A STUDY OF THE MECHANISMS INVOLVED IN THE PRODUCTION OF IODINE-DEFICIENCY GOITER

1965 ◽  
Vol 49 (4) ◽  
pp. 610-628 ◽  
Author(s):  
Hugo Studer ◽  
Monte A. Greer
Keyword(s):  
Iodine Deficiency ◽  
Elevated Serum ◽  
Extensive Study ◽  
The Body ◽  
Total Evidence ◽  
High Iodine ◽  
Tsh Secretion ◽  
Serum Tsh ◽  
Tsh Levels ◽  
Made In

ABSTRACT An extensive study of the temporal sequence of changes in thyroid function after initiation of a low iodine regimen has been made in rats. Variables measured include: thyroid weight, 131I uptake, monoiodotyrosine/diiodotyrosine (MIT/DIT) and triiodothyronine/thyroxine (T3/T4) ratios, iodide clearance, and 127I content. Also measured were protein-bound iodine (PBI), inorganic iodide and thyrotrophin (TSH) levels in the serum. Significant thyroid hypertrophy was produced during the first week and before there was a fall in serum PBI. Temporally related to the appearance of goiter were a rise in 131I uptake, MIT/DIT ratio and iodide clearance and a fall in thyroidal 127I concentration. In contrast, a fall in total thyroidal 127I appeared later and was closely correlated with a decline in serum PBI concentration and a rise in the thyroidal T3/T4 ratio. Manipulations such as hypophysectomy, injections of iodide, thyroxine or TSH, and refeeding a high iodine diet gave results consistent with the view that changes produced by iodine deficiency involve both autonomous and TSH-dependent thyroidal mechanisms. Although elevated serum TSH levels could not be demonstrated until after the first week of the iodine-deficient regimen, the total evidence of these studies permits the conclusion that increased TSH secretion is the most important factor in producing the thyroidal response to iodine deficiency. It is shown that homeostatic mechanisms allow maintenance of a normal level of circulating thyroid hormone in an iodine-deficient state until the body iodine pool becomes too severely depleted to supply adequate iodide substrate to the thyroid. The changes observed closely resemble those found in human iodine-deficient goiters. Although the large goiters produced after several weeks of an iodine-deficient regimen were hyperplastic, they could readily be converted to typical colloid goiters by feeding a high iodine diet for a few days.

scholarly journals Inhibition of pituitary type 2 deiodinase by reverse triiodothyronine does not alter thyroxine-induced inhibition of thyrotropin secretion in hypothyroid rats

2005 ◽  
Vol 153 (3) ◽  
pp. 429-434 ◽  
Author(s):  
P Cettour-Rose ◽  
T J Visser ◽  
A G Burger ◽  
F Rohner-Jeanrenaud
Keyword(s):  
Specific Inhibitor ◽  
Adult Rats ◽  
Reverse T3 ◽  
Brown Adipose ◽  
Tsh Secretion ◽  
Serum T3 ◽  
Serum T4 ◽  
Serum Tsh ◽  
Tsh Levels

Objectives: Intrapituitary triiodothyronine (T3) production plays a pivotal role in the control of TSH secretion. Its production is increased in the presence of decreased serum thyroxine (T4) concentrations and the enzyme responsible, deiodinase type 2 (D2), is highest in hypothyroidism. In order to document the role of this enzyme in adult rats we developed an experimental model that inhibited this enzyme using the specific inhibitor, reverse T3 (rT3). Methods: Hypothyroidism was induced with propylthiouracil (PTU; 0.025 g/l in drinking water) which in addition blocked deiodinase type 1 (D1) activity, responsible for the rapid clearance of rT3 in vivo. During the last 7 days of the experiment, the hypothyroid rats were injected (s.c.) for 4 days with 0.4 or 0.8 nmol T4 per 100 g body weight (bw) per day. For the last 3 days, the same amount of T4 was infused via s.c. minipumps. In additional groups, 25 nmol rT3/100 g bw per day were added to the 3-day infusion of T4. Results: Infusion of 0.4 nmol T4/100 g bw per day did not affect the high serum TSH levels, 0.8 nmol T4/100 g bw per day decreased them to 57% of the hypothyroid values. The infusions of rT3 inhibited D2 activity in all organs where it was measured: the pituitary, brain cortex and brown adipose tissue (BAT). In the pituitary, the activity was 27%, to less than 15% of the activity in hypothyroidism. Despite that, serum TSH levels did not increase, serum T4 concentrations did not change and the changes in serum T3 were minimal. Conclusions: We conclude that in partly hypothyroid rats, a 3-day inhibition of D2 activity, without concomitant change in serum T4 and minimal changes in serum T3 levels, is not able to upregulate TSH secretion and we postulate that this may be a reflection of absent or only minimal changes in circulating T3 concentrations.

