title: Lack of substantial effects of raloxifene on thyroxine-binding globulin in postmenopausal women: dependency on thyroid status.
abstract: Long-term estrogen therapy can modify thyroid hormone kinetics by increasing serum concentration of thyroxine-binding globulin (TBG). Raloxifene is a recently developed selective estrogen receptor modulator (SERM) for the treatment of osteoporosis, which possesses estrogenic and antiestrogenic properties. In a prospective and randomized study, we investigated the effects of raloxifene on TBG levels and on the serum concentrations of free thyroxine (FT4), thyroxine (T4), triiodothyronine (T3), and thyrotropin (TSH) in controls and in patients receiving TSH-suppressive doses of levothyroxine (LT4). Twenty-nine postmenopausal osteopenic (n = 14) and osteoporotic (n = 15) women were investigated over a period of 6 months. Group 1 (n = 15) included control patients and group 2 (n = 14) patients receiving TSH-suppressive dose of LT4. All patients were treated with raloxifene hydrochloride, 60 mg/d, for a period of 6 months. Serum basal TBG values were found higher in Group 1 compared to Group 2 (26.2 2 microg/mL vs. 21.4 2.1 microg/ml; p < 0.01). The TBG levels raised slightly in group 1 from 26.2 2 microg/mL to 28.6 3.1 microg/mL; p < 0.05 (in group 2 from 21.4 2.1 microg/mL to 22.2 2.3 microg/mL, not significant) after 3 months of treatment and failed to show any further significant change until the end of the study. Serum concentrations of T4, FT4, T3, and TSH levels changed insignificantly in both groups up to the completion of the study. Moreover, patients remained clinically euthyroid. Our findings may provide evidence that TBG levels, and consequently, thyroid function are not substantially affected by treatment with raloxifene. Additionally, TBG levels may also be influenced by small variations of thyroid function as subclinical hyperthyroidism.
authors.affiliation: Endocrine Unit, Evgenidion Hospital, University of Athens Medical School, Greece. ledunt@otenet.gr
authors.forename: L H
authors.initials: LH
authors.lastname: Duntas
authors.forename: E
authors.initials: E
authors.lastname: Mantzou
authors.forename: D A
authors.initials: DA
authors.lastname: Koutras
mesh_terms: D000368:Aged; D001851:Bone Diseases, Metabolic / Q000097:blood / Q000188:drug therapy; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D007700:Kinetics; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000097:blood / Q000188:drug therapy; D017698:Postmenopause / Q000097:blood*; D011446:Prospective Studies; D020849:Raloxifene Hydrochloride / Q000627:therapeutic use*; D012016:Reference Values; D020845:Selective Estrogen Receptor Modulators / Q000627:therapeutic use*; D013961:Thyroid Gland / Q000503:physiopathology*; D013972:Thyrotropin / Q000037:antagonists & inhibitors / Q000097:blood; D013974:Thyroxine / Q000097:blood / Q000627:therapeutic use; D013975:Thyroxine-Binding Proteins / Q000378:metabolism*; D014284:Triiodothyronine / Q000097:blood
chemical_list: D020845:Selective Estrogen Receptor Modulators; D013975:Thyroxine-Binding Proteins; D014284:Triiodothyronine; D020849:Raloxifene Hydrochloride; D013972:Thyrotropin; D013974:Thyroxine