SCI Nurse: Fosamex or Forteo?

[stephen212]

I'm turning 46 years old tomorrow and am 22 years post injury and probably osteoporotic for nearly all of them. I've had annual bone density studies for the past 4 years with mostly consistent findings: I'm osteoporotic but far from the worst case. Fortunately, I've made it this far without any fractures.

I've resisted osteoporosis treatment meds because it's been my understanding (mostly from threads here) that they would have little to no impact on an SCI (complete injury) not simultaneoulsy involved in an FES or similar regimen that applies mechanical stress on the bones.

My internist, also a board certified in physiatrist, is encouraging me to begin Fosamax to at least maintain as much of my present BMD as possible. He's less familiar, however, with the guidelines for prescribing bone-building Forteo for SCIs. What guidelines should guide my decision to take one or the other?

Any follow-up thoughts on beginning with Forteo for a year and then switching over to Fosamax?

[SCI-Nurse]

Forteo is actually a physiologic substance (parathormone) which regulates calcium in the body. There is really no medical reason for using them in sequence. They would probably work betteer taken together. Remember though that they do not restore normal bone density in people with SCI--they just help to maintain or prevent further deterioration in calcium stores.

RAB

[stephen212]

Originally Posted by SCI-Nurse

Forteo is actually a physiologic substance (parathormone) which regulates calcium in the body. There is really no medical reason for using them in sequence. They would probably work betteer taken together.
RAB

SCI Nurse:
The rationale for taking them in sequence is explained in the link at the bottom of my last post. A study published in the NEJM last August showed a significant increase in bone density when PaTH was used as a 1-year precursor before switching over to alendronates (e.g., Fosamax) when compared to taking only alendronates. Though the participants in the study were (surprise!) menopausal women, Wise speculated that people with SCI might benefit from the same or similar protocol. I'd like to know if he or anyone else still recommends this.

[LaoziSailor]

I have marginal Osteopenia and was originally rejected from the study because for reasons unknown my bone density had actually improved since my last scan.

Subsequently, the criteria was changed and I was admitted for http://www.clinicaltrials.gov/ct/gui/show/NCT00138866 and had to withdraw for personal reasons before I began the program.

[SCI-Nurse]

I'll ask Dr. Young to respond to the post. Sorry that I'm behind the curve.

RAB

[lynnifer]

Thanks for posting your question Stephen and the above Sailor ... I wonder if they'd take someone from Windsor for that trial? A four hour trip one way ... in winter no less ... eeeeks.

Usually I'm ousted from trials because of my pressure sores (on my sixth now woo hoo ... *grumble mumble*)

[Wise Young]

I don't know the answer because there have not been any direct comparison (that I was able to find) of the two therapies in chronic spinal cord injury. Here are a few recent studies on other kinds of osteoporosis and about the complications of the therapies:

1. Wada S (2006). [Present development of new drugs for osteoporosis.]. Clin Calcium 16: 176-81. Bisphosphonates are widely used, though gastrointestinal tolerance is a problem on daily administration. Alendronate 35 mg administered once weekly is as effective at increasing bone mineral density (BMD) as 5 mg/day in the treatment of osteoporosis. Once weekly regimen will be soon available in Japan and can reduce adverse events. Injection therapies may also circumvent this, although this introduces the smaller problem of acute phase reactions. New generation bisphosphonates (milodronate, ibandronate and zoledronate) along with anti-receptor activator of nuclear factor-kappaB ligard (RANKL) antibody are promising and eargely develoed for the treatment of osteoporosis. Raloxifene appears to have a superior safety profile to hormone replacement therapy (HRT), though its efficacy on bone may be limited, so that various new generation of selective estrogen receptor modulator (SERMs) is now underdeveloped. Anabolic agents such as teriparatide and strontium ranelate have marked effects on BMD and subsequent reduction on fracture risk. While none of these options is suitable for everyone, the range of future available therapies does mean that most patients can find an intervention that is effective and acceptable. Department of Clinical Science, Faculty of Pharmaceutical Sciences, Josai International Univesity. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16397369
   
