goitres, and a combination of both methods supports comprehensive assessments of the anatomy and function of the thyroid gland.

Causes and laboratory investigations of thyrotoxicosis

2011 ◽  
pp. 466-476 ◽  
Author(s):  
Francesco Latrofa ◽  
Paolo Vitti ◽  
Aldo Pinchera
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Laboratory Testing ◽  
Thyroid Stimulating Hormone ◽  
Clinical Syndrome ◽  
Laboratory Confirmation ◽  
Common Causes ◽  
Laboratory Investigations ◽  
Destructive Processes

The term thyrotoxicosis identifies the clinical syndrome caused by elevated circulating thyroid hormones of all sources, while the term hyperthyroidism includes only the disorders due to an increased secretion of hormones by the thyroid gland. Hyperthyroidism is the most frequent cause of thyrotoxicosis. Destructive processes involving the thyroid gland that induce unregulated discharge of preformed thyroid hormones (destructive thyrotoxicosis) and circulating thyroid hormone of extrathyroidal origin (exogenous or extrathyroidal thyrotoxicosis) are less common causes of thyrotoxicosis. Although careful history taking and physical examination often allows a diagnosis of thyrotoxicosis to be made, laboratory confirmation by measurement of thyroid-stimulating hormone (TSH) and thyroid hormone is always needed. Once thyrotoxicosis is confirmed, laboratory testing and thyroid imaging are required to identify the cause of thyrotoxicosis.

Cognitive and Behavioral Complications of Congenital Hypothyroidism

2010 ◽  
Author(s):  
Ruth D. Nass
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Brain Development ◽  
Congenital Hypothyroidism ◽  
Behavioral Problems ◽  
Thyroid Stimulating Hormone ◽  
Primary Hypothyroidism ◽  
Normal Brain ◽  
Gene Encoding ◽  
Hormone Synthesis

Congenital hypothyroidism (CH) affects approximately 1 in 3,500 newborns. There is a female preponderance. In areas of iodine insufficiency, the incidence is higher, since iodine is a key element in the synthesis of thyroid hormone. Approximately 85% of CH cases are sporadic, whereas 15% are hereditary. Thyroid hormone is essential for normal pre- and postnatal brain development. The importance of in utero thyroid hormone status is demonstrated by the fact that maternal hypothyroidism during pregnancy is known to result in cognitive and motor deficits in the offspring (Forrest 2004; Zoeller and Rovet 2004). Congenital hypothyroidism is already expressed in fetal life; maternal T4, transferred via the placenta, is not sufficient for normal brain development (Forrest 2004; Haddow et al. 1999; Opazo et al. 2008; Pop and Vulsma 2005). Prior to newborn screening, CH that went undiagnosed and untreated for more than 3 months was associated with permanent and significant mental retardation, as well as behavioral problems. Outcome is now significantly better. Children with CH have normal intelligence, although subtle and specific cognitive and behavioral problems occur. Congenital hypothyroidism can be caused by primary hypothyroidism, due to a defect of the thyroid gland, or by central hypothyroidism secondary to defective hypothalamic or pituitary regulation of thyroid hormone. Several types of primary thyroid abnormalities may occur. Thyroid dysgenesis is the result of a missing, ectopic, or hypoplastic gland. Proteins that are crucial for normal thyroid gland development include the thyroid transcription factors PAX8, TTF1, TTF2, FOXE1 and the thyroid stimulating hormone (TSH) receptor gene. Thyroid dyshormonogenesis is generally due to an autosomal recessive genetic defect in any of many stages of thyroid hormone synthesis, secretion and transport (Moreno and Visser 2007). One in 50,000 children has autosomal dominant thyroid hormone resistance (RTH) due to a mutation in the gene encoding for the TRb thyroid receptors (Hauser et al. 1993; Weiss et al. 1993). Iodine deficiency can also cause CH (endemic cretinism) (DeLange et al. 2000). Gaudino and colleagues (2005) determined the etiology of CH in 49 non-athyroid cases.

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