scholarly journals Bone metabolism during substitution therapy of primary hypothyroidism

2009 ◽  
Vol 62 (9-10) ◽  
pp. 407-411
Author(s):  
Radoslav Pejin ◽  
Nikola Curic ◽  
Branka Kovacev-Zavisic ◽  
Ljiljana Todorovic-Djilas

Introduction. The relation between thyroid hormones and bone metabolism markers in hyperthyroidism is well known. Earlier studies indicate the possibility of bone metabolism acceleration during the excessive replacement therapy with l-thyroxin in hypothyroid patients especially in one with other risk factors for bone metabolism impairment. This study evaluated the effect of physiological l-thyroxine treatment on bone metabolism in patient with primary hypothyroidism. Material and methods. In the study group of 30 hypothyroid patients individual thyroxine replacement was performed targeting euthyroid status. Bone and calcium metabolism parameters (osteocalcin-OC, alkaline phosphates-ALP, C-terminal cross-linking telopeptide type I-CL, parathormone-PTH, Ca, ionized Ca, P), thyroid hormone levels (T3, T4, TSH) were measured before treatment and when euthyroid status was achieved. Results and discussion. A significant treatment effect was observed for bone formation and resorption parameters before and during the therapy; OC (p=0.000024), CL (p=0.002648). Ionized calcium levels also showed significantly higher values in euthyroid status confirming bone metabolism acceleration during the l-thyroxine therapy (p= 0.020). Thus, calcium metabolism hormone regulators were not significantly different before and after the therapy; PTH (p=0.27). Thyroid hormone levels showed significant correlation with bone metabolism parameters before the therapy whereas this correlation was not found during therapy because of different individual l-thyroxine doses. Conclusion. It can be concluded that physiological doses of l-thyroxine therapy accelerate bone metabolism in hypothyroid patients. Thus, the argument against bone loss during physiological substitution is highly specific mutual correlation between bone formation and resorption parameters. These assumptions require further investigations in long term prospective studies in patients on replacement l-thyroxine therapy.

1998 ◽  
Vol 76 (12) ◽  
pp. 1120-1131 ◽  
Author(s):  
William N Henley ◽  
Linda L Bellush ◽  
Marc Tressler

A three-part study explored the basis for an interaction between changes in thyroid status and bulbospinal serotonin (5HT) metabolism. In experiment 1, three well-characterized models of primary hypothyroidism were all accompanied by significant increases in 5HT metabolism. In experiment 2, circulating thyroid hormone levels were experimentally varied from very low methimazole (Meth) treatment to very high (T3 implants: 2.5, 5.0, or 7.5 mg triiodothyronine). As in experiment 1, Meth led to elevated 5HT. Hyperthyroidism was accompanied by significant reductions in 5HT, while urinary norepinephrine excretion paralleled 5HT. In experiment 3, rats were subjected to Meth either 2 weeks before or after induction of diabetes with streptozotocin (Stz). Meth prevented Stz-associated reductions in 5HT and attenuated development of hyperphagia. Meth could not reverse established Stz-associated reduction in 5HT or hyperphagia, although both were slightly attenuated. Thus, although the first two experiments argue for a simple inverse relationship between circulating thyroid hormone levels and 5HT in the brain, experiment 3 demonstrated that Stz-associated decrements in 5HT could not be reversed by subsequent lowering of circulating thyroid hormone. Nor did accompanying measurements indicate that glycemic status or circulating levels of leptin were important predictors of 5HT. Thus the interaction between thyroid hormones and 5HT is both more subtle and more complex than previously thought.Key words: hypothyroidism, hyperthyroidism, serotonin, diabetes mellitus.


1980 ◽  
Vol 27 (3) ◽  
pp. 291-295 ◽  
Author(s):  
MITSUO INADA ◽  
MITSUSHIGE NISHIKAWA ◽  
KOICHI NAITO ◽  
HITOSHI ISHII ◽  
KIYOSHI TANAKA ◽  
...  

