Urine TRH immunoreactivity in hypothyroid and hyperthyroid patients

1984 ◽  
Vol 105 (4) ◽  
pp. 482-486 ◽  
Author(s):  
Anna-Stina Suhonen ◽  
Juhani Leppäluoto ◽  
Jorma Salmi
Keyword(s):  
Healthy Subjects ◽  
Ammonium Acetate ◽  
Polar Solvent ◽  
Primary Hypothyroidism ◽  
Exchange Chromatography ◽  
Reverse Phase ◽  
Before And After ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients ◽  
Serum Tsh

Abstract. Urine samples from 8 healthy subjects, from 16 patients with primary hypothyroidism and 8 patients with Graves' hyperthyroidism were pre-purified in SP-Sephadex-C-25 cation-exchange-chromatography, subjected to reverse phase high-pressure liquid chromatography (HPLC) with 0.01 M ammonium acetate pH 4 as a polar and propanol as a non-polar solvent with a 1%/min gradient and assayed in our TRH radioimmunoassay. Urine TRH-immunoreactivity levels were measured before and after 3 months of treatment with thyroxine or methimazole. The urine TRH-levels in healthy subjects were 5.5 ± 1.4 ng/l (mean ± sem, n = 8). In the hypothyroid patients, the urine TRH levels were 50.6 ±40 ng/l before and 71.7 ± 45.3 ng/l after 3 months of treatment with thyroxine. These values did not significantly differ from those in healthy subjects. The large variations were due to highly elevated values in 3 patients. In 2 hypothyroid patients with initially high urine TRH values, 67 and 657 ng/l, urine TRH was measured 5 and 18 months later and was found to have decreased to 5 and 11 ng/l. In the hyperthyroid patients, urine TRH levels were 10.3 ± 3.9 ng/l before and 8.9 ± 3.3 ng/l after the treatment with methimazole and did not differ significantly from the levels in healthy subjects. After 3 months of treatment, the hyper- and the hypothyroid patients were euthyroid. Our results show, that, except in 2 hypothyroid patients, there does not appear to be any relationship between urine TRH levels and serum TSH or thyroid hormone levels in hypothyroid and hyperthyroid patients.

scholarly journals Thyroid hormone increases mannan-binding lectin levels

2005 ◽  
Vol 153 (5) ◽  
pp. 643-649 ◽  
Author(s):  
Anne Lene Dalkjær Riis ◽  
Troels Krarup Hansen ◽  
Steffen Thiel ◽  
Claus Højbjerg Gravholt ◽  
Signe Gjedde ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Healthy Subjects ◽  
Paired Comparison ◽  
Innate Immune ◽  
Before And After ◽  
Low Levels ◽  
Mannan Binding Lectin ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients ◽  
Binding Lectin

Background: Recent studies have indicated the existence of causal links between the endocrine and immune systems and cardiovascular disease. Mannan-binding lectin (MBL), a protein of the innate immune system, may constitute a connection between these fields. Methods: To test whether thyroid hormone regulates MBL levels, we studied eight patients with Graves’ hyperthyroidism before and after methimazole therapy, eight healthy subjects before and after short-term experimental hyperthyroidism, and eight hypothyroid patients with chronic auto-immune thyroiditis before and after L-thyroxine substitution. Results: In all hyperthyroid patients, MBL levels were increased – median (range), 1886 ng/ml (1478–7344) – before treatment and decreased to 954 ng/ml (312–3222) after treatment (P = 0.01, paired comparison: Wilcoxon’s signed ranks test). The healthy subjects had MBL levels of 1081 ng/ml (312–1578). Administration of thyroid hormones to these persons induced mild hyperthyroidism and increased MBL levels significantly to 1714 ng/ml (356–2488) (P = 0.01). Two of the eight hypothyroid patients had undetectably low levels of MBL both before and after L-thyroxine substitution. The other six hypothyroid patients had decreased levels of MBL of 145 ng/ml (20–457) compared with 979 ng/ml (214–1533) after L-thyroxine substitution (P = 0.03, paired comparison: Wilcoxon’s signed ranks test). Conclusion: Our data show that thyroid hormone increases levels of MBL. MBL is part of the inflammatory complement system, and this modulation of complement activation may play a role in the pathogenesis of a number of key components of thyroid diseases.