2. Reginster JY and Sarlet N (2006). The treatment of severe postmenopausal osteoporosis : a review of current and emerging therapeutic options. Treat Endocrinol 5: 15-23. Several chemical entities have shown their ability to reduce axial and/or appendicular fractures in patients with osteoporosis. Since patients who have experienced a previous fracture are at high risk for subsequent vertebral or hip fracture, it is of prime importance to treat such patients with medications that have unequivocally demonstrated their ability to reduce fracture rates in patients with prevalent fractures. Results obtained with calcium and vitamin D, in this particular population, are not fully satisfactory and these medications are probably better used in conjunction with other therapeutic regimens. Bisphosphonates have shown their ability to reduce vertebral (alendronate, risedronate, ibandronate) and non-vertebral (alendronate, risedronate) fractures in patients with established osteoporosis. Raloxifene has also shown similar properties, notwithstanding its effect on non-vertebral fractures, which has only been derived from a post hoc analysis limited to patients with prevalent severe vertebral fractures at baseline. This compound also has interesting non-skeletal benefits, including effects on the breast and heart. Teriparatide, a bone-forming agent, promptly reduces the rate of vertebral and all non-vertebral fractures, without significant adverse effects. Strontium ranelate, the first agent shown to concomitantly decrease bone resorption and stimulate bone formation, has also shown its ability to reduce rates of vertebral and non-vertebral fractures in patients with established osteoporosis. It significantly reduces hip fractures in elderly individuals at high risk for such events. Its safety profile is also excellent. WHO Collaborating Center for Public Health Aspects of Rheumatic Diseases, Liege, Belgium. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16396515
   
3. Eastell R, Krege JH, Chen P, Glass EV and Reginster JY (2006). Development of an algorithm for using PINP to monitor treatment of patients with teriparatide. Curr Med Res Opin 22: 61-6. INTRODUCTION: Teriparatide effects are mediated via the preferential stimulation of osteoblastic activity over osteoclastic activity. Amino-terminal propeptide of type I procollagen (PINP) is an indicator of osteoblastic activity.OBJECTIVE: Develop an algorithm using PINP as an aid in the management of patients with postmenopausal osteoporosis treated with teriparatide.Research design and methods: For inclusion in this post-hoc analysis, trials had to be investigations of teriparatide 20 mug/day in postmenopausal women with osteoporosis having measurements of PINP at 3 months and bone mineral density (BMD) at 12 months. Signal-to-noise ratio was calculated for a series of markers of bone turnover in the Fracture Prevention Trial. An algorithm was developed to monitor patients treated with teriparatide using PINP.RESULTS: Three trials met inclusion criteria and included the Fracture Prevention, Forteo-Alendronate Comparator and Anabolic After Antiresorptive trials. PINP had the highest signal-to-noise ratio of all bone-turnover markers. Positive PINP responses defined as increases > 10 mug/L were observed in 77-79% of teriparatide- and in 6% of placebo-treated patients after 3 months of study drug. Mean lumbar spine BMD increases after 12 months of teriparatide in patients having PINP changes > 10 mug/L ranged from 8.3% to 9.5% and in patients with PINP changes </= 10 mug/L ranged from 5.9% to 7.6%.In the algorithm, PINP is measured at baseline and after 1-3 months of therapy. Patients with PINP increases > 10 mug/L are given a positive message. Patients with PINP increases </= 10 mug/L are assessed for adherence, teriparatide administration and storage techniques, and for the presence of medical conditions that might limit their therapeutic response, and these issues are addressed as appropriate. Patients without these issues and with PINP increases </= 10 mug/L should be given a neutral message because BMD may significantly increase with continued therapy.CONCLUSIONS: The PINP algorithm provides information regarding the anabolic response to teriparatide therapy and has the potential to identify patients requiring help with issues of adherence, injection technique, teriparatide storage, and medical problems limiting therapeutic responsiveness to teriparatide treatment. Data assessing the relationship of changes in PINP to fracture risk reduction are not available. We recommend physicians audit the use of the algorithm in practice so that improvements can be made. University of Sheffield, Sheffield, UK. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16393431
   
