FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 344:1434-1441 May 10, 2001 Number 19 Next

Abstract PDF Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

ABSTRACT

Background Once-daily injections of parathyroid hormone or its amino-terminal fragments increase bone formation and bone mass without causing hypercalcemia, but their effects on fractures are unknown.

Methods We randomly assigned 1637 postmenopausal women with prior vertebral fractures to receive 20 or 40 µg of parathyroid hormone (1-34) or placebo, administered subcutaneously by the women daily. We obtained vertebral radiographs at base line and at the end of the study (median duration of observation, 21 months) and performed serial measurements of bone mass by dual-energy x-ray absorptiometry.

Results New vertebral fractures occurred in 14 percent of the women in the placebo group and in 5 percent and 4 percent, respectively, of the women in the 20-µg and 40-µg parathyroid hormone groups; the respective relative risks of fracture in the 20-µg and 40-µg groups, as compared with the placebo group, were 0.35 and 0.31 (95 percent confidence intervals, 0.22 to 0.55 and 0.19 to 0.50). New nonvertebral fragility fractures occurred in 6 percent of the women in the placebo group and in 3 percent of those in each parathyroid hormone group (relative risk, 0.47 and 0.46, respectively [95 percent confidence intervals, 0.25 to 0.88 and 0.25 to 0.86]). As compared with placebo, the 20-µg and 40-µg doses of parathyroid hormone increased bone mineral density by 9 and 13 more percentage points in the lumbar spine and by 3 and 6 more percentage points in the femoral neck; the 40-µg dose decreased bone mineral density at the shaft of the radius by 2 more percentage points. Both doses increased total-body bone mineral by 2 to 4 more percentage points than did placebo. Parathyroid hormone had only minor side effects (occasional nausea and headache).

Conclusions Treatment of postmenopausal osteoporosis with parathyroid hormone (1-34) decreases the risk of vertebral and nonvertebral fractures; increases vertebral, femoral, and total-body bone mineral density; and is well tolerated. The 40-µg dose increased bone mineral density more than the 20-µg dose but had similar effects on the risk of fracture and was more likely to have side effects.

Parathyroid hormone stimulates bone formation and resorption and can increase or decrease bone mass, depending on the mode of administration. Continuous infusions and daily subcutaneous injections of parathyroid hormone stimulate bone formation similarly but have different effects on bone resorption and bone mass.^1,2 Continuous infusions, which result in a persistent elevation of the serum parathyroid hormone concentration, lead to greater bone resorption than do daily injections, which cause only transient increases in the serum parathyroid hormone concentration.³

Parathyroid hormone or its amino-terminal fragments and analogues prevent, arrest, or partially reverse bone loss in animals and humans.⁴ In animals, parathyroid hormone induces parallel increases in bone mass and bone strength,⁵ suggesting that treatment with parathyroid hormone may provide protection against fractures in humans. We tested this hypothesis in a study of parathyroid hormone (1-34) for the treatment of postmenopausal women with prior vertebral fractures. Parathyroid hormone (1-34) comprises the first 34 amino acids of the hormone and produces its chief biologic effects. The sponsor terminated the study early in order to evaluate the clinical relevance of the finding that osteosarcomas developed in Fischer 344 rats during a long-term toxicologic study of parathyroid hormone (1-34). Subsequent evaluation of the clinical data revealed that parathyroid hormone (1-34) was effective in preventing fractures and was well tolerated.

Methods

Study Subjects

We screened postmenopausal women at 99 centers in 17 countries for enrollment in the study. Women were eligible for enrollment if they were ambulatory, if a period of at least five years had elapsed since menopause, and if they had at least one moderate or two mild atraumatic vertebral fractures on radiographs of the thoracic and lumbar spine, and an ambulatory status.⁶ For women with fewer than two moderate fractures, an additional criterion for enrollment was a value for bone mineral density of the hip or lumbar spine that was at least 1 SD below the mean value in normal premenopausal white women (age range, 20 to 35 years). We excluded women with illnesses that affect bone or calcium metabolism, urolithiasis within the preceding 5 years, impaired hepatic function, a serum creatinine concentration exceeding 2 mg per deciliter (177 µmol per liter), or alcohol or drug abuse, as well as women who had taken drugs that alter bone metabolism within the previous 2 to 24 months (depending on the drug). The study was approved by the ethics committee at each participating center, and all women gave written informed consent.

Treatment Protocol and Follow-up Studies

All enrolled women received daily supplements of 1000 mg of calcium and 400 to 1200 IU of vitamin D. The women gave themselves daily injections of placebo for two weeks and were then randomly assigned to receive placebo or 20 or 40 µg of recombinant human parathyroid hormone (1-34) in a regimen of daily, self-administered injections. We measured serum calcium before and 4 to 6 hours after injection at base line and after 1, 3, 6, 12, 18, and 24 months of treatment, and we measured calcium and creatinine excretion in 24-hour urine specimens at base line and after 1, 6, 12, and 24 months of treatment. All tests of serum and urine samples from an individual woman were performed at one of three laboratories that used identical, cross-calibrated methods of measurement. If the post-injection serum calcium concentration was high or if urinary excretion of calcium exceeded 350 mg (8.8 mmol) per day, and if the increase persisted on repeated testing, the calcium supplement was discontinued permanently or the volume of the injected study drug was halved until the abnormality had disappeared.

All women underwent anteroposterior and lateral radiography of the thoracic and lumbar spine at base line and at the end of the study. Radiologists at a central location who knew the temporal sequence of the radiographs, but not the treatment assignments, graded each woman's vertebrae as normal (i.e., normal height) or as mildly, moderately, or severely deformed (i.e., a decrease in height of approximately 20 to 25 percent, 26 to 40 percent, or more than 40 percent, respectively).⁶ A vertebra was not graded if scoliosis, fusion, or another anomaly prevented radiographic assessment. A new vertebral fracture was reported if a normal vertebra became deformed; worsening of preexisting deformities was not analyzed. Nonvertebral fractures were documented by a review of radiographs or radiologic reports and were classified as fragility fractures (the protocol-specified end point) if the associated trauma would not have resulted in the fracture of a normal bone, in the opinion of the local investigator.

We measured the bone mineral density of the lumbar spine, proximal femur, and radius and the total-body bone mineral by dual-energy x-ray absorptiometry with the use of Hologic, Lunar, or Norland equipment. The measurements were analyzed centrally, and the results were not reported to the participating centers. We measured the bone density of the spine at base line and at 12 and 18 months, and at the end of the study in all women (as well as at 3 and 6 months in a subgroup of women); we measured the bone density of the hips (in all women), forearms (in a subgroup), and total body (in a subgroup) at base line, at 12 months, and at the end of the study. Spine and hip values are reported in grams per square centimeter, although they have been converted to standardized units, which eliminate differences in measurements attributable to the manufacturer's calibrations.⁷ Measurements of the spine excluded vertebrae with fractures or focal sclerosis. Total-body bone measurements excluded the head in order to avoid dental artifacts. The consistency of serial measurements was assessed with serial measurements of a spine phantom at each center, and the consistency of measurements among centers was assessed with measurements of a standard phantom circulated to all centers. Measurements of the phantoms were used to adjust for minor changes in the performance of the densitometer.⁸

We measured height with a stadiometer at base line and every 12 months; blood counts, serum chemical tests, and urinalysis were performed at base line and at 1, 6, 12, and 24 months. Tests of serum antibodies to parathyroid hormone (1-34), based on the specific binding of radioiodinated parathyroid hormone (1-34), were performed at base line and at 3, 12, and 24 months.

Statistical Analysis

We analyzed data for all women with at least one follow-up visit after enrollment. The rates of side effects and the proportions of women with fractures in the three study groups were compared with the use of Pearson's chi-square test. All laboratory data and bone mineral measurements were evaluated by analysis of variance, with the inclusion of terms for the treatment assignment and country. All statistical tests were two-sided.

