In conclusion, T4-suppressive therapy was associated with bone loss in postmenopausal women, which could be prevented by either calcium supplementation or intranasal calcitonin, although the latter did not provide additional benefit compared to calcium alone.All patients were receiving a stable dose of L-T4 (170 /- 60 micrograms/day or 3.0 /- 1.4 micrograms/kg. day) for more than 1 yr. All had TSH levels of 0.03 mIU/L or less and an elevated free T4 (FT4) index, but normal T3 levels.
Bone mass, most studies reported bone loss in estrogen-deprived post-. density (BMD) in women receiving T4 suppression therapy. (2-8). However.Both endogenous hyperthyroidism and exogenous thyroxine suppressive therapy have been associated with reduction in bone mineral density (BMD but the).
Although controversies exist on the possible adverse effect of T4 on bone mass, most studies reported bone loss in estrogen-deprived postmenopausal women.Although controversies exist on the possible adverse effect of T4 on bone mass, most studies reported bone loss in estrogen-deprived postmenopausal women taking suppressive doses of T4. We prospectively studied 46 postmenopausal women with carcinoma of thyroid for 2 yr to evaluate the rate of bone loss and assess whether calcium supplementation with or without.
No significant changes were detected in the bone-specific alkaline phosphatase levels. Urinary hydroxyproline excretion increased in group 3 at the end of 2 yr, but remained the same in groups 1 and 2.The calcium intake was low and averaged 507 /- 384 g/day as assessed by dietary recall. The subjects were randomized into three groups: 1) intranasal calcitonin (200 IU daily) for 5 days/week plus 1000 mg calcium daily, 2) calcium alone, or 3) placebo.
Prevention of bone loss induced by thyroxine suppressive therapy in postmenopausal women: the effect of calcium and calcitonin. Kung AW(1 Yeung SS).Total body and regional bone mineral density were measured by a dual energy x-ray absorptiometry bone densitometer at 6-month intervals. The results showed that both groups 1 and 2 had stable bone mass, whereas patients in groups 3 showed significant bone loss at the end of 2 yr (lumbar spine, 5.0, hip, 6.7, trochanter, 4.7;.
Thyroid hormone has been shown to stimulate bone resorption. Both endogenous hyperthyroidism and exogenous thyroxine suppressive therapy have been associated with reduction in bone mineral density (BMD but the patholophysiology of thyroxine-induced bone loss is not well understood.Treatment with sodium etidronate or calcitonin alone did not alter the regional BMD. Cyclical sodium etidronate, but not calcitonin, was able to prevent the bone loss induced by L-T4 treatment. L-T4 caused a dose-dependent increase in femur osteocalcin mRNA concentration.
Treatment with calcitonin resulted in 50 reduction of osteocalcin mRNA, but sodium etidronate had no effect. In conclusion, cyclical sodium etidronate prevents bone loss induced by exogenous L-T4 in rats and may be useful in preventing osteoporosis in patients given long term TSH-suppressive doses of thyroxine therapy.Bone disease with hyperthyroidism and thyroid hormone therapy. Prevention of bone loss induced by thyroxine suppressive therapy in.
Groups of 10 male Sprague-Dawley rats each weighing 320-350 g were studied before and after 3 weeks of treatment. L-T4 treatment resulted in reduction in BMDs in the lumbar spine, tail, and femur as measured by dual energy X-ray absorptiometry, but there was no correlation with the dosage of L-T4 or the serum T4 level.There were no differences between groups 1 and 2. All three groups had elevated osteocalcin levels compared with age-matched reference controls. At 1 yr, the osteocalcin level decreased in groups 1 and 2, but remained significantly raised in group 3.
J Clin Endocrinol Metab 1996 Mar;81(3 1232-6, Prevention of bone loss induced by thyroxine suppressive therapy in postmenopausal women: the effect of).First we studied the effect of L-T4 ( microgram/g body weight ip/day) on bone turnover in rats by measuring regional BMDs and osteocalcin mRNA. Next we determined whether antiresorptive agents (calcitonin 1 microU/gip/day or sodium etidronate given cyclically at 10 micrograms/g po for 3 consecutive days out of every week) could prevent bone loss.
However, careful titration of T4 dosage to maintain biochemical euthyroidism is a better way to avoid the adverse effect of T4 on bone.- Some integrative physicians and hormone experts state that if free T3 is not in the top half - or even the top quarter - of the reference range, it is not optimal.
1998;. Lamberg BA, Helenius T, Liewendahl K. Assessment of thyroxine suppression in thyroid carcinoma patients with a sensitive immunoradiometric TSH assay. Clin Endocrinol. 1986;. Braverman LE. Evaluation of thyroid status in patients with thyrotoxicosis.A baseline TSH of 5 or less usually goes up to 10-20 after giving an injection of TRH. Patients with too much thyroid hormone (thyroxine or triiodothyronine) will not show a rise in TSH when given TRH.
ADVICE : Avoid concomitant use or only undertaken with caution and appropriate monitoring. Ampicillin Atomoxetine HCl The effect and toxicity of atomoxetine could be increased by CYP2D6 inhibitor. Carbamazepine Possible increased risk of convulsions when antiepileptics given with Chloroquine.After birth, contractions stop and the feedback loop ceases. Here are a few well-known physiological processes and parameters that involve feedback loops. Pause the video here and determine which ones involve negative feedback and which ones involve positive feedback.