4. Cosman F (2005). The prevention and treatment of osteoporosis: a review. MedGenMed 7: 73. Osteoporosis is a disorder characterized by reduced bone strength, diminished bone density, and altered macrogeometry and microscopic architecture. Adult bone mass is the integral measurement of the bone mass level achieved at the peak minus the rate and duration of subsequent bone loss. There is clearly a genetic predisposition to attained peak bone mass, which occurs by a person's mid-20s. Bone loss with age and menopause are universal, but rates vary among individuals. Both peak bone mass and subsequent bone loss can be modified by environmental factors, such as nutrition, physical activity, and concomitant diseases and medications. Osteoporosis prevention requires adequate calcium and vitamin D intake, regular physical activity, and avoiding smoking and excessive alcohol ingestion. Risk of fracture determines whether medication is also warranted. A previous vertebral or hip fracture is the most important predictor of fracture risk. Bone density is the best predictor of fracture risk for those without prior adult fractures. Age, weight, certain medications, and family history also help establish a person's risk for osteoporotic fractures. All women should have a bone density test by the age of 65 or younger (at the time of menopause) if risk factors are present. Guidelines for men are currently in development. Medications include both antiresorptive and anabolic types. Antiresorptive medications--estrogens, selective estrogen receptor modulators (raloxifene), bisphosphonates (alendronate, risedronate, and ibandronate) and calcitonins--work by reducing rates of bone remodeling. Teriparatide (parathyroid hormone) is the only anabolic agent currently approved for osteoporosis in the United States. It stimulates new bone formation, repairing architectural defects and improving bone density. All persons who have had osteoporotic vertebral or hip fractures and those with a bone mineral density diagnostic of osteoporosis should receive treatment. In those with a bone mineral density above the osteoporosis range, treatment may be indicated depending on the number and severity of other risk factors. Columbia University College of Physicians and Surgeons, New York, NY, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16369451
   
5. Small RE (2005). Uses and limitations of bone mineral density measurements in the management of osteoporosis. MedGenMed 7: 3. CONTEXT: Bone mineral density (BMD) is used to diagnose osteoporosis, and often to measure efficacy in osteoporosis treatment trials; however, there is a poor correlation between lumbar spine BMD increases and vertebral fracture risk reduction in patients receiving treatment for osteoporosis. OBJECTIVE: The purpose of this article is to review the uses and limitations of BMD measurements and the relationship between BMD and bone strength. DATA SOURCE/STUDY SELECTION: A MEDLINE literature search was conducted with the terms bone mineral density , fracture , osteoporosis , and bone strength as well as the generic names of osteoporosis therapies (alendronate, risedronate, raloxifene, teriparatide, and calcitonin). Search results were limited to English language journals and articles published within the last 20 years. Published abstracts from scientific meetings were also reviewed. CONCLUSION: BMD measurement remains the most useful diagnostic tool for identifying patients with osteoporosis. Although they are helpful in guiding decisions to initiate osteoporosis treatment, subsequent changes in BMD provide an imperfect indicator of treatment efficacy. Analyses of clinical trials show an inconsistent relationship between increased spinal BMD and a decreased risk of vertebral fracture. Increased BMD accounts for less than 25% of the overall reduction in fracture risk in most instances. Consequently, fracture risk reduction itself remains the most clinically relevant therapeutic outcome of osteoporosis therapy. Virginia Commonwealth University, Richmond, Virginia, USA. ralphsmall@rcn.com http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16369382
   
6. McCarus DC (2006). Fracture prevention in postmenopausal osteoporosis: a review of treatment options. Obstet Gynecol Surv 61: 39-50. Several treatment options are available to reduce the risk of fractures in postmenopausal women with or at risk for osteoporosis. A MEDLINE search was conducted to evaluate antifracture and adverse event data of osteoporosis therapies from trials in postmenopausal women. Among the antiresorptive therapies, the bisphosphonates alendronate and risedronate have demonstrated consistent efficacy in reducing vertebral and nonvertebral fracture risk. Once-weekly alendronate and risedronate produced similar improvements in bone mineral density compared with their once-daily counterparts with similar tolerability. Daily injections of teriparatide resulted in statistically significant reductions in the risk of vertebral and nonvertebral fractures, and trials of ibandronate, raloxifene, and calcitonin nasal spray showed reductions in vertebral fracture risk. Hormone therapy has demonstrated clinical fracture risk reduction; however, safety outcomes from the Women's Health Initiative study have raised concerns regarding long-term use of these preparations. These data can guide clinical decision-making regarding the selection of an osteoporosis therapy. Target Audience: Obstetricians & Gynecologists, Family Physicians Learning Objectives: After completion of this article, the reader should be able to summarize adverse events data of osteoporosis therapies from trials in postmenopausal women, explain that only a few therapies have shown a consistent efficacy in reducing vertebral and nonvertebral fractures, and state that data from the Women's Health Initiative study have raised concerns regarding long-term use of estrogen-progestin therapy. Founder, Center for Advanced Vein Treatment & Women's Health Care, Towson, Maryland. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16359568
   