Results

Of 9347 women who were screened for the study, 7710 were not eligible or were not interested in participating. The remaining 1637 women were randomly assigned to receive placebo (544 women) or parathyroid hormone (1-34) at a dose of 20 µg per day (541 women) or 40 µg per day (552 women). The base-line characteristics of the women in the three study groups were similar (Table 1). In December 1998, all women were invited to a termination visit because the sponsor had stopped the study. The interval during which women were at risk for vertebral fractures (the period from enrollment to the final radiographic study of the spine) and nonvertebral fractures (the period from enrollment to the final visit) did not differ significantly among the three groups (Table 2 and Table 3, respectively). The cumulative duration of the study treatment in the group that received placebo, the group that received 20 µg of parathyroid hormone (1-34) per day, and the group that received 40 µg per day was 798, 779, and 774 patient-years, respectively, and the mean (±SD) duration of treatment in the three groups was 18±5, 18±6, and 17±6 months, respectively. The average rate of compliance with the regimen of injections, assessed on the basis of returned medication, ranged from 79 to 83 percent at each visit, and the rates did not differ significantly among the three groups.

View this table: [in this window] [in a new window]   Table 1. Base-Line Characteristics of 1637 Postmenopausal Women According to Whether Their Spinal Radiographs Were Adequate for Evaluation.

 

View this table: [in this window] [in a new window]   Table 2. Radiographic Evidence of New Vertebral Fractures.

 

View this table: [in this window] [in a new window]   Table 3. New Nonvertebral Fractures and New Nonvertebral Fragility Fractures.

 
Vertebral Fractures and Changes in Height

Base-line and follow-up radiographs were available for 1326 of the 1637 women (81 percent); follow-up radiographs were not available for 249 women, and an additional 62 women had pretreatment radiographs that were inadequate for evaluation. Base-line risk factors for new vertebral fractures were similar in the three groups (Table 1), as were serum 25-hydroxyvitamin D concentrations and indexes of bone turnover (data not shown). Of the 1326 women for whom adequate radiographs were available, 105 had one or more new vertebral fractures. As compared with placebo, parathyroid hormone (1-34) at the 20-µg and 40-µg doses reduced the risk of one or more new vertebral fractures by 65 and 69 percent, respectively; the risk of two or more fractures was reduced by 77 and 86 percent, respectively, and the risk of at least one moderate or severe vertebral fracture was reduced by 90 and 78 percent, respectively (Table 2). Treatment with parathyroid hormone (1-34) also reduced the total number of vertebral fractures: the number of fractures per 1000 patient-years of treatment was 136 in the placebo group, 49 in the 20-µg parathyroid hormone group, and 30 in the 40-µg group. With the 20-µg dose, a vertebral fracture was prevented for every 12 patient-years of treatment, and with the 40-µg dose, a vertebral fracture was prevented for every 10 patient-years of treatment.

New or worsening back pain was reported by 23 percent of the women in the placebo group but by only 17 percent and 16 percent of those in the 20-µg and 40-µg parathyroid hormone groups, respectively (P=0.007). These data were consistent with the radiographic findings. Among the 105 women with one or more new vertebral fractures, the mean loss in height was greater in the placebo group (–1.1 cm) than in the 20-µg and 40-µg parathyroid hormone groups (–0.2 and –0.3 cm, respectively; P=0.002). Because most women did not have new vertebral fractures, the overall mean loss in height was small and did not differ significantly among the three groups.

Nonvertebral Fractures

New nonvertebral fractures occurred in 119 women and were considered fragility fractures in 58 (Table 3). Women treated with the 20-µg dose of parathyroid hormone (1-34) and those treated with the 40-µg dose were 35 and 40 percent less likely to have one or more new nonvertebral fractures, respectively, than the women in the placebo group, and were 53 and 54 percent less likely to have one or more new nonvertebral fragility fractures. The absolute risk of one or more nonvertebral fractures was 10 percent in the placebo group and 6 percent in each parathyroid hormone group; the absolute risk of one or more nonvertebral fragility fractures was 6 percent in the placebo group and 3 percent in the two parathyroid hormone groups (relative risk, 0.47 and 0.46, respectively [95 percent confidence intervals, 0.25 to 0.88 and 0.25 to 0.86]). The cumulative incidence of one or more new nonvertebral fractures or nonvertebral fragility fractures was initially similar in the three study groups; the protective effects of parathyroid hormone treatment became evident after 9 to 12 months (Figure 1). Although the numbers of women with new nonvertebral fractures at specific skeletal sites were too small to estimate the incidence of each type of fracture, the numbers in the parathyroid hormone groups were generally smaller than — and in no case exceeded — the numbers in the placebo group (Table 3).

View larger version (12K): [in this window] [in a new window]   Figure 1. Cumulative Proportion of Women Assigned to Receive Placebo or Parathyroid Hormone (1-34) (PTH) at a Daily Dose of 20 µg or 40 µg Who Had One or More Nonvertebral Fractures (Panel A) and the Cumulative Proportion Who Had One or More Nonvertebral Fragility Fractures (Panel B) during the Study. For both panels, the respective numbers of women in the placebo group and in the 20-µg and 40-µg PTH groups were 544, 541, and 552 at base line; 497, 492, and 486 at 6 months; 477, 465, and 456 at 12 months; and 404, 400, and 390 at 18 months. P0.05 for all pairwise comparisons with placebo, by the log-rank test.

 
Bone Mineral Density and Total-Body Bone Mineral

At base line, bone mineral density was similar among the three groups at all skeletal sites; total-body bone mineral was also similar (Table 4). The mean bone mineral density of the spine was 2.6 SD below the mean value in normal young white women (mean T score, –2.6). Treatment with parathyroid hormone (1-34) resulted in significant dose-dependent increases in the bone mineral density of the spine and hip and in total-body bone mineral (Table 4). The bone mineral density of the shaft of the radius decreased from the base-line values in all three groups; the percent change in the 40-µg group, but not that in the 20-µg group, differed significantly from the percent change in the placebo group (P<0.001). As previously reported by other investigators,^9,10 this difference arose during the first year of treatment; subsequently, the bone mineral density of the radial shaft changed in parallel in all three groups (data not shown). The density of the distal radius did not differ significantly among the three groups.

View this table: [in this window] [in a new window]   Table 4. Change from Base Line in Bone Mineral Density and Total-Body Bone Mineral.

 
Adverse Events

There were no significant differences among the three groups with respect to the numbers of deaths and hospitalizations or the numbers of women in whom cardiovascular disorders, urolithiasis, or gout developed during the study. There were no cases of osteosarcoma. Cancer developed in 40 women, with a higher incidence in the placebo group (4 percent) than in the 20-µg and 40-µg parathyroid hormone groups (2 percent in each group; P=0.02 and P=0.07, respectively). A total of 32 women in the placebo group (6 percent), 35 in the 20-µg parathyroid hormone group (6 percent), and 59 in the 40-µg group (11 percent) withdrew from the study because of an adverse event. Nausea was reported by 18 percent of women taking 40 µg of parathyroid hormone, and headache was reported by 13 percent, whereas only 8 percent of women taking placebo reported each of these symptoms (P<0.001 and P=0.01, respectively); the frequencies of nausea and headache in the lower-dose parathyroid hormone group were similar to those in the placebo group. Nine percent of the women in the 20-µg parathyroid hormone group reported dizziness, and 3 percent reported leg cramps, but these symptoms were reported by only 6 percent and 1 percent of women in the placebo group, respectively (P=0.05 and P=0.02, respectively); the frequencies of dizziness and leg cramps in the 40-µg parathyroid hormone group were similar to those in the placebo group. Preinjection blood pressure and heart rate, measured at each visit, were unaffected by treatment with parathyroid hormone (1-34).

