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Use of Vitamin K₂ (Menatetrenone) and 1,25-dihydroxyvitamin D₃ in the Prevention of Bone Loss Induced by Leuprolide¹

Department of Obstetrics and Gynecology, Toride Kyodo General Hospital, Toride, Ibaraki, 302-0022 Japan

Address all correspondence and requests for reprints to: Yoshiaki Somekawa, M.D.. Toride Kyodo General Hospital, Hongo 2–1-1 Toride, Ibaraki, 302-0022 Japan. E-mail: pv2t-sigi{at}asahi-net.or.jp

The purpose of this study is to evaluate the efficacy of vitamin K₂ and 1,25-dihydroxyvitamin D₃ [1,25-(OH)₂D₃] in preventing bone loss induced by estrogen deficiency during therapy with the GnRH agonist (GnRH-a) leuprolide.

One hundred ten women (mean age, 46.2 ± 0.5 yr), receiving leuprolide therapy for estrogen-dependent diseases (such as endometriosis and uterine leiomyomas), were randomly allocated into four groups (group A, leuprolide only; group B, leuprolide with vitamin K₂; group C, leuprolide with 1,25-(OH)₂D₃; and group D, leuprolide with vitamin K₂ and 1,25-(OH)₂D₃). Bone mineral density of the lumbar spine was measured by dual-energy x-ray absorptiometry before and after 6 months of treatment. Bone formation and resorption markers were also measured before and after 6 months of treatment.

There were no significant differences in the background parameters among the four groups. Bone mineral density was reduced in all four groups, but the percent changes varied slightly, at -5.25% (group A), -3.72% (P < 0.05 vs. group A) (group B), -4.13% (group C), and -3.59% (P < 0.01 vs. group A) (group D), respectively. Bone formation markers were significantly increased in all four groups, and the percent changes of bone formation markers were highest in group B.

Bone resorption markers also increased significantly in all four groups after treatment of 6 months. Group B tended to have the highest percent changes of bone resorption markers among the four groups, but these increases were not significantly different between any of the groups.

Vitamin K₂, especially when combined with 1,25-(OH)₂D₃, can partially prevent bone loss caused by estrogen deficiency. However, because this effect is attributable mainly to the activation of bone formation, it is not sufficient to eliminate bone loss induced by GnRH-a therapy.

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