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Biomedical subjects

N H Bell

Publications and source records attributed to N H Bell.

At least 37 records · Page 2Linked to original sources
PubMed1997

Hormone replacement therapy in postmenopausal women: urinary N-telopeptide of type I collagen monitors therapeutic effect and predicts response of bone mineral density.

PURPOSE: To assess the ability of the urinary N-telopeptide of type I collagen (NTx) to monitor and predict therapeutic effects of hormone replacement therapy (HRT) in postmenopausal women. PATIENTS AND METHODS: To assess the relationship between baseline or change in NTx (predictive variable), and change in lumbar and hip bone mineral density (BMD; outcome variable), we conducted a 2-year randomized controlled study at academic university and private practice medical centers in 236 healthy women 1 to 3 years postmenopausal; 227 women completed the study. Women received estrogen plus progesterone plus calcium (treated group) or calcium alone (control group). RESULTS: In the treated group NTx significantly (P < 0.0001) decreased, and spine and hip BMD significantly (P < 0.00001 and P < 0.005, respectively) increased; in the control group NTx did not change but BMD decreased significantly (P < 0.01). Subjects in the highest quartiles for baseline NTx (67 to 188 units) or decreasing NTx (-66% to -87%) through 6 months demonstrated the greatest gain in BMD in response to HRT (P < 0.05 and P < 0.005). For every increase of 30 units in baseline NTx the odds of gain in BMD in response to HRT increased by a factor of 5.0 (95% confidence interval [CI] 1.9 to 13.3); for every 30% decrease in NTx through 6 months, the odds of gaining BMD in response to HRT increased by a factor of 2.6 (95% CI 1.6 to 4.4). In the control group an increase of 30 units in mean NTx across the study indicated a higher odds of losing BMD by a factor of 3.2 (95% CI 1.6 to 6.5). A high baseline NTx (> 67 units) indicated a 17.3 times higher risk of BMD loss if not treated with HRT. CONCLUSION: These data support the clinical utility of NTx to monitor the antiresorptive effect of HRT in recently postmenopausal women, and to predict changes in BMD in response to HRT.

Absorptiometry, Photon↗
PubMed1997

Increments in bone mineral density of the lumbar spine and hip and suppression of bone turnover are maintained after discontinuation of alendronate in postmenopausal women.

PURPOSE: Previously we have reported a significant increase in bone mineral density (BMD) of the spine and the hip and reductions in biochemical indices of bone turnover in postmenopausal women with osteoporosis treated with alendronate at various doses over 1 to 2 years. We have followed BMD and biochemical parameters in these patients for 1 or 2 years after discontinuation of alendronate to determine resolution of alendronate effects. PATIENTS AND METHODS: Participants received daily oral doses of placebo, 5 or 10 mg of alendronate for 2 years, or 20 or 40 mg of alendronate for 1 year followed by 1 year of placebo. No treatment was given in the third year of study. RESULTS: Lumbar spine BMD changes in the 5- and 10-mg groups (-1.4 and -0.4%) were similar to those in the placebo group (-1.2%) 1 year after discontinuation of drug and lumbar spine BMD changes in the 20- and 40-mg groups (-1.2% and 0.8%) were similar to those in the placebo group (-0.9%) 2 years after discontinuation of drug. BMD of the total hip followed the same pattern of resolution. The difference in BMD between alendronate and placebo groups at the end of alendronate treatment was maintained up to 2 years. Residual reductions in the bone resorption markers urinary deoxypyridinoline (D-Pyr) and collagen type 1 cross-linked N telopeptides and the bone formation markers serum bone-specific alkaline phosphatase and osteocalcin remained for 1 year after discontinuation of 5 and 10 mg of alendronate and for 2 years after discontinuation of 20 and 40 mg of alendronate, other than return of D-Pyr to baseline 1 year after cessation of treatment with the 5- and 10-mg doses. CONCLUSIONS: A residual decrease in bone turnover may be found up to 2 years after discontinuation of alendronate. Accelerated bone loss is not observed when treatment is discontinued. However, continuous therapy with alendronate is required to achieve a continuous gain in BMD.