Serum 3'-monoiodothyronine levels in normal subjects and in patients with thyroid and non-thyroid disease

1981 ◽  
Vol 97 (4) ◽  
pp. 454-460 ◽  
Author(s):  
C. Kirkegaard ◽  
J. Faber ◽  
D. Cohn ◽  
K. Kølendorf ◽  
H. Francis Thomsen ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Normal Subjects ◽  
Serum Levels ◽  
Endogenous Depression ◽  
Lower Detection Limit ◽  
Specific Radioimmunoassay ◽  
Lower Detection ◽  
Before And After ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients

Abstract. Serum 3'-monoiodothyronine (3'-T1) levels were estimated by means of a specific radioimmunoassay (RIA) preceded by an ethanol extraction. The recovery of 3'-T1 was in mean (± sem) 110 ± 9%, and the lower detection limit was 23 pmol/l. Serum levels of 3'-T1 in 34 euthyroid healthy subjects were (median (range)) 55 pmol/l (<23-168 pmol/l), in 13 hyperthyroid patients 133 pmol/l (70-265 pmol/l) (P < 0.01) and in 13 hypothyroid patients <23 pmol/l (<23-68 pmol/l) (P <0.01). In 11 patients with chronic renal failure serum 3'-T1 levels were highly increased 285 pmol/l (115-1538 pmol/l) (P < 0.01) and correlated inversely to creatinine clearance (R = −0.68, P < 0.05). In patients with liver cirrhosis serum 3'-T1 levels were unaffected, whereas in 19 patients with endogenous depression studied before and after recovery from the depression serum levels decreased from 70 pmol/l (< 23-248 pmol/l) to 30 pmol/l (<23-95 pmol/l (P < 0.01). Administration of propranolol 40 mg b. i. d. for 2 weeks did not affect serum 3'-T1 levels. The study shows that 3'-T1 is present in serum from euthyroid man and varies with thyroid function. Further, it is suggested that 3'-T1 in contrast to other iodothyronines primarily is eliminated by the kidneys.

Efficiency of Organic Binding of Trapped Iodide in Sporadic Goiter, Evaluated by the Decrease of Radioiodide Clearance

1977 ◽  
Vol 16 (04) ◽  
pp. 168-173
Author(s):  
Dige-Petersen Harriet
Keyword(s):  
Gamma Camera ◽  
Elevated Serum ◽  
Primary Hypothyroidism ◽  
Relative Decrease ◽  
Single Detector ◽  
The Difference ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients ◽  
Normal Controls ◽  
Serum Tsh

SummaryThe decrease of early thyroid radioiodide clearance was determined in 33 patients with sporadic simple goiter, in 21 normal controls, in 38 hyperthyroid, and 9 hypothyroid patients. The clearance was measured between 5 and 30 min after injection of the tracer, 132I or 123 I, using a single detector system or a gamma camera, respectively. The decrease of clearance was given as the difference between the thyroid radioiodide clearance (ml blood/min) from 5–10 min and 25–30 min post injection.The relative decrease of clearance was similar in controls and in patients with simple goiter, indicating a normal binding efficiency of trapped iodide in the patients. The median 5–10 min clearance of controls was 85 ml blood/min, and of the patients 125 ml/min, the median decrease of clearance was 26 and 36 ml/min, respectively, i. e. about 30% in both groups; the higher early clearance values correlated significantly with the higher decreases. In the hyperthyroid patients the relative decrease was less pronounced, indicating that the increased iodide trapping in these patients was accompanied by a proportionately greater binding efficiency. In patients with primary hypothyroidism and elevated serum TSH levels the fractional binding of trapped iodide did not differ from normal.It was concluded that minor degrees of organic binding defects could not be demonstrated in patients with sporadic simple goiter.

Effect of thyroid function on serum somatomedin activity

1981 ◽  
Vol 96 (4) ◽  
pp. 491-497 ◽  
Author(s):  
Josef Marek ◽  
Marie Schüllerová ◽  
Olga Schreiberová ◽  
Zdeňka Límanová
Keyword(s):  
Thyroid Hormones ◽  
Replacement Therapy ◽  
Primary Hypothyroidism ◽  
Embryonic Chick ◽  
Mean Values ◽  
Before And After ◽  
And Function ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients

Abstract. To obtain more information about a possible role of somatomedins in mediating the effects of thyroid hormones on the development and function of epiphyseal cartilage, somatomedin activity, measured on the basis of 35S incorporation in embryonic chick cartilage, was studied in thyrotoxic patients before and after treatment with carbimazole or surgery and in a group of patients with primary hypothyroidism. In 29 hyperthyroid patients mean values of somatomedin were 1.29 ± 0.03 sem and differed significantly (P < 0.01) from normals (1.04 ± 0.03). In 15 carbimazole treated patients and in 5 operated patients with thyrotoxicosis somatomedin levels fell from 1.29 ± 0.04 to 1.03 ± 0.04 (P < 0.01) when the patients became euthyroid. Correspondingly, somatomedin levels in 12 untreated hypothyroid patients (0.82 ± 0.04) were significantly less than in normals (P < 0.01) and increased from 0.77 ± 0.09 to 1.14 ± 0.13 (P < 0.05) in 4 patients on replacement therapy. In conclusion: somatomedin levels rise when thyroid hormones are present in excess, and fall when these are deficient. This suggests that thyroid hormones are important regulators of somatomedin levels.

THYROID FUNCTION AND PLASMA CYCLIC AMP RESPONSE TO INTRAVENOUS GLUCAGON

1977 ◽  
Vol 85 (4) ◽  
pp. 760-768 ◽  
Author(s):  
S. Nistrup Madsen
Keyword(s):  
Cyclic Amp ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Healthy Subjects ◽  
Blood Levels ◽  
Sensitive Test ◽  
Normal Response ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients

ABSTRACT The glucagon stimulated increase in plasma cyclic AMP has been studied in 17 healthy subjects, in 13 hyperthyroid and in 14 hypothyroid patients. Six hyperthyroid and 2 hypothyroid patients were re-investigated after at least 15 months of treatment. The results show: 1) The glucagon stimulated cyclic AMP response is significantly increased in hyperthyroid patients considered as a group, and is reduced in patients with hypothyroidism. 2) Three hyperthyroid and 4 hypothyroid patients showed a normal response to iv glucagon, indicating that the plasma cyclic AMP response to iv glucagon is not a sensitive test for the evaluation of peripheral thyroid states. This suggests that the effects of thyroid hormones in the liver does not necessarily follow the effects in other tissues. 3) Re-investigation of treated patients showed that the cyclic AMP response can be normalized by treatment, both in hyperthyroidism and in hypothyroidism. However, in patients treated for hyperthyroidism a hyper-response to glucagon can continue after blood levels of thyroid hormones are reduced to normal. This suggests an inertia in the loss of the hyper-response to glucagon, once a hyperfunction has been induced. A similar inertia in the loss of glucagon sensitivity in hypothyroidism could explain the large number of normal tests in hypothyroid patients.

Free thyroxine, free triiodothyronine, and thyrotropin concentrations in hypothyroid and thyroid carcinoma patients receiving thyroxine therapy

1987 ◽  
Vol 116 (3) ◽  
pp. 418-424 ◽  
Author(s):  
K. Liewendahl ◽  
T. Helenius ◽  
B.-A. Lamberg ◽  
H. Mähönen ◽  
G. Wägar
Keyword(s):  
Thyroid Carcinoma ◽  
Equilibrium Dialysis ◽  
Primary Hypothyroidism ◽  
Free Thyroxine ◽  
Suppressive Therapy ◽  
Free Triiodothyronine ◽  
Thyroxine Therapy ◽  
Thyroxine Replacement ◽  
Hypothyroid Patients ◽  
Serum Tsh

Abstract. Free thyroxine (FT4) and free triiodothyronine (FT3) concentrations in serum were measured by direct equilibrium dialysis methods in patients receiving thyroxine replacement or suppression therapy. Four of 50 hypothyroid patients euthyroid on replacement therapy (mean thyroxine dose 120 μg/day) had supra-normal FT4 concentrations, whereas the FT3 concentrations were normal in all. Forty-one of 56 operated thyroid carcinoma patients on suppressive therapy (mean thyroxine dose 214 μg/day) had raised FT4 concentrations, whereas the FT3 concentration was elevated in only one patient. There was a large difference in mean FT4 values for hypothyroid and thyroid carcinoma patients (17.2 vs 29.5 pmol/l), whereas the difference in mean FT3 values was small (5.0 vs 6.1 pmol/l), suggesting a decreased peripheral conversion of T4 to T3 with increasing concentrations of FT4. Serum TSH concentrations, as determined by an immunoradiometric assay, varied from < 0.02 to 11.9 mU/l in treated hypothyroid patients; 21 patients (42%) had values outside the reference limits. As a single test, serum TSH is therefore not very useful for the assessment of adequate thyroxine dosage in patients with primary hypothyroidism. In thyroid carcinoma patients, the TSH concentrations were < 0.18 mU/l; 45 patients had values < 0.02 mU/l indicating sufficient suppression of TSH secretion in the majority of cases. On the basis of these results we recommend the combination of FT3 and TSH tests for monitoring thyroxine replacement and suppression therapy. FT4 appears less useful than FT3 for this purpose even if special reference values values were adopted for each patient group.

