scholarly journals Reducing Effect of Nadolol on Serum Levels of Free Thyroid Hormones in Hyperthyroidism.

1994 ◽  
Vol 41 (6) ◽  
pp. 717-723
Author(s):  
TAKU KASHIWAI ◽  
HISATO TADA ◽  
HARUO TAMAKI ◽  
YOH HIDAKA ◽  
ERIKO ITO ◽  
...  
1985 ◽  
Vol 108 (2) ◽  
pp. 211-216 ◽  
Author(s):  
G. Benker ◽  
C. Splittstößer ◽  
H. Meinhold ◽  
Th. Olbricht ◽  
D. Reinwein

Abstract. Bovine TSH was administered iv to 10 normal volunteers in doses of 2.5, 7.5, 15 and 30 mU/kg. Brisk elevations of serum diiodotyrosine occurred already after the smallest dose (mean, + 183%) while larger doses had only slight additional effects. T3 rose much higher than T4 (+71% compared to +23% after 15 mU bTSH/kg), and free thyroid hormones exhibited changes similar to total T3 and total T4. The mean absolute increase in serum fT3 ranged from 2.03 to 9.04 pmol/l and proved to be an easily measurable parameter for the TSH effect. Dose-response effects were seen for the increases of fT4, fT3 and T3. TBG and rT3 did not change but the degradation product 3,3'-T2 showed large increments of serum levels. There was no correlation between the response of T3 and T4, fT3 and fT4, or diiodotyrosine and any of the other parameters of thyroid function. The interindividual differences in the magnitude of thyroid hormone response to TSH were considerable, and there was no relationship between this response and thyroid volume by ultrasound. We conclude that direct stimulation of the thyroid gland with bTSH in small doses leads to consistent increases of thyroid hormones, especially T3 and fT3, that the response varies between individuals, and that the precursor diiodotyrosine is released together with thyroid hormones.


1990 ◽  
Vol 29 (01) ◽  
pp. 40-43 ◽  
Author(s):  
W. Langsteger ◽  
P. Költringer ◽  
P. Wakonig ◽  
B. Eber ◽  
M. Mokry ◽  
...  

This case report describes a 38-year-old male who was hospitalized for further clarification of clinically mild hyperthyroidism. His increased total hormone levels, the elevated free thyroid hormones and the elevated basal TSH with blunted response to TRH strongly suggested a pituitary adenoma with inappropriate TSH incretion. Transmission computed tomography showed an intrasellar expansion, 16 mm in diameter. The neoplastic TSH production was confirmed by an elevated alpha-subunit and a raised molar alpha-sub/ATSH ratio. However, T4 distribution on prealbumin (PA, TTR), albumin (A) and thyroxine binding globulin (TBG) showed a clearly increased binding to PA (39%), indicating additional prealbumin-associated hyperthyroxinemia. The absolute values of PA, A and TBG were within the normal range. After removal of the TSH-producing adenoma, basal TSH, the free thyroid hormones and T4 binding to prealbumin returned to normal. Therefore, the prealbumin-associated hyperthyroxinemia had to be interpreted as a transitory phenomenon related to secondary hyperthyroidism (T4 shift from thyroxine binding globulin to prealbumin) rather than a genetically conditioned anomaly of protein binding.


2021 ◽  
Vol 16 ◽  
Author(s):  
Reihaneh Rezaee ◽  
Masoud Mohebbi ◽  
Mozhgan Afkhamizadeh ◽  
Mohammad Ali Yaghoubi ◽  
Mona Najaf Najafi ◽  
...  