2002 ◽  
Vol 50 (1) ◽  
pp. 93-100 ◽  
Author(s):  
T. Keçeci ◽  
E. Keskin

The effect of dietary zinc (Zn) supplementation on plasma Zn and serum thyroid hormones was evaluated in healthy male Merino lambs and Angora goats. A total of 12 lambs and 12 goats were divided into two equal groups as control and Zn groups in separate experiments. The lambs and goats of the control groups were fed basal rations alone. The Zn contents of these rations prepared for lambs and goats were 40 mg/kg and 35 mg/kg in dry matter (DM), respectively. Both species of animals in the Zn groups were fed a basal ration supplemented with zinc sulphate adjusted to 250 mg Zn/kg diet in DM. The feeding trial lasted for 12 weeks in lambs and 8 weeks in goats. Blood samples were taken from the jugular vein at 4-week intervals. Both animal species in the Zn groups had higher plasma Zn values than the controls throughout the experimental period, except in the 4th week in goats. However, the levels of serum total thyroxine (T4) and triiodothyronine (T3) were lower in the lambs and goats of the Zn groups, except in the 4th week, as compared to those in the controls. Moreover, serum total thyroid hormone levels of the goats were higher at the 4th week than at the 8th week. Although there was a decrease in the levels of free thyroxine and triiodothyronine of both small ruminant species in the Zn groups when compared to the controls, these alterations were not statistically significant. These results may show that zinc supplementation to the diet at this dose reduces total thyroid hormone levels in small ruminants but does not yet impair the euthyroid status of the organism.


2007 ◽  
Vol 157 (2) ◽  
pp. 221-223 ◽  
Author(s):  
Anastasios Papadimitriou ◽  
Dimitrios T Papadimitriou ◽  
Anna Papadopoulou ◽  
Polyxeni Nicolaidou ◽  
Andreas Fretzayas

Introduction: A recent study on TSH receptor (TSHR) null mice suggested that skeletal loss occurring in hyperthyroidism is caused by the low TSH rather than high thyroid hormone levels. The aim of this study was to examine whether low TSH results in osteoporosis in the human. Subjects and methods: We determined bone mineral density (BMD) and markers of bone metabolism in two male siblings aged 9.8 and 6.8 years with isolated TSH deficiency, due to a mutation of the TSH β-subunit gene. BMD was measured in the lumbar spine (L1–L4) by dual-energy X-ray absorptiometry. Laboratory investigation included the determination of serum calcium, phosphate, 25-hydroxy-vitamin D, parathyroid hormone concentrations, and urine calcium (Ca)/creatinine (Cr) ratio. Osteoblast activity was measured by serum bone alkaline phosphatase and osteocalcin levels, and osteoclast activity by urine cross-linked amino-terminal, carboxy-terminal telopeptides of type I collagen and deoxypyridinoline concentrations. Results: BMD of both patients was within the normal range for age and sex; z-scores were −0.55 and −0.23 for patients 1 and 2 respectively. Serum calcium, phosphate, urine Ca/Cr ratio, and specific markers of bone metabolism were also within normal range. Conclusion: In childhood, chronic extremely low TSH levels, in the face of normal thyroid hormone levels, are not related to bone loss.


1978 ◽  
Vol 133 (3) ◽  
pp. 211-218 ◽  
Author(s):  
D. G. McLarty ◽  
W. A. Ratcliffe ◽  
J. G. Ratcliffe ◽  
J. G. Shimmins ◽  
A. Goldberg

SummaryThe prevalence of abnormal serum total thyroxine (T4) and triiodothyronine (T3) concentrations were determined in 1,206 in-patients in two associated psychiatric hospitals. The biochemical pattern of primary hypothyroidism occurred in five females and one male (prevalence 0.5 per cent), but in only one patient was the diagnosis clinically obvious. Eight patients (all female) were clinically hyperthyroid (prevalence 0.7 per cent), of whom six were previously undiagnosed. There was no evidence that phenothiazines or benzodiazepine therapy had any significant effect on thyroid hormone levels. The small differences in thyroid hormone levels between psychiatric diagnostic groups could be explained by differences in age distribution.


1992 ◽  
Vol 36 (6) ◽  
pp. 573-578 ◽  
Author(s):  
George Phillppou ◽  
Demetrios A. Koutras ◽  
Gregory Plperlngos ◽  
Athanasslos Souvatzoglou ◽  
Spyrldon D. Moulopoulos

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