Because subcutaneous injections of parathyroid hormone (1-34) have the greatest effect on serum calcium during the first four to six hours after injection, we measured serum calcium before and four to six hours after an injection of parathyroid hormone (1-34) at each visit. The preinjection measurements (performed 16 to 24 hours after the previous injection) were usually normal. Mild hypercalcemia (defined as a calcium concentration that exceeded 10.6 mg per deciliter [2.6 mmol per liter]) occurred at least once in 2 percent of the women in the placebo group, 11 percent of those in the 20-µg parathyroid hormone group, and 28 percent of those in the 40-µg group. Of the high serum calcium values, 95 percent were less than 11.2 mg per deciliter (2.80 mmol per liter) in the 20-µg group, and 95 percent were less than 11.8 mg per deciliter (2.95 mmol per liter) in the 40-µg group; in only about one third of the women with high serum calcium concentrations were the values high on retesting, which was usually performed within a few weeks. Women who did not have hypercalcemia during the first six months of treatment seldom had it later. The study protocol required permanently halving the injected dose of medication in women with persistent hypercalcemia after a reduction in calcium intake; this occurred in 3 women in the placebo group (<1 percent), 15 in the 20-µg group (3 percent), and 62 in the 40-µg group (11 percent). Treatment was withdrawn because of repeatedly elevated serum calcium concentrations in one woman in the placebo group, one in the 20-µg group, and nine in the 40-µg group.

Serum 25-hydroxyvitamin D and calcitriol concentrations were similar in the three groups at base line. Serum calcitriol concentrations increased significantly from the base-line values in each parathyroid hormone group and did not change in the placebo group. The mean 24-hour urinary calcium excretion increased slightly during parathyroid hormone (1-34) treatment (by 30 mg [0.75 mmol] per day), but the incidence of hypercalciuria (a value for urinary calcium excretion that exceeded 300 mg [7.5 mmol] per day) did not increase. Serum magnesium concentrations decreased slightly in both parathyroid hormone groups, and serum uric acid concentrations rose by 13 to 20 percent during treatment with parathyroid hormone at a dose of 20 µg per day and by 20 to 25 percent at a dose of 40 µg per day, without clinical sequelae. An average of five weeks after the cessation of treatment, serum calcium, magnesium, and uric acid concentrations had returned to or approached pretreatment values. Serum creatinine concentrations and creatinine clearance were unaffected by parathyroid hormone (1-34) treatment. Circulating antibodies to parathyroid hormone (1-34) developed in 1 woman in the placebo group (<1 percent), 15 women in the 20-µg group (3 percent), and 44 in the 40-µg group (8 percent), but these antibodies had no discernible effects on any of the other measurements.

Discussion

Daily injections of parathyroid hormone (1-34) at a dose of 20 µg and daily injections at a dose of 40 µg increased the bone mineral density of the spine by 9 and 13 percentage points more than did placebo, and reduced the risk of new vertebral fractures by 65 and 69 percent, respectively, as compared with placebo. These benefits exceed those reported for other treatments in similar women. In studies using similar analyses, alendronate (10 mg per day) reduced the risk of new vertebral fractures by 48 percent,^11,12,13 risedronate (5 mg per day) by 41 percent,¹⁴ an intermittent regimen of cyclical etidronate by 44 percent,^15,16 and raloxifene (60 mg per day) by 30 percent.¹⁷ Estimates of a 40 to 50 percent reduction in the risk of vertebral fractures with estrogen treatment are based on cohort and case–control studies or small placebo-controlled, prospective trials.^18,19 Salmon calcitonin nasal spray has inconsistent effects on the risk of vertebral fractures,²⁰ and the effects of supplemental calcitriol,^21,22 vitamin D,^23,24,25,26 and calcium²⁷ on this end point cannot be estimated on the basis of the published data.

Daily treatment with parathyroid hormone (1-34) reduced the risk of nonvertebral fractures by 35 percent at the 20-µg dose and by 40 percent at the 40-µg dose and reduced the risk of nonvertebral fragility fractures by 53 and 54 percent, respectively. In similar women, alendronate reduced the risk of nonvertebral fractures by 20 percent,¹² risedronate by 39 percent,¹⁴ and raloxifene by 10 percent.¹⁷ The effects of etidronate^15,16 and calcitonin²⁰ on the risk of nonvertebral fractures are not known. Vitamin D^23,26 and calcitriol²² reduced the risk of nonvertebral fractures by 50 to 60 percent in some studies, but the effects of parathyroid hormone in our study are in addition to any effect of vitamin D, since all the women received vitamin D and calcium supplements.

These antifracture benefits make it important to understand the clinical relevance of the osteosarcomas found in rats given parathyroid hormone (1-34) in a standard carcinogenicity bioassay. In that study, the rats were given nearly lifetime daily injections of parathyroid hormone (1-34). The occurrence of osteosarcoma was dose-dependent, and the tumors developed after parathyroid hormone (1-34) had induced osteosclerosis. Parathyroid hormone (1-34) did not increase the incidence of tumors in other tissues in rats, nor were osteosarcomas found in monkeys that had undergone bilateral oophorectomy and then been given daily doses that were 4 to 10 times the maximal dose in humans over a period of 18 months. In standard tests, parathyroid hormone (1-34) is neither mutagenic nor genotoxic. In prior studies involving a total of nearly 1000 patients, treatment with parathyroid hormone (1-84), parathyroid hormone (1-34), or parathyroid hormone (1-38) for up to three years did not increase the incidence of bone tumors.²⁸ Osteosarcomas are rare in adults, and chronic primary hyperparathyroidism is not associated with an increased risk of osteosarcoma.^29,30

In summary, the clinical benefits of parathyroid hormone (1-34) reflect its ability to stimulate bone formation and thereby increase bone mass and strength. This hormone appears to be effective in preventing fractures in postmenopausal women with osteoporosis.

Supported by Eli Lilly.

Dr. Eriksen owns stock in Eli Lilly.

We are indebted to Drs. Hunter Heath III and John T. Potts, Jr., for their comments on the manuscript and to Ms. Michele Y. Hill for editorial assistance and assistance in the preparation of the manuscript.

Source Information

From Massachusetts General Hospital and Harvard Medical School, Boston (R.M.N.); the University of California, San Francisco (C.D.A., H.K.G.); Fundación de Investigaciones Metabólicas, Buenos Aires, Argentina (J.R.Z.); the University of Western Australia and Sir Charles Gairdner Hospital, Perth, Australia (R.P.); Eli Lilly, Indianapolis (G.A.G., O.W., B.H.M.); Polycliniques Universitaires L. Brull, Liege, Belgium (J.-Y.R.); St. Joseph's Health Center, London, Ont., Canada (A.B.H.); Aarhus Amtssygehus, Aarhus, Denmark (E.F.E.); and Rambam Medical Center, Haifa, Israel (S.I.-S.).

Other authors were Dan Mellström, Department of Geriatrics, University of Göteborg, Göteborg, Sweden; Erik S. Oefjord, Bergen Osteoporosesenter, Paradis, Norway; Ewa Marcinowska-Suchowierska, Klinika Chorob Wewnetrznych, Warsaw, Poland; Jorma Salmi, Koskiklinikka, Tampere, Finland; Henk Mulder, Medisch Onderzoekscentrum Gcp, De Bilt, the Netherlands; Johan Halse, Betanien Med Lab, Oslo, Norway; and Andrzej Z. Sawicki, Warszawskie Centrum Osteoporozy, Warsaw, Poland.

Address reprint requests to Dr. Mitlak at Eli Lilly, Inc., Lilly Corporate Center, Indianapolis, IN 46285-2680, or at b.mitlak{at}lilly.com.