7. Hamdy RC, Chesnut CH, 3rd, Gass ML, Holick MF, Leib ES, Lewiecki ME, Maricic M and Watts NB (2005). Review of treatment modalities for postmenopausal osteoporosis. South Med J 98: 1000-14; quiz 1015-7, 1048. This review summarizes and updates data presented at recent annual Southern Medical Association conferences on postmenopausal osteoporosis. As part of any osteoporosis treatment program, it is important to maintain adequate calcium and 25-hydroxyvitamin D levels either through diet or supplementation. Among the available pharmacologic therapies, the bisphosphonates alendronate and risedronate have demonstrated the most robust fracture risk reductions-approximately 40 to 50% reduction in vertebral fracture risk, 30 to 40% in nonvertebral fracture risk, and 40 to 60% in hip fracture risk. Ibandronate, a new bisphosphonate, has demonstrated efficacy in reducing vertebral fracture risk. Salmon calcitonin nasal spray and raloxifene demonstrated significant reductions in vertebral fracture risk in pivotal studies. Teriparatide significantly reduced vertebral and nonvertebral fracture risk. Drugs on the horizon include strontium ranelate, which has been shown to reduce vertebral and nonvertebral fracture risk, and zoledronic acid, an injectable bisphosphonate that increased bone density with once-yearly administration. East Tennessee State University, Johnson City, TN 37614, USA. Hamdy@etsu.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16295815
   
8. Nevitt MC, Chen P, Dore RK, Reginster JY, Kiel DP, Zanchetta JR, Glass EV and Krege JH (2006). Reduced risk of back pain following teriparatide treatment: a meta-analysis. Osteoporos Int 17: 273-80. Vertebral fractures are the most common osteoporotic fracture and may result in back pain with functional limitations and diminished quality of life. Teriparatide [rhPTH (1-34)] has been shown to increase bone mass and reduce the risk of vertebral and other osteoporotic fractures. The aim of this study was to evaluate the effects of teriparatide on the risk of back pain in patients with osteoporosis. A systematic review of the literature was performed, and five trials were identified and included in our analyses. All trials were randomized, double-blinded, and parallel with either new vertebral fracture ( n =1) or bone mineral density as the primary endpoint ( n =4). Four studies were in postmenopausal women with osteoporosis, and one was in men with idiopathic or hypogonadal osteoporosis. Two trials were placebo controlled, two trials were alendronate controlled, and one trial involved teriparatide plus hormone replacement therapy versus hormone replacement therapy alone. Reports of back pain, defined as new or worsened back pain after initiating the study drug, were obtained from adverse event databases, and the risk of back pain was analyzed using a multivariate Cox proportional hazards model. Results were not statistically heterogeneous ( P =0.60) across trials, and there were no differences between groups administered teriparatide 20 or 40 mcg/day doses ( P =0.64). The rates of back pain, moderate or severe back pain, and severe back pain per 100 patient-years were numerically lower in the teriparatide versus comparator groups in each study. Compared with the pooled comparator, patients in the pooled teriparatide group had reduced risk for any back pain [relative risk, 0.66 (95% CI, 0.55-0.80)], moderate or severe back pain [relative risk, 0.60 (95% CI, 0.48-0.75)] and severe back pain [relative risk, 0.44 (95% CI, 0.28-0.68)]. Separate meta-analyses comparing teriparatide versus placebo or antiresorptive drugs gave similar results. In conclusion, patients randomized to teriparatide had a reduced risk of new or worsening back pain compared to patients randomized to placebo, hormone replacement therapy or alendronate. University of California San Francisco, San Francisco, CA, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16142502
   
