Fractures are not a feature in the natural history of treated hypothyroidism, whereas CAD is a common cause of death in these patients.
For the whole group and for the male subgroup, serum calcium was significantly lower in patients than in controls, presumably as a result of previous thyroid surgery and radioiodine ablation, although there were no differences in serum parathyroid hormone or alkaline phosphatase (table II).
For the whole group, there were no differences between patients and controls apart from a small difference in physical activity score (p 0.05). In subgroup analysis there were no significant differences between patients and controls in inorganic phosphate, alkaline phosphatase, or parathyroid hormone (table II).
P B, Sunningdale, Berks. See WDDTY vol 6 no 7 for information about the inaccuracies of thyroid testing. We'll be covering natural methods of stimulating the thyroid in an upcoming issue, so please keep reading.
It was the only drug that didn't have any! Twenty years on, the story has changed, as it normally does. I feel it is important for patients to seek other ways of stimulating the thyroid into normal action, rather than resorting to thyroxine, and ending up with my problem.
Although effective antithyroid treatment means that the association of overt thyrotoxicosis and osteoporotic fractures is now rare, lately much attention has focused on the potential effect of mild to moderate hyperthyroidism on bone mineral density.
Several studies have used single or dual photon absorptiometry to define the influence of thyroxine treatment on bone mineral density. Most of these studies examined small numbers of patients, not grouped for age, sex, or menopausal status, and with varied histories of thyroid disease and doses of thyroxine administered.
Serum thyrotropin was below the limit of assay detection ( 0.05 Mu/l) in 13 premenopausal female patients, 20 postmenopausal women, and 2 men. Thyrotropin was below the normal range but detectable in 5 of the remaining 14 patients and within the normal range in 9.
We suggest that thyroxine alone does not have a significant effect on bone mineral density and hence on risk of osteoporotic fractures. Introduction The relation between thyroid disease and osteoporosis was first recognised 100 years ago.
Studies of the effect of thyroxine replacement therapy on bone mineral density have given conflicting results; the reductions in bone mass reported by some have prompted recommendations that prescribed doses of thyroxine should be reduced.
Subjects with hypoparathyroidism were excluded. Each patient had received a constant dose of thyroxine since thyroidectomy; in most the dose was sufficient to suppress thyrotropin concentrations to below normal. The mean thyroxine dose was similar in women and men (premenopausal women 217 range 10-300 /day; postmenopausal women /day; men /day as was the duration of.
The in-vivo precision was 1.6 for measurements of femoral neck, 3.2 for Ward's triangle, 2.2 for femoral trochanter, and 0.8 (anterior-posterior) and 3.6 (lateral) for lumbar spine. A Z score was calculated for each bone density measurement from the mean (SD) for the relevant control group (Z score patient's value - group mean ö group.
Hormones are really important to bone strength. Hormones are chemicals made by glands that travel throughout the body and have many effects on growth, maturation, energy, weight, and bone strength. Sex hormones (estrogen made in the ovary of females and testosterone made by the testes in males) control ability to reproduce.
I went to a lab for tests which showed up magnesium and zinc deficiencies, but an osteoporosis profile showed no lack of calcium! You cannot imagine my disappointment when I had my second scan yesterday showing a 10 per cent drop in my spine and slightly less in my hip.
BMD and cholesterol concentrations were compared between those with suppressed and normal thyrotrophin concentrations and between those with and without a past history of thyrotoxicosis. No patient had a pathological fracture.