Syndrome of'inappropriate secretion of thyroid-stimulating hormone' by partial target organ resistance to thyroid hormones

1981 ◽  
Vol 97 (3) ◽  
pp. 361-368 ◽  
Author(s):  
J. Salmerón De Diego ◽  
C. Alonso Rodriguez ◽  
A. Salazar Orlando ◽  
P. Sanchez Garcia Cervigon ◽  
E. Caviola Mutazzi ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Elevated Serum ◽  
Pituitary Tumour ◽  
Thyroid Stimulating Hormone ◽  
Target Organ ◽  
Resistance To Thyroid Hormones ◽  
Serum Thyroid Hormone ◽  
Serum Tsh ◽  
Tsh Levels ◽  
Stimulating Hormone

Abstract. A 74 year old woman was found to have elevated serum thyroid-stimulating hormone (TSH) levels and elevated serum thyroid hormone levels, with clinical euthyroidism. There was no evidence of a pituitary tumour. TSH levels increased substantially during methimazole therapy. Administration of dexamethasone was followed by a prompt fall in serum TSH levels. Triiodothyronine (T3) was administered over a period of 20 days in doses from 25 μg to as much as 100 μg daily causing a rise in serum T3 above 700 ng/100 ml, a decline of T4 and a blunting of the response to thyrotrophinreleasing hormone (TRH), with normal metabolic responses (pulse rate, photomotogram, cholesterol). These results suggest that the patient's disorder is due to partial target organ resistance to thyroid hormones.

Subclinical hypothyroidism: treat or watch?

2021 ◽  
pp. 98-108
Author(s):  
I. A. Tsanava ◽  
S. V. Bulgakova ◽  
A. V. Melikova
Keyword(s):  
Thyroid Hormones ◽  
Subclinical Hypothyroidism ◽  
Metabolic Disorders ◽  
Reference Range ◽  
Cognitive Disorders ◽  
The Body ◽  
Relationship Of ◽  
The Relationship ◽  
Serum Tsh ◽  
Tsh Levels

Manifest hypothyroidism occurs in more than 5 % of the population, while prevalence of subclinical hypothyroidism is much higher and reaches 15 %. In the practice of an endocrinologist, in most cases, the diagnosis and treatment of manifest hypothyroidism does not raise questions, while subclinical changes in thyroid hormones quite often generate a lot of discussions. The generally accepted reference range for TSH up to 4.50 μIU / ml is in conflict with data showing that more than 95 % of healthy people with euthyroidism have serum TSH levels up to 2.5 μIU / ml. At the same time, a lot of data has been accumulated on the effect of even slightly altered levels of thyroid hormones and TSH on various tissues, organs and systems of the body, especially on the cardiovascular, nervous and reproductive systems. This review analyzes the results of studies aimed at studying the relationship of subclinical hypothyroidism with cardiovascular and metabolic disorders, cognitive disorders, pathology of pregnant women.

Rapid adaptations of serum thyrotrophin, triiodothyronine and reverse triiodothyronine levels to short-term starvation and refeeding

1984 ◽  
Vol 105 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Jean-Noel Hugues ◽  
Albert G. Burger ◽  
A. Eugene Pekary ◽  
Jerome M. Hershman
Keyword(s):  
Serum Cortisol ◽  
Starvation Period ◽  
Short Term ◽  
Mean Values ◽  
Fed State ◽  
Tsh Secretion ◽  
The Mean ◽  
Serum Tsh ◽  
Tsh Levels

