Effects of raloxifene therapy on the anticoagulant system Raloksifen tedavisinin antikoagülan sistem üzerine olan etkileri
Jinekoloji ve Obstetrik Dergisi, cilt.19, sa.4, ss.222-227, 2005 (Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 19 Sayı: 4
- Basım Tarihi: 2005
- Dergi Adı: Jinekoloji ve Obstetrik Dergisi
- Derginin Tarandığı İndeksler: Scopus, TR DİZİN (ULAKBİM)
- Sayfa Sayıları: ss.222-227
- Anahtar Kelimeler: Antithrombin III, Fibrinogen, Protein C, Protein S, Raloxifene, Venous Thromboembolism
- Sağlık Bilimleri Üniversitesi Adresli: Hayır
Özet
OBJECTIVE: Raloxifene therapy is associated with a 7.5-3 fold increase in the risk for venous thromboembolism. This study has been designed to determine the effects of raloxifene on the natural anticoagulant system in postmenopausal women. STUDY DESIGN: Sixty postmenopausal, osteoporotic women were enrolled to this prospective randomized double-blind study. Thirty patients were treated with raloxifene hydrochloride (60 mg/day) + calcium (600 mg/day) + vitamin D (400 IU/day) and thirty patients with calcium (600 mg/day) and vitamin D (400 IU/day) as a control group for a year. Fibrinogen and antithrombin III levels with protein S and C activities were measured in all patients at base-line, and after 12 months of treatment. Results at baseline and after treatment were compared with each other and control group. RESULTS: There were no statistically significant difference between the baseline and after treatment levels of fibrinogen. Statistically significant 8.7%, 13.8% and 16% reductions of plasma antithrombin III, protein S and C levels were observed at 12 months of raloxifene therapy, respectively (p<0.05). But these reductions were not statistically significant when compared to control group (p>0.05). CONCLUSION: Raloxifene therapy is associated with a significant reduction in plasma protein C, protein S and antithrombin III levels after 12 months of therapy. Although, these reductions didn't reach to the statistically significant levels when compared to the control group, might explain the mechanism of the increased risk of venous thromboembolism in raloxifene users.