9. McClung MR, San Martin J, Miller PD, Civitelli R, Bandeira F, Omizo M, Donley DW, Dalsky GP and Eriksen EF (2005). Opposite bone remodeling effects of teriparatide and alendronate in increasing bone mass. Arch Intern Med 165: 1762-8. BACKGROUND: Antiresorptive agents for the treatment of osteoporosis suppress bone remodeling and reestablish bone turnover at a lower rate to reduce bone loss. Recombinant teriparatide (human parathyroid hormone 1-34) stimulates bone formation, increases bone mass, and improves bone microarchitecture. We contrasted the effects of once-daily doses of 20 mug of teriparatide and 10 mg of alendronate sodium on bone mineral density (BMD) and markers of bone turnover. METHODS: Markers of bone turnover and areal BMD were assessed in 203 postmenopausal women with osteoporosis in an 18-month randomized parallel double-blind study; volumetric BMD was measured in a subset of women. RESULTS: Teriparatide significantly increased markers of bone turnover that peaked at 6 months (serum procollagen type I N-terminal propeptide, 218%, and urinary N-telopeptide corrected for creatinine, 58%; P<.001); alendronate significantly decreased the markers at 6 months (-67% and -72%, respectively; P<.001). At 18 months, areal and volumetric spine BMDs were significantly higher with teriparatide than with alendronate (10.3% vs 5.5% [P<.001] and 19.0% vs 3.8% [P<.01], respectively). Areal femoral neck BMD was significantly higher than baseline in the teriparatide and alendronate groups (3.9% and 3.5%, respectively). There were no significant differences in trabecular femoral neck BMD between the teriparatide and alendronate groups (4.9% and 2.2%, respectively). Cortical volumetric femoral neck BMD was significantly different between the teriparatide and alendronate groups (-1.2% and 7.7%, respectively; P = .05). CONCLUSION: Two distinct options for the management of osteoporosis lead to increases in BMD by opposite mechanisms of action on bone remodeling. Oregon Osteoporosis Center, Providence Portland Medical Center, Portland, OR 97213, USA. mmcclung@orost.com http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16087825
   
10. Miller PD, Shergy WJ, Body JJ, Chen P, Rohe ME and Krege JH (2005). Longterm reduction of back pain risk in women with osteoporosis treated with teriparatide compared with alendronate. J Rheumatol 32: 1556-62. OBJECTIVE: To compare the effects on back pain of teriparatide versus alendronate, we analyzed the reporting of back pain in a head to head comparator trial and a followup study. METHODS: In the comparator trial, women were randomized to receive either daily self-injected teriparatide 40 microg plus an oral placebo (n = 73), or daily oral alendronate 10 mg plus self-injected placebo (n = 73). Treatment was for a median 14 months. After completion of the comparator trial, 72% of these patients enrolled in a nontreatment followup study. Adverse events were recorded at each comparator trial visit and followup study visit, and the incidence of new or worsening back pain in each group was compared. RESULTS: During the comparator trial, compared with women randomized to alendronate 10 mg, women randomized to teriparatide 40 microg had reduced risk for any back pain (relative risk 0.27, 95% CI 0.09-0.82) and moderate or severe back pain (relative risk 0.19, 95% CI 0.04-0.86). The differences in the reporting of back pain between the teriparatide treated women and the alendronate treated women were sustained during an interval including the comparator trial plus 18 additional months. During an interval including the comparator trial plus 30 additional months, teriparatide treated patients had numerically fewer occurrences of back pain and moderate or severe back pain. CONCLUSION: Compared with women randomized to alendronate 10 mg, women randomized to teriparatide 40 microg had reduced risk of back pain during the trial and 2.5 years of followup. Colorado Center for Bone Research, Lakewood, 80227, USA. millerccbr@aol.com http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16078334
    
