IOF World Congress on Osteoporosis

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This summary of late-breaking news that will emerge from Lisbon has been prepared by Professor Ego Seeman, a member of IOF's board, editor of Progress in Osteoporosis and contributing editor to Osteoporosis Action.

A special plenary session devoted to late-breaking news will be held in Session VIII, 11.45-12.45 on Tuesday, May 14, 2002:

For the complete Lisbon program and other press briefings please see the Congress website:

The complete book of abstracts will be available on arrival as part of the registration package.

Oral presentations are identified as O, posters as P.

Predicting who will respond to drug therapy

Antiresorptive therapies reduce vertebral fracture risk and increase BMD. Although a single measurement of BMD is a predictor of fracture risk, the evidence that the increase in BMD in response to treatment predicts the reduction in fracture risk is weak. Indeed, two recent reviews examining the same data derived from about 14 randomized double blind trials come to opposite conclusions. In one analysis, Wasnich and Miller conclude that the increment in BMD explains most of the reduction in risk while Cummings et al report that only a small proportion of the risk reduction is explained by the increase in BMD.

The reasons for these differing interpretations are not clear. The controversy is instructive as it raises several questions. If the change in BMD is not a predictor or surrogate measure of fracture risk reduction why repeat a BMD measurement at all? Are there other predictors of fracture risk reduction that can be used in clinical practise to help us identify persons likely to respond to treatment early? What is the structural and biomechanical basis underlying the reduction in fracture risk using antiresorptive drugs?

Eastell et al examined whether the early decreases in vertebral fracture risk reported following risedronate could be explained by the early decrease in bone resorption markers (O42). The median CTX decrease during 3 – 6 months with placebo was 18% and 60% with risedronate 5mg/day. The respective median NTX decreases were 22% and 51% respectively. These changes in CTX and NTX accounted for two-thirds of the spine fracture risk reduction suggesting that these measurements may be useful in predicting who will and will not respond to drug therapy.

Bauer et al also examined the association between changes in biochemical measures of bone remodeling and the reduction in nonvertebral fractures in the Fracture Intervention Trial (O44). During 3.6 years, 72 hip and 786 non-spine fractures were confirmed and 336 women had incident vertebral fractures. A change in one or more biochemical markers was associated with the risk of hip, non-spine, and vertebral fracture in the treated group. The reductions in BAP, CTX, P1NP were associated with significant reductions in spine fracture risk of around 20%. The reduction in markers was also associated with a reduction in hip and nonspine fractures of about 10% but the coinfidence intervals around the risk reduction included unity.

Severity of spine fracture deformities predictors of vertebral and nonvertebral fracture

The presence of a spine fracture is one of the most important predictors of further fracture. However, whether mild deformities are predictors of vertebral (VF) and nonvertebral (NVF) fracture is uncertain. Delmas et al examined this issue in the placebo group of MORE (n = 2576) (O43). Prevalent VF severity predicted VF and NVF risk at 3 years; women with most severe deformities had a greater incidence of new fractures risks for VF and NVF (38% and 14% for grade 3, 24% and 8% for grade 2, 10% and 7% for grade 1 and 4% and 6% in those with no prevalent deformity. The number of prevalent VF and baseline BMD predicted VF risk, but severity of deformity was the only predictor of NVF risk. Women with grade 3 had the highest fracture incidence. In these women, raloxifene 60 mg/day decreased the risk of new VF [RR 0.73 (95% CI 0.54, 0.99)] and NVF [RR 0.53 (95% CI 0.29, 0.99)] at 3 years.

Sniffing estrogen

Christiansen et al report that nasal inhalation of 17B-estradiol (E2) in 386 early postmenopaiusal women assigned to intranasal E2 150mcg/d or 300mcg/d or placebo over 2 years cyclically combined with micronised progesterone (200mg/d) (O41). After 24 months, 150 and 300mcg/d S21400 increased spine BMD by 2.2% and 4% respectively, and increased femoral neck BMD by 0.07% and 1.15% respectively, whereas in the placebo group, BMD decreased by -3.50% and -4.02% in the spine and femoral neck respectively. S21400 (150 and 300mcg/d) decreased urinary CTX by -40.0% and -46.1% respectively and serum osteocalcin by -21.8% and -27.2% respectively.

A new kid on the block – Strontium Ranelate

Strontium ranelate increases bone formation and decreases bone resorption, increasing BMD. The results of the SOTI study are presented for the first time at this meeting (O45). In this 3 year study 2g/day orally administered drug was given in a double-blind, randomised, placebo-controlled trial involving 12 countries and 1649 women mean age 70 years; 87.5% of patients had at least one prevalent vertebral fracture (average:2.2 per patient). After the first year, the number of women having new vertebral fractures was reduced by about 50% [44 (6.1%) vs 85 (11.8%) in placebo]. The incidence of patients having at least one clinical spine fracture was halved (3.1% vs 6.4%, p=0.003). For the whole 3 years, a 41% reduction in relative risk of experiencing a first new vertebral fracture (semi-quantitative) was observed, 139 vs 222 (placebo) (RR=0.59, 95%CI 0.48;0.73) in the intent-to-treat population. A relative risk reduction during the third year of 51% is consistent with sustained efficacy. Bone specific alkaline phosphatase increased while serum CTX decreased. The lumbar BMD increased in the treated group compared to the placebo (+11.4% vs -1.3% respectively, p<0.001). The drug is a welcomed new orally effective and safe treatment of vertebral osteoporosis with a unique mechanism of action.