References

1. Podbesek R, Edouard C, Meunier PJ, et al. Effects of two treatment regimes with synthetic human parathyroid hormone fragment on bone formation and the tissue balance of trabecular bone in greyhounds. Endocrinology 1983;112:1000-1006. [Abstract]
2. Hock JM, Gera I. Effects of continuous and intermittent administration and inhibition of resorption on the anabolic response of bone to parathyroid hormone. J Bone Miner Res 1992;7:65-72. [ISI][Medline]
3. Tam CS, Heersche JN, Murray TM, Parsons JA. Parathyroid hormone stimulates the bone apposition rate independently of its resorptive action: differential effects of intermittent and continuous administration. Endocrinology 1982;110:506-512. [Abstract]
4. Dempster DW, Cosman F, Parisien M, Shen V, Lindsay R. Anabolic actions of parathyroid hormone on bone. Endocr Rev 1993;14:690-709. [Erratum, Endocr Rev 1994;15:261.] [CrossRef][ISI][Medline]
5. Turner CH, Wang T, Hirano T, et al. In primates, treatment with PTH (1-34), LY333334, increases bone strength at trabecular bone sites without compromising the strength of cortical bone. J Bone Miner Res 1999;14:Suppl 1:S414-S414.abstract 
6. Genant HK, Wu CY, van Kuijk C, Nevitt MC. Vertebral fracture assessment using a semiquantitative technique. J Bone Miner Res 1993;8:1137-1148. [ISI][Medline]
7. Lu Y, Ye K, Mathur AK, Hui S, Fuerst TP, Genant HK. Comparative calibration without a gold standard. Stat Med 1997;16:1889-1905. [CrossRef][ISI][Medline]
8. Lu Y, Mathur AK, Blunt BA, et al. Dual X-ray absorptiometry quality control: comparison of visual examination and process-control charts. J Bone Miner Res 1996;11:626-637. [ISI][Medline]
9. Neer R, Slovik D, Daly M, Lo C, Potts J, Nussbaum S. Treatment of postmenopausal osteoporosis with daily parathyroid hormone plus calcitriol. In: Christiansen C, Overgaard K, eds. Osteoporosis 1990: proceedings of the Third International Symposium on Osteoporosis. Copenhagen, Denmark: Osteopress ApS, 1990:1314-7.
10. Hodsman AB, Steer BM, Fraher LJ, Drost DJ. Bone densitometric and histomorphometric responses to sequential human parathyroid hormone (1-38) and salmon calcitonin in osteoporotic patients. Bone Miner 1991;14:67-83. [CrossRef][ISI][Medline]
11. Liberman UA, Weiss SR, Bröll J, et al. Effect of oral alendronate on bone mineral density and the incidence of fractures in postmenopausal osteoporosis. N Engl J Med 1995;333:1437-1443. [Free Full Text]
12. Black DM, Cummings SR, Karpf DB, et al. Randomised trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Lancet 1996;348:1535-1541. [CrossRef][ISI][Medline]
13. Cummings SR, Black DM, Thompson DE, et al. Effect of alendronate on risk of fracture in women with low bone density but without vertebral fractures: results from the Fracture Intervention Trial. JAMA 1998;280:2077-2082. [Free Full Text]
14. Harris ST, Watts NB, Genant HK, et al. Effects of risedronate treatment on vertebral and nonvertebral fractures in women with postmenopausal osteoporosis: a randomized controlled trial. JAMA 1999;282:1344-1352. [Free Full Text]
15. Storm T, Thamsborg G, Steiniche T, Genant HK, Sørensen OH. Effect of intermittent cyclical etidronate therapy on bone mass and fracture rate in women with postmenopausal osteoporosis. N Engl J Med 1990;322:1265-1271. [Abstract]
16. Watts NB, Harris ST, Genant HK, et al. Intermittent cyclical etidronate treatment of postmenopausal osteoporosis. N Engl J Med 1990;323:73-79. [Abstract]
17. Ettinger B, Black DM, Mitlak BH, et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: results from a 3-year randomized clinical trial. JAMA 1999;282:637-645. [Erratum, JAMA 1999;282:2124.] [Free Full Text]
18. Lufkin EG, Wahner HW, O'Fallon WM, et al. Treatment of postmenopausal osteoporosis with transdermal estrogen. Ann Intern Med 1992;117:1-9.
19. Lindsay R, Hart DM, Forrest C, Baird C. Prevention of spinal osteoporosis in oophorectomised women. Lancet 1980;2:1151-1154. [ISI][Medline]
20. Chesnut CH, Silverman SL, Andriano K, et al. A randomized trial of nasal spray salmon calcitonin in postmenopausal women with established osteoporosis: the Prevent Recurrence of Osteoporotic Fractures study. Am J Med 2000;109:267-276. [CrossRef][ISI][Medline]
21. Ott SM, Chesnut CH. Calcitriol treatment is not effective in postmenopausal osteoporosis. Ann Intern Med 1989;110:267-274.
22. Tilyard MW, Spears GFS, Thomson J, Dovey S. Treatment of postmenopausal osteoporosis with calcitriol or calcium. N Engl J Med 1992;326:357-362. [Abstract]
23. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D₃ and calcium to prevent hip fractures in elderly women. N Engl J Med 1992;327:1637-1642. [Abstract]
24. Heikinheimo RJ, Inkovaara JA, Harju EJ, et al. Annual injection of vitamin D and fractures of aged bones. Calcif Tissue Int 1992;51:105-110. [CrossRef][ISI][Medline]
25. Lips P, Graafmans WC, Ooms ME, Bezemer PD, Bouter LM. Vitamin D supplementation and fracture incidence in elderly persons: a randomized, placebo-controlled clinical trial. Ann Intern Med 1996;124:400-406. [Free Full Text]
26. Dawson-Hughes B, Harris SS, Krall EA, Dallal GE. Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med 1997;337:670-676. [Free Full Text]
27. Reid IR, Ames RW, Evans MC, Gamble GD, Sharpe SJ. Long-term effects of calcium supplementation on bone loss and fractures in postmenopausal women: a randomized controlled trial. Am J Med 1995;98:331-335. [CrossRef][ISI][Medline]
28. Horwitz M, Stewart A, Greenspan SL. Sequential parathyroid hormone/alendronate therapy for osteoporosis -- robbing Peter to pay Paul? J Clin Endocrinol Metab 2000;85:2127-2128. [Free Full Text]
29. Palmer M, Adami HO, Krusemo UB, Ljunghall S. Increased risk of malignant diseases after surgery for primary hyperparathyroidism: a nationwide cohort study. Am J Epidemiol 1988;127:1031-1040. [Free Full Text]
30. Wermers RA, Khosla S, Atkinson EJ, et al. Survival after the diagnosis of hyperparathyroidism: a population-based study. Am J Med 1998;104:115-122. [CrossRef][ISI][Medline]

The following additional investigators participated in the study: Argentina — C.A. Mautalen, Buenos Aires; Austria — G. Leb, Astrid Fahrieitner, H. Dobnig, Graz; Belgium — J.P. Devogelaer, Brussels; J.-M. Kaufman, Ghent; Canada — J.P. Brown, Sainte-Foy, Que.; D.A. Hanley, Calgary, Alta.; R.G. Josse, G.A. Hawker, S. Mann, Toronto; W.P. Olszynski, Saskatoon, Sask.; L.G. Ste.-Marie, Montreal; M.O. Al-Daker, Regina, Sask.; C.K. Yuen, Winnipeg, Man.; S. Kaiser, St. John's, Newf.; A.B. Cranney, Ottawa, Ont.; K.G. Siminoski, Edmonton, Alta.; Czech Republic — J. Stepan, Prague; O. Topolcan, V. Vyskocil, Plzen-Bory; V. Palicka, Kralove; Denmark — L. Hyldstrup, Hvifovre; P. Laurberg, Aalborg, Otto Grove, Varde; H. Beck-Nielsen, Odense; Finland — E. Alhava, Kuopio; M. Kormano, Turku; P. Salmela, K. Rontgen, J.E. Heikkinen, Oulu; J. Salmi, Tampere; M. Valimaki, I. Arnala, Helsinki; J. Saltevo, Jyvaskyla; Hungary — G. Poor, J. Szuecs, Budapest; L. Gaspar, Szeged; Israel — A. Karasik, I. Vered, Tel-Hashomer; E. Segal, Haifa; Italy — C. Gennari, Siena; G. Crepaldi, L. Sartori, Padua; A. Pinchera, Pisa; G. Mazzuoli, Rome; M. Passeri, Parma; G. Bianchi, Arenzano; New Zealand — N.L. Gilchrist, Canterbury; Norway — J.B. Michelsen, Kristiansand; J.A. Falch, Oslo; E. Mohr, Haugesund; S.S. Gudnason, Bergen; U. Syversen, Trondheim; Poland — M. Talalaj, P. Kapuscinski, J. Borowicz, E. Sawicka, J. Lesnicki, A. Olak-Popko, Warsaw; T. Miazgowski, J. Ogonowski, S. Czekalski, Szczecin; Sweden — S. Ljunghall, K. Larsson, Uppsala; M. Palmer, Orebro; G. Toss, Linkoping; M. Saaf, Stockholm; United States — M.A. Bolognese, Gaithersburg, Md.; C. Mckeever, Houston; L. Avioli (deceased), St. Louis; E.S. Orwoll, Portland, Oreg.; M. Greenwald, Palm Springs, Calif.; R.D. Wasnich, Honolulu; S.R. Weiss, San Diego, Calif.; W. Briney, Denver; C. Gallagher, Omaha, Nebr.; O.S. Gluck, Phoenix, Ariz.; M.H. Davidson, Chicago; S.C. English, Billings, Mont.; N.M. Lunde, Arden Hills, Minn.; M.R. Khairi, Indianapolis; J. Rosenstock, Dallas; A.A. Licata, Cleveland; A.L. Burshell, New Orleans; C.E. Lewis, Birmingham, Ala.; A.L. Mulloy, Augusta, Ga.; M.P. Ettinger, Stuart, Fla.; A. Virshup, West Palm Beach, Fla.; S.B. Ward, Philadelphia; N. Wei, Frederick, Md.; J. Stock, Morristown, N.J.; S. Wallach, R. Bockman, New York; C.J. Rosen, Bangor, Me.; C.E. Waud, Worcester, Mass.; R. Marcus, Palo Alto, Calif.; R. Levy, Olympia, Wash.; S.S. Miller, San Antonio, Tex.; S. Songcharoen, Jackson, Miss.; K.D. Schlessel, Willingboro, N.J.; L.M. Cohen, Sarasota, Fla.; V.K. Piziak, Temple, Tex.; S. Scumpia, Austin, Tex.; R.R. Stoltz, Evansville, Ind.