Abstract. Nutrition influences thyroid function at the level of TSH secretion, at the level of monodeiodination, and possibly elsewhere. In order to study the effect of starvation on TSH secretion, 8 healthy male volunteers fasted for 30 h and were then refed with 800 kcal. Refeeding was performed at 19.00 h and blood was sampled at 20 min intervals until midnight. Control experiments were performed in the same subjects both when they were normally fed and when the starvation period was prolonged a further 5 h until midnight. Starvation decreased serum TSH levels to below 1 mU/l, and without refeeding the nocturnal peak of the TSH nycthemeral rhythm was abolished. With refeeding serum TSH tended to increase towards midnight and was significantly higher than during starvation. However, the serum TSH levels remained significantly below those at the same time of the day in the absence of a preceding starvation period. Serum T3 levels were significantly lower than in the fed state. The mean values were 1.84 ± 0.03 vs 2.30 ± 0.06 nmol/l (120 ±2 vs 150 ± 4 ng/100 ml, mean ± sem P < 0.01). Refeeding did not result in a measurable change in serum T3 concentration (1.80 ± 0.05 nmol/l; 120 ± 3 ng/100 ml, mean ± sem, n.s.). The contrary was true for rT3 levels which increased in starvation and tended to fall with refeeding, but this decrease was not significant. As glucocorticoids have been implicated in the control of monodeiodination and TSH secretion, serum cortisol levels were also measured. They did not differ during the 3 experimental periods. The results show that short-term starvation and refeeding may be a valuable tool for studying in vivo control of TSH secretion. The results show that short-term starvation and refeeding may be a valuable tool for studying in vivo control of TSH secretion.

EFFECT OF PROLONGED ORAL ADMINISTRATION OF TRH ON PLASMA LEVELS OF THYROTROPHIN AND PROLACTIN IN NORMAL INDIVIDUALS AND IN PATIENTS WITH PRIMARY HYPOTHYROIDISM

1977 ◽  
Vol 85 (4) ◽  
pp. 744-752 ◽  
Author(s):  
Harald M. M. Frey ◽  
Egil Haug
Keyword(s):  
Elevated Serum ◽  
Primary Hypothyroidism ◽  
Trh Test ◽  
Normal Individuals ◽  
Term Administration ◽  
Maximal Rise ◽  
Trh Receptor ◽  
Serum Tsh ◽  
Tsh Levels

ABSTRACT Forty mg TRH/day was given orally for 3 weeks to 10 euthyroid women and 10 women with primary hypothyroidism on low replacement doses of thyroxine. Once weekly oral TRH was replaced by an iv TRH-test (0.4 mg) with measurement of serum concentration of TSH, prolactin (PRL), thyroxine (T4), triiodothyronine (T3) and cholesterol. In the normal group, mean serum T4 concentration increased after one week and remained elevated. Serum TSH concentration showed a slight tendency to decline. Maximal rise in TSH concentration after iv TRH (ΔTSH) fell from a mean of 4.0 ng/ml to 1.4 ng/ml within one week and stayed low. T3, cholesterol, PRL and ΔPRL were normal and unchanged throughout. In the hypothyroid group T4, T3, cholesterol, PRL and ΔPRL were not influenced by the TRH administration. In 2 patients (with the highest serum T4 concentrations) serum TSH concentration was normal and resistant to iv TRH. Of the 8 patients with elevated TSH, basal level and ΔTSH did not change in 2 (with subnormal T4 levels and the highest TSH levels). In the other 6 (with intermediate T4 levels) basal TSH fell from a mean of 10.1 ng/ml to 4.2 ng/ml, and ΔTSH from 10.0 ng/ml to 3.3 ng/ml after three weeks. It is concluded that in addition to feed-back effect of thyroid hormones, the pituitary response to long-term administration of TRH is determined by other factors. Among these may be reduced pituitary TRH receptor capacity and the activity of the TSH producing cells.

Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness

1994 ◽  
Vol 130 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Nicola Custro ◽  
Vincenza Scafidi ◽  
Salvatore Gallo ◽  
Alberto Notarbartolo
Keyword(s):  
Thyroid Hormone ◽  
Healthy Subjects ◽  
Normal Subjects ◽  
Healthy Individuals ◽  
Circadian Variations ◽  
Tsh Secretion ◽  
Thyroid Hormone Levels ◽  
Rhythmic Change ◽  
Serum Tsh ◽  
Tsh Levels

Custro N, Scafidi V, Gallo S, Notarbartolo A. Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness. Eur J Endocrinol 1994;130:132–6. ISSN 0804–4643. Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l, The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay from midnight (0 degrees) of the highest level in the rhythm) was −9.9 degrees. In contrast, severely ill patients showed only slight and anticipated elevations of serum TSH levels (mesor 0.93 mU/l, amplitude 0.22 mU/l, acrophase +82.4 degrees). Moreover, whereas the episodic TSH secretion in healthy individuals consisted of 5–8 pulses/24 h, mainly clustered around midnight, only one pulse of reduced amplitude was detected in two of the eight severely ill patients and no pulses in the other six. Since earlier studies have indicated that the loss of TSH pulsatility is associated with the relative insensitivity of the thyrotrophs to low thyroid hormone levels and our analytical procedures have demonstrated that 24 h pulsatile pattern of TSH closely overlapped with baseline TSH secretion, it seems reasonable to assume that low-thyroid-hormone state, deficient pulsatile TSH secretion and altered nyctohemeral TSH periodicity do not coincide by chance, but that there is a causal relationship between such abnormalities in severely ill patients. Nicola Custro, Cattedra di Patologia Medica, Via del Vespro, n.141, 90127 Palermo, Italy

RELATIONSHIP BETWEEN PEROXIDASE ACTIVITY AND SERUM TSH, T4 AND T3 LEVELS IN RATS IN THE COURSE OF IODINE DEFICIENCY

1978 ◽  
Vol 88 (3) ◽  
pp. 499-505 ◽  
Author(s):  
B. M. Nataf ◽  
P. Fragu ◽  
S. Ben Othman
Keyword(s):  
Iodine Deficiency ◽  
Peroxidase Activity ◽  
Control Diet ◽  
Early Period ◽  
Iodine Content ◽  
Thyroid Peroxidase ◽  
Wet Weight ◽  
Iodine Treatment ◽  
Serum Tsh ◽  
Tsh Levels

ABSTRACT The relationship between peroxidase activity and serum TSH, T4 and T3 levels was investigated in the course of iodine deficiency in rats. Rats were maintained either on a control diet with a relatively high iodine content (600 μg/kg of 127I), or on a low iodine diet (30 μg/kg of 127I). Twenty days after the low iodine treatment, the thyroid iodine [127I] concentration was half that of control value (647 ± 52 and 1241 ± 72 μg/g of wet weight, respectively). However, no significant changes in serum T4, T3, TSH were found at 20 days even though an early increase in peroxidase activity was observed. It was only at 35 days of iodine deficiency, when the concentration of iodine in the gland averaged 260 μg/g of wet weight that serum T4 and TSH levels started to be significantly modified. From day 35 to day 70, a significant and progressive decrease of plasma T4 concentration was observed, and it levelled off thereafter. The changes of serum T3 were much smaller than those of T4. A significant increase in serum TSH level was noted at 35 days. Thereafter TSH levels increased rapidly and progressively (205 % increase over control at 70 days and 643 % at 80 days). From day 35 until day 80 of the low iodine treatment, the thyroid peroxidase activity and the serum TSH level varied concomitantly. Our results suggest that for an iodine content between 5 and 2 μg per thyroid gland, the high cellular peroxidase activity observed could be correlated with an increase in circulating TSH, due to a decrease of T4. In contrast, in the early period of iodine deficiency, no correlation was found between peroxidase activity and serum T4, T3 and TSH levels.

scholarly journals Levels of T4 and TSH in mother's blood and in cord blood at the time of delivery

2013 ◽  
Vol 11 (1) ◽  
pp. 6-10
Author(s):  
K Agrawal ◽  
BH Paudel ◽  
PN Singh ◽  
S Majhi ◽  
H Pokhrel ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Blood Serum ◽  
Cord Blood ◽  
Iodine Deficiency ◽  
Elevated Serum ◽  
Reproductive Age ◽  
Average Weight ◽  
Cord Blood Serum ◽  
Serum T4 ◽  
Tsh Levels