Background and Objective: Subclinical hypothyroidism can potentially develop to overt hypothyroidism. Thyroid hormones have substantial roles in metabolism and glucose homeostasis and thus are closely related to determinant factors of metabolic syndromes, such as obesity and insulin resistance. Osteocalcin is considered a predictor of metabolic conditions in thyroid diseases. This study aimed to investigate the effect of levothyroxine vs. placebo on serum osteocalcin levels in patients with subclinical hypothyroidism. Methods: This randomized clinical trial was performed on 30 patients with subclinical hypothyroidism who were referred to the endocrine clinics of Ghaem and Imam Reza hospitals in Mashhad, Iran. After giving informed consent, patients were randomly divided into intervention (50 µg/day levothyroxine for 2 months) and control (placebo) groups. Serum levels of osteocalcin, thyroid hormones, lipid profile, insulin, and fasting glucose, as well as other clinical and anthropometric data, were measured at baseline and at the end of the study. SPSS was used to analyze the data and P<0.05 was considered significant. Results: Mean age in the intervention and control groups was 35.07 ± 9.94 and 31.30 ± 4.30, respectively (P=0.20). There was no significant difference between osteocalcin levels before and after the intervention in either of the groups (P=0.54). TSH level was significantly decreased in the levothyroxine group after the intervention (P<0.01). T4 level was significantly increased in the intervention group (P=0.02). Conclusion: Levothyroxine had no significant effect on increasing the levels of serum osteocalcin in patients with subclinical hypothyroidism. We have registered the trial in the Iranian registry of clinical trials (IRCT) with the registration code IRCT20171129037677N1.


1995 ◽  
Vol 21 (3) ◽  
pp. 671-680 ◽  
Author(s):  
M. C. Arufe ◽  
B. Arias ◽  
R. Durán ◽  
M. Alfonso

1985 ◽  
Vol 69 (2) ◽  
pp. 113-121 ◽  
Author(s):  
C. A. Ollis ◽  
S. Tomlinson ◽  
D. S. Munro

Graves’ disease is the commonest form of hyperthyroidism in which excessive production of thyroid hormones by the hyperplastic overactive thyroid gland produces elevated serum levels of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). Many of the manifestations of Graves’ disease, increased basal metabolic rate, increased heart rate, heat intolerance, sweating and nervousness, can be attributed to the peripheral actions of the excess thyroid hormones. The pathogenesis of many of the other dramatic features of Graves’ disease, such as the eye involvement or localized skin changes, is not fully understood, but circulating immunoglobulins with thyroid stimulating activity are almost certainly linked to excess thyroid hormone production and thereby cause the hyperthyroidism.


1984 ◽  
Vol 26 (5) ◽  
pp. 633-634 ◽  
Author(s):  
J. A. Franklyn ◽  
M. C. Sheppard ◽  
D. B. Ramsden

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1306-1313 ◽  
Author(s):  
Lutz Schomburg ◽  
Cornelia Riese ◽  
Marten Michaelis ◽  
Emine Griebert ◽  
Marc O. Klein ◽  
...  

The thyroid gland is rich in selenium (Se) and expresses a variety of selenoproteins that are involved in antioxidative defense and metabolism of thyroid hormones (TH). Se deficiency impairs regular synthesis of selenoproteins and adequate TH metabolism. We recently generated mice that lack the plasma Se carrier, selenoprotein P (SePP). SePP-knockout mice display decreased serum Se levels and manifest growth defects and neurological abnormalities partly reminiscent of thyroid gland dysfunction or profound hypothyroidism. Thus, we probed the TH axis in developing and adult SePP-knockout mice. Surprisingly, expression of Se-dependent 5′-deiodinase type 1 was only slightly altered in liver, kidney, or thyroid at postnatal d 60, and 5′-deiodinase type 2 activity in brain was normal in SePP-knockout mice. Thyroid gland morphology, thyroid glutathione peroxidase activity, thyroid Se concentration, and serum levels of TSH, T4, or T3 were within normal range. Pituitary TSHβ transcripts and hepatic 5′-deiodinase type 1 mRNA levels were unchanged, indicating regular T3 bioactivity in thyrotropes and hepatocytes. Cerebellar granule cell migration as a sensitive indicator of local T3 action during development was undisturbed. Collectively, these findings demonstrate that low levels of serum Se or SePP in the absence of other challenges do not necessarily interfere with regular functioning of the TH axis. 5′-deiodinase isozymes are preferentially supplied, and Se-dependent enzymes in the thyroid are even less-dependent on serum levels of Se or SePP than in brain. This indicates a top priority of the thyroid gland and its selenoenzymes with respect to the hierarchical Se supply within the organism.


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