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Treatment of postmenopausal osteoporosis with slow-release sodium fluoride: final report of a randomized controlled trial
Abstract
section
/ Maturitas
Background: A number of factors contribute to increased risk of coronary heart disease (CHD) among postmenopausal women, including atherogenic changes in serum cholesterol profiles, weight gain, and decreases in physical activity during the menopause. To date, no study has attempted to prevent elevations in primary CHD risk factors as women experience menopause. Methods: A sample of 536 healthy premenopausal women, ages 4450, were recruited for an ongoing 5-year randomized prevention trial testing whether increases in lowdensity lipoprotein cholesterol (LDL-C) and body weight can be prevented during the menopause with a dietary and behavioral intervention. The aim was to reduce total dietary and saturated fat and cholesterol, prevent weight gain, and increase physical activity levels. Changes in CHD risk factors after the first 6 months of treatment were analyzed comparing 253 intervention and 267 assessment-only control participants. Results: The intervention group showed significant reductions in total cholesterol ( - 0.34 mmol/l), LDL-C ( 0.28 mmol/l), triglycerides (- 0.04 mmol/l), weight ( - 4.8 kg), waist-hip ratio (-O.OOS), systolic blood pressure (- 3.5 mmHg), diastolic blood pressure (- 2.2 mmHg), serum glucose levels (- 0.06 mmol/l), and HDL-C ( - 0.06 mmol/l) and significant increases in physical activity ( + 383 kcal). No significant changes were observed in the control group. Conclusion. Six-month results suggested that participants were receptive to the preventive approach to CHD risk reduction and were successful in making initial positive lifestyle changes. Follow-up data will evaluate long-term adherence to the intervention and the interaction between adherence and physiological changes during menopause. 95290221
Treatment of postmenopausal osteoporosis sodium fluoride: final report of a randomized
with slow-release controlled trial
Pak C.Y.C.; Sakhaee K.; Adams-Huet B.; Piziak V.; Peterson R.D.: Poindexter J.R. Texas University Boulevard, Dallas,
SW Medical Center, TX 75235-8885, USA
5323
Harry
Hines
ANN. INTERN. MED. 1995 123/6 (401-408) Objective: To test whether slow-release sodium fluoride inhibits spinal fractures and is safe to use. Design: Placebo-controlled randomized trial. Interventions: Slow-release sodium fluoride, 25 mg twice daily, in four ICmonth cycles (12 months receiving sodium fluoride followed by 2 months not receiving it) compared with placebo. Calcium citrate, 400 mg calcium twice daily, continuously in both groups. Patients: 48 of 54 patients who received sodium fluoride and 51 of 56 patients who received placebo completed at least 1 year of the study. All patients had postmenopausal osteoporosis. Results: Compared with the placebo group, the fluoride group had a lower individual vertebral fracture rate (0.0640.182 per patient-year compared with 0.205-0.297 per patient-year; P = 0.002) a higher unadjusted fracture-free rate (85.4% compared with 56.9%; P = O.OOl), and a greater survival estimate (relative risk, 0.3 (95% CI, 0.12-0.76)) for new fractures. The recurrent spinal fracture rate did not differ be-
24 (1996)
121
119-123
tween the two groups. The fluoride group had a substantial increase in L2--L4 bone mass of 4-5X per year for 4 years. a mean increase in femoral neck bone density of 2.38 --3.33”/0 per year, and no change in radial shaft bone density. The frequency with which minor side effects and appendicular fractures occurred was similar in the two groups; no patients developed microfractures or gastric ulcers. Conclusion: Slowrelease sodium fluoride and calcium citrate administered for 4 years inhibits new vertebral fractures (but not recurrent fractures), augments spinal and femoral neck bone mass, and is safe to use. 95283186
Role of calcium and vitamin D in the prevention treatment of postmenopausal osteoporosis: an overview
and
the
Kaufman J.M. AZ Gent, Department Belgium
Unit jbr Osteoporosis, Metabolic of’ Endocrinology, De Pintelaan
Bone Diseases, 185, 9000 Gent,
CLIN. RHEUMATOL. 1995 14 SUPPL. 3 (9-13) When discussing the use of calcium and vitamin D in the prevention and the treatment of osteoporosis one can make a distinction between the use as dietary supplementation to correct or prevent deficiencies, and the pharmacologic use of higher doses, whether or not in association with other drugs. However, in practical terms it is not always possible to clearly make this distinction. Available evidence suggests that increasing the calcium intake can favourably affect the buildup of bone mass in adolescence. In this population. the daily consumption of calcium in the diet should, optimally, be at least 1200 mg/day. In view of the lack of data pertaining to the effect on the final peak bone mass, there is at present time no basis for the systematic administration of calcium supplements to healthy children and adolescents. Calcium supplementation, aiming at a total calcium intake of at least 1500 mg/day, has a partial protective effect on postmenopausal bone loss, this effect being documented mainly in women more than 5 years after menopause. In the present state of our knowledge, there is no established role for vitamin D supplementation in the prevention of postmenopausal osteoporosis. except in elderly patients presenting with a higher risk for relative vitamin D deficiency and with low calcium intake. The results of a controlled trial suggest that in institutionalised elderly patients, systematic administration of calcium and vitamin D supplements can substantially reduce the risk of hip fracture. In the treatment of established postmenopausal osteoporosis, calcium supplementation has only a role as a general adjuvant therapeutic measure and as a specific complement to the treatment with other active compounds. There are indications that treatment with calcidol or calcitriol has. a positive effect on the evolution of bone mass, but awaiting further confirmation of a favourable effect on the incidence of osteoporotic fractures, treatment with these drugs remains experimental. 95308820