scholarly journals Recent evidence sets therapeutic targets for levothyroxine-treated patients with primary hypothyroidism based on risk of death

2021 ◽  
Vol 184 (2) ◽  
pp. C1-C3
Author(s):  
Petros Perros ◽  
Krishnarajah Nirantharakumar ◽  
Laszlo Hegedüs
Keyword(s):  
Large Population ◽  
Indirect Evidence ◽  
Thyroid Stimulating Hormone ◽  
Primary Hypothyroidism ◽  
Normal Serum ◽  
Normal Range ◽  
Ample Evidence ◽  
Risk Of Death ◽  
Hypothyroid Patients ◽  
Serum Tsh

Since the introduction of sensitive assays for serum thyroid-stimulating hormone (TSH) clinicians have advised hypothyroid patients to adjust the dose of levothyroxine (L-T4) in order to achieve a normal serum TSH. A minority of patients are dissatisfied with this treatment strategy and experience symptoms. Some indirect evidence suggests that a normal serum TSH may not necessarily reflect euthyroidism at the tissue level in patients treated with L-T4. Increasingly hypothyroid patients demand higher doses of L-T4 or liothyronine (L-T3) or animal thyroid extract, often purchased online, and titrate the dose against symptoms, although ample evidence suggests that combination treatment (L-T4 with L-T3) is no more effective than L-T4 alone. Community surveys show that up to 53% of treated hypothyroid patients at any time have a serum TSH outside the normal range. The recommendation by guidelines that the upper limit of the normal range for serum TSH should not be exceeded is supported by robust evidence and is generally accepted by clinicians and patients. However, until recently the lower limit of serum TSH for optimal L-T4 replacement has been controversial. New evidence obtained by two independent large population studies over the past two years has shown that mortality of hypothyroid patients treated with levothyroxine is increased when the serum TSH exceeds or is reduced outside the normal reference range. It is estimated that the implementation of a policy of normalising serum TSH in hypothyroid patients will reduce the risk of death of 28.3 million people in the USA and Europe alone.

EFFECT OF THYROTROPHIN RELEASING HORMONE (TRH) IN PATIENTS WITH PITUITARY DISORDERS

1977 ◽  
Vol 85 (3) ◽  
pp. 479-487 ◽  
Author(s):  
J. Lindholm ◽  
H. Dige-Petersen ◽  
L. Hummer ◽  
P. Rasmussen ◽  
O. Korsgaard
Keyword(s):  
Pituitary Tumour ◽  
Thyroid Stimulating Hormone ◽  
Trh Test ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Basal Serum ◽  
Chromophobe Adenoma ◽  
Before And After ◽  
Hypothyroid Patients ◽  
Serum Tsh

ABSTRACT The secretion and biological activity of thyroid stimulating hormone (TSH) were studied in 22 patients with a pituitary tumour (17 acromegalics and 5 patients with a chromophobe adenoma) and in 36 hypophysectomized patients (16 acromegalics and 20 with a chromophobe adenoma). Thyroid function was assessed by serum thyroxine (T4), serum triiodothyronine (T3), and thyroxine-binding globulin (TBG) concentration. Serum TSH was measured before and after injection of TSH releasing hormone (TRH), and in 19 hypophysectomized patients the T3 response after TRH was measured. In addition a TRH test was performed 1–2 weeks after surgery in 11 patients. The basal serum TSH did not differ from euthyroid control values in any of the groups and no late effect of hypophysectomy was observed. Subnormal peak TSH values were seen in 10 out of 37 euthyroid patients, whereas 9 out of 11 hypothyroid patients responded normally. Hypophysectomy caused an immediate but transient decrease in peak TSH in patients with a chromophobe adenoma only. The rise in serum T3 after TRH was significantly lower in hypophysectomized patients than in controls. An increase in TSH was followed by a T3 response in all patients except in 4 out of 8 euthyroid acromegalics. In patients operated on for a chromophobe adenoma the T3 response was correlated with serum T4, whereas this was not the case in acromegalics.