11. Arlot M, Meunier PJ, Boivin G, Haddock L, Tamayo J, Correa-Rotter R, Jasqui S, Donley DW, Dalsky GP, Martin JS and Eriksen EF (2005). Differential effects of teriparatide and alendronate on bone remodeling in postmenopausal women assessed by histomorphometric parameters. J Bone Miner Res 20: 1244-53. An 18-month randomized double-blind study was conducted in postmenopausal women with osteoporosis to compare the effects of once-daily teriparatide 20 microg with alendronate 10 mg on bone histomorphometry. Biopsies were obtained from 42 patients. Indices of bone formation were significantly higher after 6 or 18 months of teriparatide compared with alendronate treatment. INTRODUCTION: Alendronate and teriparatide increased BMD, assessed by DXA, by different mechanisms of action, supported by changes in biochemical markers of bone turnover. The purpose of this cross-sectional study was to explore the differential effects of these two osteoporosis treatments at the bone tissue level by examining bone histomorphometric parameters of bone turnover after either 6 or 18 months of treatment. MATERIALS AND METHODS: Patients were a cohort from a randomized parallel double-blind study conducted to compare the effects of once-daily teriparatide 20 microg and alendronate 10 mg in postmenopausal women with osteoporosis. Transiliac crest bone biopsies were obtained after tetracycline double labeling from 42 patients treated for 6 months (n = 23) or 18 months (n = 14); 5 additional patients were biopsied from contralateral sides at 6 and 18 months. Biopsy specimens adequate for quantitative analysis were analyzed by 2D histomorphometry from 17 patients at 6 months (teriparatide, n = 8; alendronate, n = 9) and 15 patients at 18 months (teriparatide, n = 8; alendronate, n = 7). Data were analyzed by two-sample tests. RESULTS: Histomorphometric indices of bone formation were significantly and markedly greater in the teriparatide group than in the alendronate group at 6 and 18 months, whereas indices of bone resorption were only significantly greater in the teriparatide group than in the alendronate group at 6 months. Bone formation and activation frequency were significantly lower at 18 months compared with 6 months in the teriparatide group, returning to levels comparable with untreated postmenopausal women. In the teriparatide group, the peak in histomorphometric bone formation indices coincided with peak levels for N-terminal propeptide of type I collagen, a biochemical marker of bone formation. The degree of mineralization was lower at 18 months than at 6 months with treatment in both groups but was not different between groups. CONCLUSIONS: These results confirm the opposite mechanisms of action of teriparatide and alendronate on bone remodeling and confirm the bone formation effect of teriparatide. Laboratoire d'Histodynamique Osseuse and INSERM Unit 403, Faculty of Medicine R. Laennec, Lyon, France. Monique.Arlot@sante.univ-lyon1.fr http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15940379
    
12. Stevenson M, Lloyd Jones M, De Nigris E, Brewer N, Davis S and Oakley J (2005). A systematic review and economic evaluation of alendronate, etidronate, risedronate, raloxifene and teriparatide for the prevention and treatment of postmenopausal osteoporosis. Health Technol Assess 9: 1-160. OBJECTIVES: To establish the clinical effectiveness and cost-effectiveness of selective oestrogen receptor modulators, bisphosphonates and parathyroid hormone (subject to licensing) for the prevention and treatment of osteoporosis and the prevention of osteoporotic fractures in postmenopausal women. DATA SOURCES: Electronic databases. REVIEW METHODS: Studies that met the review's entry criteria were eligible for inclusion in the meta-analyses provided that they reported fracture incidence in terms of the number of patients suffering fractures. Meta-analysis was carried out using the random-effects model. A model was constructed to estimate the cost-effectiveness of osteoporosis interventions. The model calculated the number of fractures that occurred and provided the costs associated with osteoporotic fractures, and the quality-adjusted life-years (QALYs). In addition, the conditions of breast cancer and coronary heart disease (CHD) were modelled, as some interventions have been shown to affect the risk of these conditions. RESULTS: Ninety randomised controlled trials (RCTs) met the inclusion criteria. They related to the five interventions (alendronate, etidronate, risedronate, raloxifene and teriparatide) and to five comparators (calcium, calcium plus vitamin D, calcitriol, hormone replacement therapy and exercise), as well as placebo or no treatment. All five interventions have been shown to reduce the risk of vertebral fracture in women with severe osteoporosis with adequate calcium intakes. However, none of these drugs has been demonstrated, by direct comparison, to be significantly more effective than either each other or the other active interventions reviewed in this report. The intervention costs of treating all osteoporotic women, for a period of 5 years, were in the region of pound900--1500 million for alendronate, etidronate, risedronate and raloxifene. The cost per QALY ratios fell dramatically with age. Assuming the risks of a woman with severe osteoporosis at the threshold of osteoporosis, no treatment had a cost per QALY below pound35,000 at 50 years of age. At 60 years of age, the cost per QALY of raloxifene was pound26,000 assuming no impact on hip fractures, and pound31,000 assuming an adverse effect. However, these results are driven by the effect on breast cancer and the assumptions made regarding this disease state. No other intervention had a cost per QALY below pound35,000. When analyses were conducted assuming that the fracture risk is doubled at each site, alendronate and risedronate had cost per QALY ratios below pound 30,000 at all ages. For women at the threshold of osteoporosis, without a prior fracture and aged 70 years, the cost per QALY of the three bisphosphonates ranged from pound34,000 to pound41,000. Raloxifene had a cost per QALY of pound23,000, assuming no effect on hip fracture, given assumptions regarding breast cancer. At 80 years of age, the cost per QALY of alendronate and risedronate was below pound20,000. This was true for etidronate when incorporating observational data, but the value rose to pound69,000 when only RCT data were used. No other intervention had a cost per QALY below pound35,000. It was assumed that doubling the risk of fracture for women without a prior fracture would give results similar to patients at the threshold of osteoporosis with a prior fracture. CONCLUSIONS: Of the five interventions, only raloxifene appeared to reduce the risk of vertebral fracture in postmenopausal women unselected for low bone mineral density (BMD). However, as the full data have not been made public, there is some uncertainty regarding this result. None of the five interventions has been shown to reduce the risk of non-vertebral fracture in women unselected for low BMD. All of the proposed interventions provided gains in QALYs compared with no treatment in women with sufficient calcium and vitamin D intakes. The size of the QALY gain for each intervention was strongly related to the age of the patient. The estimated costs varied widely for the interventions. These net costs were markedly different by age, with some interventions becoming cost-saving at higher age ranges in patients with a prior fracture. Areas for future research include: the evidence base for the efficacy of fracture prevention in the very elderly, reanalysis of raloxifene using a dedicated breast cancer and CHD model, and more trials considering the cost-effectiveness of teriparatide. School of Health and Related Research (ScHARR), University of Sheffield, UK. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15929857
13. Scharla S and Reichenhall B (2005). [Optimal osteoporosis strategy?]. Krankenpfl J 43: 65. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15912853