section
/ Maturitas
Background: A number of factors contribute to increased risk of coronary heart disease (CHD) among postmenopausal women, including atherogenic changes in serum cholesterol profiles, weight gain, and decreases in physical activity during the menopause. To date, no study has attempted to prevent elevations in primary CHD risk factors as women experience menopause. Methods: A sample of 536 healthy premenopausal women, ages 4450, were recruited for an ongoing 5-year randomized prevention trial testing whether increases in lowdensity lipoprotein cholesterol (LDL-C) and body weight can be prevented during the menopause with a dietary and behavioral intervention. The aim was to reduce total dietary and saturated fat and cholesterol, prevent weight gain, and increase physical activity levels. Changes in CHD risk factors after the first 6 months of treatment were analyzed comparing 253 intervention and 267 assessment-only control participants. Results: The intervention group showed significant reductions in total cholesterol ( - 0.34 mmol/l), LDL-C ( 0.28 mmol/l), triglycerides (- 0.04 mmol/l), weight ( - 4.8 kg), waist-hip ratio (-O.OOS), systolic blood pressure (- 3.5 mmHg), diastolic blood pressure (- 2.2 mmHg), serum glucose levels (- 0.06 mmol/l), and HDL-C ( - 0.06 mmol/l) and significant increases in physical activity ( + 383 kcal). No significant changes were observed in the control group. Conclusion. Six-month results suggested that participants were receptive to the preventive approach to CHD risk reduction and were successful in making initial positive lifestyle changes. Follow-up data will evaluate long-term adherence to the intervention and the interaction between adherence and physiological changes during menopause. 95290221
Treatment of postmenopausal osteoporosis sodium fluoride: final report of a randomized
with slow-release controlled trial
Pak C.Y.C.; Sakhaee K.; Adams-Huet B.; Piziak V.; Peterson R.D.: Poindexter J.R. Texas University Boulevard, Dallas,
SW Medical Center, TX 75235-8885, USA
5323
Harry
Hines
ANN. INTERN. MED. 1995 123/6 (401-408) Objective: To test whether slow-release sodium fluoride inhibits spinal fractures and is safe to use. Design: Placebo-controlled randomized trial. Interventions: Slow-release sodium fluoride, 25 mg twice daily, in four ICmonth cycles (12 months receiving sodium fluoride followed by 2 months not receiving it) compared with placebo. Calcium citrate, 400 mg calcium twice daily, continuously in both groups. Patients: 48 of 54 patients who received sodium fluoride and 51 of 56 patients who received placebo completed at least 1 year of the study. All patients had postmenopausal osteoporosis. Results: Compared with the placebo group, the fluoride group had a lower individual vertebral fracture rate (0.0640.182 per patient-year compared with 0.205-0.297 per patient-year; P = 0.002) a higher unadjusted fracture-free rate (85.4% compared with 56.9%; P = O.OOl), and a greater survival estimate (relative risk, 0.3 (95% CI, 0.12-0.76)) for new fractures. The recurrent spinal fracture rate did not differ be-
24 (1996)
121
119-123
tween the two groups. The fluoride group had a substantial increase in L2--L4 bone mass of 4-5X per year for 4 years. a mean increase in femoral neck bone density of 2.38 --3.33”/0 per year, and no change in radial shaft bone density. The frequency with which minor side effects and appendicular fractures occurred was similar in the two groups; no patients developed microfractures or gastric ulcers. Conclusion: Slowrelease sodium fluoride and calcium citrate administered for 4 years inhibits new vertebral fractures (but not recurrent fractures), augments spinal and femoral neck bone mass, and is safe to use. 95283186
Role of calcium and vitamin D in the prevention treatment of postmenopausal osteoporosis: an overview
and
the
Kaufman J.M. AZ Gent, Department Belgium
Unit jbr Osteoporosis, Metabolic of’ Endocrinology, De Pintelaan
Bone Diseases, 185, 9000 Gent,
CLIN. RHEUMATOL. 1995 14 SUPPL. 3 (9-13) When discussing the use of calcium and vitamin D in the prevention and the treatment of osteoporosis one can make a distinction between the use as dietary supplementation to correct or prevent deficiencies, and the pharmacologic use of higher doses, whether or not in association with other drugs. However, in practical terms it is not always possible to clearly make this distinction. Available evidence suggests that increasing the calcium intake can favourably affect the buildup of bone mass in adolescence. In this population. the daily consumption of calcium in the diet should, optimally, be at least 1200 mg/day. In view of the lack of data pertaining to the effect on the final peak bone mass, there is at present time no basis for the systematic administration of calcium supplements to healthy children and adolescents. Calcium supplementation, aiming at a total calcium intake of at least 1500 mg/day, has a partial protective effect on postmenopausal bone loss, this effect being documented mainly in women more than 5 years after menopause. In the present state of our knowledge, there is no established role for vitamin D supplementation in the prevention of postmenopausal osteoporosis. except in elderly patients presenting with a higher risk for relative vitamin D deficiency and with low calcium intake. The results of a controlled trial suggest that in institutionalised elderly patients, systematic administration of calcium and vitamin D supplements can substantially reduce the risk of hip fracture. In the treatment of established postmenopausal osteoporosis, calcium supplementation has only a role as a general adjuvant therapeutic measure and as a specific complement to the treatment with other active compounds. There are indications that treatment with calcidol or calcitriol has. a positive effect on the evolution of bone mass, but awaiting further confirmation of a favourable effect on the incidence of osteoporotic fractures, treatment with these drugs remains experimental. 95308820