Abstract PDF Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

This article has been cited by other articles:

• Miller, P. D., Delmas, P. D., Lindsay, R., Watts, N. B., Luckey, M., Adachi, J., Saag, K., Greenspan, S. L., Seeman, E., Boonen, S., Meeves, S., Lang, T. F., Bilezikian, J. P., for the Open-label Study to Determine How Prior Th, (2008). Early Responsiveness of Women with Osteoporosis to Teriparatide After Therapy with Alendronate or Risedronate. J. Clin. Endocrinol. Metab. 93: 3785-3793 [Abstract] [Full Text]  
• Horwitz, M. J., Stewart, A. F. (2008). Hypoparathyroidism: Is It Time for Replacement Therapy?. J. Clin. Endocrinol. Metab. 93: 3307-3309 [Full Text]  
• Winer, K. K., Sinaii, N., Peterson, D., Sainz, B. Jr., Cutler, G. B. Jr. (2008). Effects of Once Versus Twice-Daily Parathyroid Hormone 1-34 Therapy in Children with Hypoparathyroidism. J. Clin. Endocrinol. Metab. 93: 3389-3395 [Abstract] [Full Text]  
• Ono, N., Nakashima, K., Rittling, S. R., Schipani, E., Hayata, T., Soma, K., Denhardt, D. T., Kronenberg, H. M., Ezura, Y., Noda, M. (2008). Osteopontin Negatively Regulates Parathyroid Hormone Receptor Signaling in Osteoblasts. J. Biol. Chem. 283: 19400-19409 [Abstract] [Full Text]  
• Ishani, A., Blackwell, T., Jamal, S. A., Cummings, S. R., Ensrud, K. E., for the MORE Investigators, (2008). The Effect of Raloxifene Treatment in Postmenopausal Women with CKD. J. Am. Soc. Nephrol. 19: 1430-1438 [Full Text]  
• Nemeth, E. F. (2008). Anabolic Therapy for Osteoporosis: Calcilytics. IBMS BoneKEy 5: 196-208 [Abstract] [Full Text]  
• Nielsen, D., Ryg, J., Nissen, N., Nielsen, W., Knold, B., Brixen, K. (2008). Multidisciplinary patient education in groups increases knowledge on osteoporosis: A randomized controlled trial. Scand J Public Health 36: 346-352 [Abstract]  
• Gehrig, L., Lane, J., O'Connor, M. I. (2008). Osteoporosis: Management and Treatment Strategies for Orthopaedic Surgeons. JBJS 90: 1362-1374 [Full Text]  
• Black, D. M., Bouxsein, M. L., Palermo, L., McGowan, J. A., Newitt, D. C., Rosen, E., Majumdar, S., Rosen, C. J., for the PTH Once-Weekly Research (POWR) Group, (2008). Randomized Trial of Once-Weekly Parathyroid Hormone (1-84) on Bone Mineral Density and Remodeling. J. Clin. Endocrinol. Metab. 93: 2166-2172 [Abstract] [Full Text]  
• Cole, Z., Dennison, E., Cooper, C. (2008). Update on the treatment of post-menopausal osteoporosis. Br Med Bull 86: 129-143 [Abstract] [Full Text]  
• Pearsall, R. S., Canalis, E., Cornwall-Brady, M., Underwood, K. W., Haigis, B., Ucran, J., Kumar, R., Pobre, E., Grinberg, A., Werner, E. D., Glatt, V., Stadmeyer, L., Smith, D., Seehra, J., Bouxsein, M. L. (2008). A soluble activin Type IIA receptor induces bone formation and improves skeletal integrity. Proc. Natl. Acad. Sci. USA 105: 7082-7087 [Abstract] [Full Text]  
• Grundberg, E., Brandstrom, H., Lam, K. C. L., Gurd, S., Ge, B., Harmsen, E., Kindmark, A., Ljunggren, O., Mallmin, H., Nilsson, O., Pastinen, T. (2008). Systematic assessment of the human osteoblast transcriptome in resting and induced primary cells. Physiol. Genomics 33: 301-311 [Abstract] [Full Text]  
• Liu, H., Paige, N. M., Goldzweig, C. L., Wong, E., Zhou, A., Suttorp, M. J., Munjas, B., Orwoll, E., Shekelle, P. (2008). Screening for Osteoporosis in Men: A Systematic Review for an American College of Physicians Guideline. ANN INTERN MED 148: 685-701 [Abstract] [Full Text]  
• Edwards, B. J., Migliorati, C. A. (2008). Osteoporosis and Its Implications for Dental Patients. Journal of the American Dental Association 139: 545-552 [Abstract] [Full Text]  
• Rozental, T. D., Makhni, E. C., Day, C. S., Bouxsein, M. L. (2008). Improving Evaluation and Treatment for Osteoporosis Following Distal Radial Fractures. A Prospective Randomized Intervention. JBJS 90: 953-961 [Abstract] [Full Text]  
• Yu, S., Franceschi, R. T., Luo, M., Zhang, X., Jiang, D., Lai, Y., Jiang, Y., Zhang, J., Xiao, G. (2008). Parathyroid Hormone Increases Activating Transcription Factor 4 Expression and Activity in Osteoblasts: Requirement for Osteocalcin Gene Expression. Endocrinology 149: 1960-1968 [Abstract] [Full Text]  
• Pioszak, A. A., Xu, H. E. (2008). Molecular recognition of parathyroid hormone by its G protein-coupled receptor. Proc. Natl. Acad. Sci. USA 105: 5034-5039 [Abstract] [Full Text]  
• Stroup, J., Kane, M. P., Abu-Baker, A. M. (2008). Teriparatide in the treatment of osteoporosis. Am J Health Syst Pharm 65: 532-539 [Abstract] [Full Text]  
• Anastasilakis, A. D, Goulis, D. G, Polyzos, S. A, Gerou, S., Pavlidou, V., Koukoulis, G., Avramidis, A. (2008). Acute changes in serum osteoprotegerin and receptor activator for nuclear factor-{kappa}B ligand levels in women with established osteoporosis treated with teriparatide. Eur J Endocrinol 158: 411-415 [Abstract] [Full Text]  
• Boonen, S., Marin, F., Obermayer-Pietsch, B., Simoes, M. E., Barker, C., Glass, E. V., Hadji, P., Lyritis, G., Oertel, H., Nickelsen, T., McCloskey, E. V., for the EUROFORS Investigators, (2008). Effects of Previous Antiresorptive Therapy on the Bone Mineral Density Response to Two Years of Teriparatide Treatment in Postmenopausal Women with Osteoporosis. J. Clin. Endocrinol. Metab. 93: 852-860 [Abstract] [Full Text]  
• Lloyd, S. A.J., Travis, N. D., Lu, T., Bateman, T. A. (2008). Development of a low-dose anti-resorptive drug regimen reveals synergistic suppression of bone formation when coupled with disuse. J. Appl. Physiol. 104: 729-738 [Abstract] [Full Text]  
• MacLaughlin, E. J., Raehl, C. L. (2008). ASHP Therapeutic Position Statement on the Prevention and Treatment of Osteoporosis in Adults. Am J Health Syst Pharm 65: 343-357 [Full Text]  