Background: In conditions of maternal iodine deficiency, the frequency distribution of neonatal thyroid stimulating hormone (TSH) is shifted towards elevated values. Elevated serum TSH in the neonates indicates insufficient supply of thyroid hormones to the neonates, a major complication of iodine deficiency. Objectives: To determine the cord blood serum T4 and TSH levels and interrelationships with maternal thyroid hormones. Method: cord blood serum T4 and TSH levels of 45 consecutive newborns born at BPKIHS, Dharan, Nepal and maternal T4 and TSH levels were analyzed using ELISA based kits. Results: The mean age of mothers was 23.73± 3.86 years and average weight of the neonates was 3.038±0.45 Kg. The median levels of maternal and neonatal T4 were 1.09 ng/dl and 1.26 ng/ dl respectively. The corresponding median TSH levels were 3.71 mIU/L and 11.9 mIU/L. The maternal and neonatal levels of T4 were positively correlated. In 36 mothers who had TSH level within euthyroid range (0.3-6.2 mIU/L, Thyroid lab of BPKIHS), 22 neonates (61.11%) had TSH levels above 10 mIU/L. Among 9 mothers having TSH levels above 6.2 mIU/L, 7 (77.77%) neonates had TSH levels above 10 mIU/L. Conclusion: Overall 29 (64.44%) neonates had TSH level above 10 mIU/L which indicates mild degree of iodine deficiency. Iodine supplementation is required before pregnancy in majority of women of reproductive age. Health Renaissance, January-April 2013; Vol. 11 No.1; 6-10 DOI: http://dx.doi.org/10.3126/hren.v11i1.7593

Pharmacokinetics of 3,5,3'-triiodothyroacetic acid and its effects on serum TSH levels

1989 ◽  
Vol 121 (5) ◽  
pp. 651-658 ◽  
Author(s):  
C. Menegay ◽  
C. Juge ◽  
A. G. Burger
Keyword(s):  
Time Course ◽  
Kinetic Studies ◽  
Volume Of Distribution ◽  
Potency Ratio ◽  
Control Serum ◽  
Tsh Secretion ◽  
Dose Response Effect ◽  
Acid Administration ◽  
Serum Tsh ◽  
Tsh Levels

Abstract. 3,5,3'-triiodothyroacetic acid is an effective inhibitor of TSH secretion in central hyperthyroidism. Serum 3,5,3'-triiodothyroacetic acid was measured with an RIA preceded by immunoprecipitation. An anti-3,5,3'-triiodothyroacetic acid antibody was obtained in rabbits, using 3,5,3'-triiodothyroacetic acid coupled to hemocyanin and diazotized benzidine as antigen (crossreactivity with T4, T3, tetraiodothyroacetic acid was 0.2, 1.1, and 5%, respectively). Endogenous 3,5,3'-triiodothyroacetic acid levels could not be detected in 14 euthyroid, 10 hypothyroid and 10 hyperthyroid sera (detection limit 0.055 nmol/l). Kinetic studies were performed in 6 healthy male subjects who received an oral and an iv dose of 1050 μg of 3,5,3'-triiodothyroacetic acid. The serum measurements were analysed according to a non-compartmental method. The half-life of 3,5,3'-triiodothyroacetic acid was 6 h 22 min ± 29 min, the volume of distribution was 114 ± 9 1/70 kg, and the plasma clearance rate was 298 ± 14 1 · (70 kg)−1 · day−1. Highest 3,5,3'-triiodothyroacetic acid levels were measured after 40 min (for T3 2–3 h) and its absorption was 67±6%. The nadir of the mean TSH levels was 0.72 ± 0.09 mU/l 6 h after 3,5,3'-triiodothyroacetic acid administration. However, the time course of serum TSH response did not differ from that obtained after administration of 37.5 μg T3. The dose-response effect for TSH was studied using oral doses of 350, 700, 1400 and 2800 μg 3,5,3'-triiodothyroacetic acid. TSH was measured 9 h after 3,5,3'-triiodothyroacetic acid administration at 17.00 h, and compared with control serum TSH levels obtained at 08.00 h (1.53 ± 0.11) and at 17.00 h the day before the test (1.87 ± 0.11). They were 1.05 ± 0.15 (N = 9, mean ± sem), 0.83 ± 0.08 (N = 24), 0.66 ± 0.06 (N = 24), and 0.43 ± 0.02 mU/l (N = 6), respectively. In conclusion, TSH inhibition by 3,5,3'-triiodothyroacetic acid is similar to T3, with a potency ratio of 1 to 18.

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