Endocrine Abstracts (2010) 22 P115

Extraosseous effects of raloxifene in osteoporotic postmenopausal women

Arántzazu Sebastián-Ochoa1, Diego Fernandez-Garcia1, Rebeca Reyes García2 & Manuel Muñoz Torres3

1Servicio Endocrinologìa y Nutrición, Hospital Virgen de la Victoria, Málaga, Spain; 2Servicio Endocrinologìa y Nutrición, Hospital Rafael Mendez, Lorca, Murcia, Spain; 3Servicio Endocrinologìa y Nutrición, Unidad de Metabolismo Óseo, Hospital Universitario San Cecilio, Granada, Spain.

Raloxifene is a selective estrogen receptor modulator which has shown to decrease bone resorption, increase bone density and reduce vertebral fracture rate in women with postmenopausal osteoporosis. Recent studies have shown a decrease on breast cancer incidence after raloxifene treatment. Although the mechanism is not clear, its mixed agonist and antagonist properties in different tissues could partially explain this effect.

Objective: To evaluate the effects of a 12 month administration of raloxifene on serum gonadotropin, thyrotropin (TSH), serum free T4 (FT4), 17βestradiol (E2), sex hormone-binding globulin (SHBG), dehydroepiandrosterone (DHEAs), testosterone, insulin-like growth factor (IGF1) and insulin-like growth factor binding protein 3 (IGFBP3).

Design: Forty seven postmenopausal women (mean age 63±7 years) with densitometric criteria of osteoporosis were treated with raloxifene 60 mg/day for 12 months. Serum IGF1, FSH, LH, E2 (kit DSL-39100 3rd Generation Estradiol RIA, Diagnostic System Laboratories, Inc., Texas, USA), DHEAs, testosterone, TSH, and anthropometric parameters were evaluated at baseline and after 12 months of treatment.

Results: No significant variations in serum FSH, LH, testosterone, SHBG, TSH, FT4 values were observed. Serum E2 (17.93±8 vs 23.2±6.8; P=0.001) and DHEAs (P=0.001) levels increased after one year of treatment with raloxifene. Serum IGF1 (133.6 vs 88.8; P=0.001) and IGF1/IGFBP3 ratio (48.23 vs 33.4; P<0.01) were both decreased after one year of raloxifene treatment.

Conclusions: Antineoplastic action of raloxifene treatment can be mediated at least in part by the decrease in IGF1 and E2 levels.

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