• MacLean, C., Newberry, S., Maglione, M., McMahon, M., Ranganath, V., Suttorp, M., Mojica, W., Timmer, M., Alexander, A., McNamara, M., Desai, S. B., Zhou, A., Chen, S., Carter, J., Tringale, C., Valentine, D., Johnsen, B., Grossman, J. (2008). Systematic Review: Comparative Effectiveness of Treatments to Prevent Fractures in Men and Women with Low Bone Density or Osteoporosis. ANN INTERN MED 148: 197-213 [Abstract] [Full Text]  
• Kunzendorf, U., Kramer, B. K., Arns, W., Braun, J., Grossmann, J., Pietruck, F., Schmidt-Gayk, H., Schwarz, A., Ziegler, E., Sperschneider, H., Wuthrich, R. P., Nonnast-Daniel, B., Schindler, R., Renders, L. (2008). Bone disease after renal transplantation. Nephrol Dial Transplant 23: 450-458 [Full Text]  
• Barnes, G. L., Kakar, S., Vora, S., Morgan, E. F., Gerstenfeld, L. C., Einhorn, T. A. (2008). Stimulation of Fracture-Healing with Systemic Intermittent Parathyroid Hormone Treatment. JBJS 90: 120-127 [Abstract] [Full Text]  
• Garnero, P., Vergnaud, P., Hoyle, N. (2008). Evaluation of a Fully Automated Serum Assay for Total N-Terminal Propeptide of Type I Collagen in Postmenopausal Osteoporosis. Clin. Chem. 54: 188-196 [Abstract] [Full Text]  
• Dawson-Hughes, B., Chen, P., Krege, J. H. (2007). Response to Teriparatide in Patients with Baseline 25-Hydroxyvitamin D Insufficiency or Sufficiency. J. Clin. Endocrinol. Metab. 92: 4630-4636 [Abstract] [Full Text]  
• Saag, K. G., Shane, E., Boonen, S., Marin, F., Donley, D. W., Taylor, K. A., Dalsky, G. P., Marcus, R. (2007). Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis. NEJM 357: 2028-2039 [Abstract] [Full Text]  
• Li, X., Qin, L., Bergenstock, M., Bevelock, L. M., Novack, D. V., Partridge, N. C. (2007). Parathyroid Hormone Stimulates Osteoblastic Expression of MCP-1 to Recruit and Increase the Fusion of Pre/Osteoclasts. J. Biol. Chem. 282: 33098-33106 [Abstract] [Full Text]  
• Tylavsky, F. A., Ryder, K. M., Li, R., Park, V., Womack, C., Norwood, J., Carbone, L. D., Cheng, S. (2007). Preliminary Findings: 25(OH)D Levels and PTH Are Indicators of Rapid Bone Accrual in Pubertal Children. J. Am. Coll. Nutr. 26: 462-470 [Abstract] [Full Text]  
• Lee, S. H., Gupta, M. K., Han, D. W., Han, S. Y., Uhm, S. J., Kim, T., Lee, H. T. (2007). Development of Transgenic Chickens Expressing Human Parathormone Under the Control of a Ubiquitous Promoter by Using a Retrovirus Vector System. Poult. Sci. 86: 2221-2227 [Abstract] [Full Text]  
• Miller, P. D., Bilezikian, J. P., Diaz-Curiel, M., Chen, P., Marin, F., Krege, J. H., Wong, M., Marcus, R. (2007). Occurrence of Hypercalciuria in Patients with Osteoporosis Treated with Teriparatide. J. Clin. Endocrinol. Metab. 92: 3535-3541 [Abstract] [Full Text]  
• Johnston, S., Andrews, S., Shen, V., Cosman, F., Lindsay, R., Dempster, D. W., Iida-Klein, A. (2007). The Effects of Combination of Alendronate and Human Parathyroid Hormone(1 34) on Bone Strength Are Synergistic in the Lumbar Vertebra and Additive in the Femur of C57BL/6J Mice. Endocrinology 148: 4466-4474 [Abstract] [Full Text]  
• Canalis, E., Giustina, A., Bilezikian, J. P. (2007). Mechanisms of Anabolic Therapies for Osteoporosis. NEJM 357: 905-916 [Full Text]  
• Bruyere, O., Roux, C., Detilleux, J., Slosman, D. O., Spector, T. D., Fardellone, P., Brixen, K., Devogelaer, J.-P., Diaz-Curiel, M., Albanese, C., Kaufman, J.-M., Pors-Nielsen, S., Reginster, J.-Y. (2007). Relationship between Bone Mineral Density Changes and Fracture Risk Reduction in Patients Treated with Strontium Ranelate. J. Clin. Endocrinol. Metab. 92: 3076-3081 [Abstract] [Full Text]  
• Blake, G. M, Fogelman, I. (2007). The role of DXA bone density scans in the diagnosis and treatment of osteoporosis. Postgrad. Med. J. 83: 509-517 [Abstract] [Full Text]  
• Su, J.-L., Yang, C.-Y., Zhao, M., Kuo, M.-L., Yen, M.-L. (2007). Forkhead Proteins Are Critical for Bone Morphogenetic Protein-2 Regulation and Anti-tumor Activity of Resveratrol. J. Biol. Chem. 282: 19385-19398 [Abstract] [Full Text]  
• Roux, C., Briot, K., Horlait, S., Varbanov, A., Watts, N. B, Boonen, S. (2007). Assessment of non-vertebral fracture risk in postmenopausal women. Ann Rheum Dis 66: 931-935 [Abstract] [Full Text]  
• Kingsley, L. A., Chirgwin, J. M., Guise, T. A. (2007). Breaking new ground to build bone. Proc. Natl. Acad. Sci. USA 104: 10753-10754 [Full Text]  
• Samadfam, R., Xia, Q., Goltzman, D. (2007). Pretreatment with Anticatabolic Agents Blunts But Does Not Eliminate the Skeletal Anabolic Response to Parathyroid Hormone in Oophorectomized Mice. Endocrinology 148: 2778-2787 [Abstract] [Full Text]  
• Suliburk, J. W., Perrier, N. D. (2007). Primary Hyperparathyroidism. The Oncologist 12: 644-653 [Abstract] [Full Text]  
• Whyte, M. P., Mumm, S., Deal, C. (2007). Adult Hypophosphatasia Treated with Teriparatide. J. Clin. Endocrinol. Metab. 92: 1203-1208 [Abstract] [Full Text]  
• Greenspan, S. L., Bone, H. G., Ettinger, M. P., Hanley, D. A., Lindsay, R., Zanchetta, J. R., Blosch, C. M., Mathisen, A. L., Morris, S. A., Marriott, T. B., for the Treatment of Osteoporosis with Parathyroid, (2007). Effect of Recombinant Human Parathyroid Hormone (1-84) on Vertebral Fracture and Bone Mineral Density in Postmenopausal Women with Osteoporosis: A Randomized Trial. ANN INTERN MED 146: 326-339 [Abstract] [Full Text]  
• Antoniucci, D. M., Sellmeyer, D. E., Bilezikian, J. P., Palermo, L., Ensrud, K. E., Greenspan, S. L., Black, D. M. (2007). Elevations in Serum and Urinary Calcium with Parathyroid Hormone (1-84) with and without Alendronate for Osteoporosis. J. Clin. Endocrinol. Metab. 92: 942-947 [Abstract] [Full Text]  
• Serra, A. L., Savoca, R., Huber, A. R., Hepp, U., Delsignore, A., Hersberger, M., Wuthrich, R. P. (2007). Effective control of persistent hyperparathyroidism with cinacalcet in renal allograft recipients. Nephrol Dial Transplant 22: 577-583 [Abstract] [Full Text]  
• Poole, K. E S, Compston, J. E (2006). Osteoporosis and its management. BMJ 333: 1251-1256 [Full Text]  