[LaoziSailor]

Hey Lynnifer,

Originally Posted by lynnifer

Thanks for posting your question Stephen and the above Sailor ... I wonder if they'd take someone from Windsor for that trial? A four hour trip one way ... in winter no less ... eeeeks.

Usually I'm ousted from trials because of my pressure sores (on my sixth now woo hoo ... *grumble mumble*)

I am presently organizing all my papers and don't have the study's letter handy. If I recall the study was carried out over 18 months where you would take the Risedronate (or placebo) once a week after waking up and sitting upright for 45 minutes (very important). The study was also going to supply Calcium and Vitamin D (I think?) for the duration.
They wanted to see you 12 times during the study for scans so maybe it wouldn't be too bad as far as the Windsor-Toronto roundtrip.
Why don't you give Michelle or Anita a call and see where it goes from there?

My apologies to CCers, the following should really be another thread and I'm hijacking this one for the sake of continuity to Lynnifer's post.

BTW, about your sores. Are they Stage II or worse? I ask because if they are Stage II, I have some "Dragon's Blood" (Croton lechleri) that you would be welcome to, if they are worse I'd rather not. PM or email me for more details.
http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum and if you go to the "Display" pull-dowm menu and choose "Related Articles" you'll have a full day (or more) of reading / research.

I grew up in Peru and the stuff was known since time immemorial. I tried to get "clinical trials" started at Lyndhurst and faced the proverbial "wall" -- "no, we can't because the Health Protection Branch (HPB) will have us fill out forms up to our yin-yang before they'll allow that.'
They used to have the URL http://www.hc-sc.gc.ca/hpb/index_e.html which doesn't work anymore, the closest I've gotten is http://www.hc-sc.gc.ca/dhp-mps/index_e.html.

[DavidGrahamFL]

I just started Forteo (I'm 57; broke my hip mountain bike riding; family practice physician was suspicious; BMD -2.5...another story).

I just took the Forteo "class" and started this week.

Probably Lilly spin, but the class instructor made a specific comment to the effect that the "gain" in bone density shows up in the second year and not so much in the first year.

So, at least according to the Lilly instructor, taking it for a year and then switching to Fosamax or something similar might negate some/all of the drug's usefulness.

Maybe someone with access to the clinical studies can look at the data.