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Journal of Clinical Endocrinology & Metabolism, Vol 80, 2480-2484, Copyright © 1995 by Endocrine Society
ARTICLES |
AK Hogasen, L Nordsletten, AO Aasen and JA Falch
Department of Pediatric Research, National Hospital, Oslo, Norway.
Interleukin-1 (IL-1) is a potent stimulator of bone resorption, and a causal role for IL-1 has been suggested in postmenopausal bone loss. We have examined IL-1 beta release in vitro by peripheral blood mononuclear cells (PBMC) isolated from nonosteoporotic women 9-15 yr after menopause. These women had presented 6 yr previously with significant differences in the rate of early postmenopausal bone loss. Ten women with low rates of bone loss (median 2.0% per year) and 10 women with high rates of bone loss (median 4.9% per year) were included in the study. The women with a high rate of bone loss had a significantly lower bone mass of the lumbar vertebrae compared with that of the other group, but there were no differences in biochemical markers of bone metabolism between the groups (pyridinoline/creatinine ratio in urine and collagen 1 c-terminal telopeptide and bone gla protein in serum). Moreover, there was no difference in spontaneous IL- 1 beta release by PBMCs between the two groups and no correlation between IL-1 beta release and present bone turnover, as judged by biochemical markers. Treatment of PBMCs with 10 nmol/L 17 beta- estradiol in vitro significantly stimulated IL-1 beta production in both groups. We conclude that IL-1 beta production by PBMCs in vitro does not correlate with the rate of early postmenopausal bone loss.
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