• Rey, A., Manen, D., Rizzoli, R., Caverzasio, J., Ferrari, S. L. (2006). Proline-rich Motifs in the Parathyroid Hormone (PTH)/PTH-related Protein Receptor C Terminus Mediate Scaffolding of c-Src with beta-Arrestin2 for ERK1/2 Activation. J. Biol. Chem. 281: 38181-38188 [Abstract] [Full Text]  
• Cummings, S. R. (2006). A 55-Year-Old Woman With Osteopenia. JAMA 296: 2601-2610 [Abstract] [Full Text]  
• Pazianas, M., Compher, C., Schiavone-Gatto, P., Kinosian, B. P. (2006). Intestinal Failure-Associated Metabolic Bone Diseases and Response to Teriparatide. Nutr Clin Pract 21: 605-609 [Abstract] [Full Text]  
• Jolette, J., Wilker, C. E., Smith, S. Y., Doyle, N., Hardisty, J. F., Metcalfe, A. J., Marriott, T. B., Fox, J., Wells, D. S. (2006). Defining a Noncarcinogenic Dose of Recombinant Human Parathyroid Hormone 1-84 in a 2-Year Study in Fischer 344 Rats. Toxicol Pathol 34: 929-940 [Abstract] [Full Text]  
• Lentle, B., Worsley, D. (2006). Osteoporosis Redux. JNM 47: 1945-1959 [Full Text]  
• Lewiecki, E. M., Laster, A. J. (2006). Clinical Applications of Vertebral Fracture Assessment by Dual-Energy X-Ray Absorptiometry. J. Clin. Endocrinol. Metab. 91: 4215-4222 [Abstract] [Full Text]  
• Chung, D. J., Castro, C. H. M., Watkins, M., Stains, J. P., Chung, M. Y., Szejnfeld, V. L., Willecke, K., Theis, M., Civitelli, R. (2006). Low peak bone mass and attenuated anabolic response to parathyroid hormone in mice with an osteoblast-specific deletion of connexin43. J. Cell Sci. 119: 4187-4198 [Abstract] [Full Text]  
• Xue, Y., Karaplis, A. C., Hendy, G. N., Goltzman, D., Miao, D. (2006). Exogenous 1,25-Dihydroxyvitamin D3 Exerts a Skeletal Anabolic Effect and Improves Mineral Ion Homeostasis in Mice that Are Homozygous for Both the 1{alpha}-Hydroxylase and Parathyroid Hormone Null Alleles. Endocrinology 147: 4801-4810 [Abstract] [Full Text]  
• Turner, R. T., Lotinun, S., Hefferan, T. E., Morey-Holton, E. (2006). Disuse in adult male rats attenuates the bone anabolic response to a therapeutic dose of parathyroid hormone. J. Appl. Physiol. 101: 881-886 [Abstract] [Full Text]  
• Wildschut, H. I.J., Peters, T.J., Weiner, C. P. (2006). Screening in women's health, with emphasis on fetal Down's syndrome, breast cancer and osteoporosis. Hum Reprod Update 12: 499-512 [Abstract] [Full Text]  
• Finkelstein, J. S., Leder, B. Z., Burnett, S.-A. M., Wyland, J. J., Lee, H., de la Paz, A. V., Gibson, K., Neer, R. M. (2006). Effects of Teriparatide, Alendronate, or Both on Bone Turnover in Osteoporotic Men. J. Clin. Endocrinol. Metab. 91: 2882-2887 [Abstract] [Full Text]  
• Jakob, F., Marin, F., Martin-Mola, E., Torgerson, D., Fardellone, P., Adami, S., Thalassinos, N.C., Sykes, D., Melo-Gomes, J., Chinn, C., Nicholson, T., Cooper, C. (2006). Characterization of patients with an inadequate clinical outcome from osteoporosis therapy: the Observational Study of Severe Osteoporosis (OSSO). QJM 99: 531-543 [Abstract] [Full Text]  
• Hodsman, A., Papaioannou, A., Cranney, A. (2006). Clinical practice guidelines for the use of parathyroid hormone in the treatment of osteoporosis.. CMAJ 175: 48-48 [Full Text]  
• Cranney, A., Papaioannou, A., Zytaruk, N., Hanley, D., Adachi, J., Goltzman, D., Murray, T., Hodsman, A., for the Clinical Guidelines Committee of Osteoporo, (2006). Parathyroid hormone for the treatment of osteoporosis: a systematic review.. CMAJ 175: 52-59 [Abstract] [Full Text]  
• Tsukiyama, K., Yamada, Y., Yamada, C., Harada, N., Kawasaki, Y., Ogura, M., Bessho, K., Li, M., Amizuka, N., Sato, M., Udagawa, N., Takahashi, N., Tanaka, K., Oiso, Y., Seino, Y. (2006). Gastric Inhibitory Polypeptide as an Endogenous Factor Promoting New Bone Formation after Food Ingestion. Mol. Endocrinol. 20: 1644-1651 [Abstract] [Full Text]  
• Mittelman, S. D., Hendy, G. N., Fefferman, R. A., Canaff, L., Mosesova, I., Cole, D. E. C., Burkett, L., Geffner, M. E. (2006). A Hypocalcemic Child with a Novel Activating Mutation of the Calcium-Sensing Receptor Gene: Successful Treatment with Recombinant Human Parathyroid Hormone. J. Clin. Endocrinol. Metab. 91: 2474-2479 [Abstract] [Full Text]  
• Pickard, B. W., Hodsman, A. B., Fraher, L. J., Watson, P. H. (2006). Type 1 Parathyroid Hormone Receptor (PTH1R) Nuclear Trafficking: Association of PTH1R with Importin {alpha}1 and {beta}. Endocrinology 147: 3326-3332 [Abstract] [Full Text]  
• Cockayne, S., Adamson, J., Lanham-New, S., Shearer, M. J., Gilbody, S., Torgerson, D. J. (2006). Vitamin K and the Prevention of Fractures: Systematic Review and Meta-analysis of Randomized Controlled Trials.. Arch Intern Med 166: 1256-1261 [Abstract] [Full Text]  
• Liu, H., Michaud, K., Nayak, S., Karpf, D. B., Owens, D. K., Garber, A. M. (2006). The Cost-effectiveness of Therapy With Teriparatide and Alendronate in Women With Severe Osteoporosis.. Arch Intern Med 166: 1209-1217 [Abstract] [Full Text]  
• Nayak, S., Olkin, I., Liu, H., Grabe, M., Gould, M. K., Allen, I. E., Owens, D. K., Bravata, D. M. (2006). Meta-analysis: accuracy of quantitative ultrasound for identifying patients with osteoporosis.. ANN INTERN MED 144: 832-841 [Abstract] [Full Text]  
• Sanchez, A. J., Aranda-Michel, J. (2006). Liver Disease and Osteoporosis. Nutr Clin Pract 21: 273-278 [Abstract] [Full Text]  
• Yakar, S., Bouxsein, M. L, Canalis, E., Sun, H., Glatt, V., Gundberg, C., Cohen, P., Hwang, D., Boisclair, Y., LeRoith, D., Rosen, C. J (2006). The ternary IGF complex influences postnatal bone acquisition and the skeletal response to intermittent parathyroid hormone.. J Endocrinol 189: 289-299 [Abstract] [Full Text]  
• Donahue, S. W., Galley, S. A., Vaughan, M. R., Patterson-Buckendahl, P., Demers, L. M., Vance, J. L., McGee, M. E. (2006). Parathyroid hormone may maintain bone formation in hibernating black bears (Ursus americanus) to prevent disuse osteoporosis. J. Exp. Biol. 209: 1630-1638 [Abstract] [Full Text]  
