Format

Send to

Choose Destination
See comment in PubMed Commons below
J Endocrinol Invest. 1991 Jun;14(6):451-5.

Effect of thyroxine therapy on bone metabolism in substituted hypothyroid patients with normal or suppressed levels of TSH.

Author information

1
Department of Medicine E, Frederiksberg Hospital, Denmark.

Abstract

The statement that pituitary hyperthyroidism reflects peripheral hyperthyroidism is still controversial. To evaluate a possible relationship between the calcium and the thyroid metabolism, 29 women with thyroxine (T4) substituted hypothyroidism were examined. They were separated into two groups, one with normal (0.15 to 6 mU/l) and one with suppressed TSH (less than 0.15 mU/l). All the women were judged euthyroid both by their T4 and T3 and by their clinics. The daily dose of T4 (median 0.15 mg in both groups) had been unchanged and TSH level had been stable during the previous six months. Bone mineral content (BMC) of the lumbar spine, bone mineral density (BMD) of left and right collum femoris, serum alkaline phosphatase activity (AP), serum concentration of osteocalcin (Ost) and urinary excretion of hydroxyproline/creatine (Hpr/crea) were similar in the two groups. Furthermore, sex- hormone-binding-globulin (SHBG) was equal in the two groups, but significantly higher than in normals (p less than 0.01). A significant positive correlation was found between serum Ost and Hpr/crea (p less than 0.05) indicating a balanced state where bone formation equals bone resorption. AP failed to correlate to Ost and Hpr/crea because the AP raises from both bone and liver of bone and liver metabolism whereas the two others predominantly reflect bone metabolism. SHBG, being a marker of liver metabolism, was elevated in both groups, probably because of the oral administration of T4. Our data suggest that euthyroid, T4 substituted patients have a normal calcium metabolism whether TSH levels are suppressed or not.

PMID:
1774441
DOI:
10.1007/BF03346838
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center