Platelet and adipocyte thermogenesis in hypothyroid patients: a microcalorimetric study

1985 ◽  
Vol 108 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Stig Valdemarsson ◽  
Birger Fagher ◽  
Pavo Hedner ◽  
Mario Monti ◽  
Peter Nilsson-Ehle
Keyword(s):  
Thyroid Hormones ◽  
Heat Production ◽  
Healthy Subjects ◽  
Mean Value ◽  
Metabolic Effects ◽  
Adipocyte Size ◽  
Before And After ◽  
The Mean ◽  
Hypothyroid Patients ◽  
Adequate Method

Abstract. Direct microcalorimetry was used for measurements of heat production in cell suspensions of platelets and adipocytes, obtained from hypothyroid patients before and after 3 months on full l-thyroxine substitution. Platelet heat production was significantly lower than normal before treatment and increased in all 10 patients studied; the mean value increased from 51.3 ± 1.6 fW/cell before to 57.1 ± 1.8 fW/cell after therapy (P< 0.001). Similarily, adipocyte heat production was initially significantly lower than normal and increased during treatment in all 6 patients investigated. The mean value for heat production per adipocyte was 18.8 ± 1.7 pW/cell before and 32.4 ± 2.5 pW/cell after therapy (P < 0.025), which is still below the level recorded in lean healthy subjects. The adipocyte size did not change significantly. The increase in adipocyte heat production was correlated to the increase in S-triiodothyronine levels (r = 0.84, P <0.05). In hypothyroidism, the total metabolic activity seems to be comparatively more reduced in adipocytes than in platelets. A difference may exist between these cells with regard to recovery of normal metabolic acitivity during treatment for hypothyroidism. Direct microcalorimetry appears to be an adequate method for monitoring net metabolic effects of thyroid hormones in these cells.

Influence of dopaminergic inhibition on serum levels of thyrotrophin and prolactin in patients with hypothyroidism before and after prolonged oral administration of TRH

1983 ◽  
Vol 104 (2) ◽  
pp. 183-188 ◽  
Author(s):  
Harald M. M. Frey ◽  
Egil Haug
Keyword(s):  
Oral Administration ◽  
Serum Levels ◽  
Primary Hypothyroidism ◽  
Dopamine Antagonist ◽  
Trh Stimulation ◽  
Before And After ◽  
The Mean ◽  
Pre Treatment ◽  
Serum Tsh

Abstract. Forty mg TRH/day given orally for 3 weeks to 8 patients with mild primary hypothyroidism decreased serum TSH from a mean of 4.0 ng/ml ± 1.2 (se) to 2.0 ng/ml ± 0.4 (49%), and their mean incremental TSH response to iv TRH was equally reduced from 8.6 ng/ml ± 2.5 to 4.0 ng/ml ± 1.9 (46%). In the same patients serum Prl was 8.2 ng/ml ± 2.2 before oral TRH treatment and 6.6 ng/ml ± 1.5 (81%) after treatment, and the mean incremetal Prl response to iv TRH was reduced from 43.5 ng/ml ± 5.0 to 35.9 ng/ml ± 7.5(83%). The oral administration of 10 mg of the dopamine antagonist metoclopramide increased mean serum TSH from 0.6 ng/ml ± 0.1 (se) to 0.7 ng/ml ± 0.1 (120%) in euthyroid subjects and from 4.0 ng/ml ±1.2 to 5.7 ng/ml ± 1.6 (145%) in patients with primary hypothyroidism, and mean serum Prl from 8.6 ng/ml ± 0.8 to 109.5 ng/ml ± 24.3 (1251%) and from 8.2 ng/ml ± 2.2 to 119.6 ng/ml ± 45.5(1460%), respectively. The incremental TSH responses to iv TRH increased 2.3-fold in euthyroid subjects pre-treated with metoclopramide, while no change was observed in the TSH responsiveness in patients with primary hypothyroidism following metoclopramide pre-treatment. In the euthyroid subjects metoclopramide treatment had no effect on the Prl response to iv TRH. In the primary hypothyroid group metoclopramide pre-treatment caused a reduced Prl response to iv TRH in more than 50% of the patients. It is concluded that long-term TRH treatment decreased the serum levels of TSH and Prl as well as the incremental increases in TSH and Prl to iv TRH stimulation in patients with primary hypothyroidism. Long-term TRH treatment did not change the TSH and Prl responses to the dopamine antagonist metoclopramide.

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