• Koo, W. W.K., Hockman, E. M., Dow, M. (2006). Palm olein in the fat blend of infant formulas: effect on the intestinal absorption of calcium and fat, and bone mineralization.. J. Am. Coll. Nutr. 25: 117-122 [Abstract] [Full Text]  
• Bauer, D. C., Garnero, P., Bilezikian, J. P., Greenspan, S. L., Ensrud, K. E., Rosen, C. J., Palermo, L., Black, D. M., for the PTH and Alendronate (PaTH) Research Group, (2006). Short-Term Changes in Bone Turnover Markers and Bone Mineral Density Response to Parathyroid Hormone in Postmenopausal Women with Osteoporosis. J. Clin. Endocrinol. Metab. 91: 1370-1375 [Abstract] [Full Text]  
• Young, N., Mikhalkevich, N., Yan, Y., Chen, D., Zheng, W.-p. (2005). Differential Regulation of Osteoblast Activity by Th Cell Subsets Mediated by Parathyroid Hormone and IFN-{gamma}. J. Immunol. 175: 8287-8295 [Abstract] [Full Text]  
• Potts, J. T (2005). Parathyroid hormone: past and present. J Endocrinol 187: 311-325 [Abstract] [Full Text]  
• Bellido, T., Ali, A. A., Gubrij, I., Plotkin, L. I., Fu, Q., O'Brien, C. A., Manolagas, S. C., Jilka, R. L. (2005). Chronic Elevation of Parathyroid Hormone in Mice Reduces Expression of Sclerostin by Osteocytes: A Novel Mechanism for Hormonal Control of Osteoblastogenesis. Endocrinology 146: 4577-4583 [Abstract] [Full Text]  
• Castro, M., Nikolaev, V. O., Palm, D., Lohse, M. J., Vilardaga, J.-P. (2005). Turn-on switch in parathyroid hormone receptor by a two-step parathyroid hormone binding mechanism. Proc. Natl. Acad. Sci. USA 102: 16084-16089 [Abstract] [Full Text]  
• Karlsson, M. K., Gerdhem, P., Ahlborg, H. G. (2005). The prevention of osteoporotic fractures. J Bone Joint Surg Br 87-B: 1320-1327 [Full Text]  
• Black, D. M., Bilezikian, J. P., Ensrud, K. E., Greenspan, S. L., Palermo, L., Hue, T., Lang, T. F., McGowan, J. A., Rosen, C. J., the PaTH Study Investigators, (2005). One Year of Alendronate after One Year of Parathyroid Hormone (1-84) for Osteoporosis. NEJM 353: 555-565 [Abstract] [Full Text]  
• Cosman, F., Nieves, J., Zion, M., Woelfert, L., Luckey, M., Lindsay, R. (2005). Daily and Cyclic Parathyroid Hormone in Women Receiving Alendronate. NEJM 353: 566-575 [Abstract] [Full Text]  
• Rosen, C. J. (2005). Postmenopausal Osteoporosis. NEJM 353: 595-603 [Full Text]  
• Vieth, R., Cole, D. E.C., Krege, J. H., Donley, D. W., Marcus, R., Licata, A. A. (2005). Teriparatide, Osteoporosis, Calcium, and Vitamin D. NEJM 353: 634-635 [Full Text]  
• McClung, M. R., San Martin, J., Miller, P. D., Civitelli, R., Bandeira, F., Omizo, M., Donley, D. W., Dalsky, G. P., Eriksen, E. F. (2005). Opposite Bone Remodeling Effects of Teriparatide and Alendronate in Increasing Bone Mass. Arch Intern Med 165: 1762-1768 [Abstract] [Full Text]  
• Hodsman, A. B., Bauer, D. C., Dempster, D. W., Dian, L., Hanley, D. A., Harris, S. T., Kendler, D. L., McClung, M. R., Miller, P. D., Olszynski, W. P., Orwoll, E., Yuen, C. K. (2005). Parathyroid Hormone and Teriparatide for the Treatment of Osteoporosis: A Review of the Evidence and Suggested Guidelines for Its Use. Endocr. Rev. 26: 688-703 [Abstract] [Full Text]  
• Maimoun, L, Simar, D, Malatesta, D, Caillaud, C, Peruchon, E, Couret, I, Rossi, M, Mariano-Goulart, D (2005). Response of bone metabolism related hormones to a single session of strenuous exercise in active elderly subjects. Br. J. Sports. Med. 39: 497-502 [Abstract] [Full Text]  
• Paschalis, E. P., Glass, E. V., Donley, D. W., Eriksen, E. F. (2005). Bone Mineral and Collagen Quality in Iliac Crest Biopsies of Patients Given Teriparatide: New Results from the Fracture Prevention Trial. J. Clin. Endocrinol. Metab. 90: 4644-4649 [Abstract] [Full Text]  
• Raisz, L. G. (2005). Screening for Osteoporosis. NEJM 353: 164-171 [Full Text]  
• Dobnig, H., Sipos, A., Jiang, Y., Fahrleitner-Pammer, A., Ste-Marie, L.-G., Gallagher, J. C., Pavo, I., Wang, J., Eriksen, E. F. (2005). Early Changes in Biochemical Markers of Bone Formation Correlate with Improvements in Bone Structure during Teriparatide Therapy. J. Clin. Endocrinol. Metab. 90: 3970-3977 [Abstract] [Full Text]  
• Barbier, J.-R., Gardella, T. J., Dean, T., MacLean, S., Potetinova, Z., Whitfield, J. F., Willick, G. E. (2005). Backbone-methylated Analogues of the Principle Receptor Binding Region of Human Parathyroid Hormone: EVIDENCE FOR BINDING TO BOTH THE N-TERMINAL EXTRACELLULAR DOMAIN AND EXTRACELLULAR LOOP REGION. J. Biol. Chem. 280: 23771-23777 [Abstract] [Full Text]  
• Fogelman, I., Blake, G. M (2005). Strontium ranelate for the treatment of osteoporosis. BMJ 330: 1400-1401 [Full Text]  
• Liu, P.-Q., Tan, S., Mendel, M. C., Murrills, R. J., Bhat, B. M., Schlag, B., Samuel, R., Matteo, J. J., de la Rosa, R., Howes, K., Reik, A., Case, C. C., Bex, F. J., Young, K., Gregory, P. D. (2005). Isogenic Human Cell Lines for Drug Discovery: Regulation of Target Gene Expression by Engineered Zinc-Finger Protein Transcription Factors. J Biomol Screen 10: 304-313 [Abstract]  
• Yamaguchi, M., Ogata, N., Shinoda, Y., Akune, T., Kamekura, S., Terauchi, Y., Kadowaki, T., Hoshi, K., Chung, U.-I., Nakamura, K., Kawaguchi, H. (2005). Insulin Receptor Substrate-1 Is Required for Bone Anabolic Function of Parathyroid Hormone in Mice. Endocrinology 146: 2620-2628 [Abstract] [Full Text]  
• Licata, A. A. (2005). Osteoporosis, Teriparatide, and Dosing of Calcium and Vitamin D. NEJM 352: 1930-1931 [Full Text]  
• Reginster, J.-Y. (2005). Treatment of postmenopausal osteoporosis. BMJ 330: 859-860 [Full Text]  
• Strewler, G. J. (2005). A 64-Year-Old Woman With Primary Hyperparathyroidism. JAMA 293: 1772-1779 [Full Text]  
• Alkhiary, Y. M., Gerstenfeld, L. C., Krall, E., Westmore, M., Sato, M., Mitlak, B. H., Einhorn, T. A. (2005). Enhancement of Experimental Fracture-Healing by Systemic Administration of Recombinant Human Parathyroid Hormone (PTH 1-34). JBJS 87: 731-741 [Abstract] [Full Text]