Adult↗
PubMed1996

Comparison of nonrandomized trials with slow-release sodium fluoride with a randomized placebo-controlled trial in postmenopausal osteoporosis.

The results of slow-release sodium fluoride (SR-NaF) treatment in two nonrandomized trials involving 65 patients with postmenopausal osteoporosis from the primary site and 121 patients from collaborative sites were compared with those obtained from 54 treated patients and 56 patients taking placebo from a randomized controlled trial. Spinal fracture data were analyzed separately in mild to moderate bone loss of lumbar spine (baseline L2-L4 bone density [BD] > or = 65% young normal) and in severe bone loss (BD < 65%). Since demographic and fracture data were similar among fluoride-treated patients from the three trials at each stratum of bone loss, their data were combined. In mild to moderate bone loss, SR-NaF treatment in the combined group virtually eliminated new spinal fractures with 96.6% of patients remaining fracture-free. The Fluoride group had a markedly lower individual vertebral fracture rate (0.025 vs. 0.188/patient year, p = 0.0001) and group vertebral fracture rate (0.029 vs. 0.175/patient year, relative risk [RR] 0.12, p = 0.0001) than the Placebo group. In severe bone loss, the combined treated group had a significantly lower new spinal fracture rate than the Placebo group, although the differences were not as marked (group vertebral fracture rate of 0.150 vs. 0.276/patient year, RR 0.54, p = 0.03). In the combined fluoride-treated group, the L2-L4 bone mass rose by 4-6%/year for 4 years, and the femoral neck BD increased by 1-2%/year during first 2 years. The radial shaft BD did not change. The Placebo group did not show a change in bone mass at any site. The prevalence (percentage) of patients with related gastrointestinal side effects and nonvertebral fracture rates did not differ significantly between the combined SR-NaF group and the Placebo group (hip fracture rate of 0.0045/patient year in SR-NaF and 0.0053/patient year in Placebo; appendicular fracture other than hip (see text) rate of 0.0193/patient year in SR-NaF and 0.0159/patient year in Placebo). A subgroup analysis showed a low baseline L2-L4 BD, high prevalent spinal fractures, and reduced body weight to be important determinants of the development of spinal fracture during SR-NaF treatment. Concomitant medications (estrogen, vitamin D, thiazide and thyroid hormone) were not independent predictors of the spinal fracture risk. Only 17% of fluoride-treated patients were nonresponders (new spinal fractures or a fall/no change in L2-L4 bone mass). Thus, the effects of SR-NaF treatment on the spinal fracture rate from nonrandomized trials were similar to those of the treated group of the randomized trial but different from those of the Placebo group. The similarity of response of nonrandomized trials with that of the randomized controlled trial and the resultant combined analysis further validate the efficacy and safety of SR-NaF in the treatment of postmenopausal osteoporosis.

Bone Density↗
PubMed1996

Ovarian status influences the skeletal effects of tamoxifen in adult rats.

Tamoxifen (TAM), an antiestrogen used in adjuvant therapy for breast cancer, is currently being evaluated for prevention of breast cancer in premenopausal and postmenopausal disease-free women. In light of this clinical application in young women, the skeleton's potential predisposition for osteoporosis following long-term treatment with an antiestrogen is a concern. In postmenopausal women being treated for breast cancer TAM was shown to prevent bone loss. There is little information, however, about the skeletal effects of TAM in premenopausal women. Previous animal studies in ovariectomized (OVX'd) rats have consistently reported TAM to prevent cancellous and cortical bone loss. The effects of TAM on ovary-intact animals, however, are not well established. We have performed a histomorphometric analysis in order to evaluate the influence of ovarian function on the skeletal effects of long-term TAM treatment in the laboratory animal model. Six-month-old rats were implanted subcutaneously with pellets designed for the controlled release of TAM at a dose (5 mg/3 wks) previously shown to be effective at antagonizing short-term bone loss in OVX'd growing rats. TAM acted as an estrogen agonist on cortical bone measurements in tibia of ovary-intact as well as OVX'd rats. In cancellous bone of OVX'd rats, TAM reduced indices of bone formation and resorption and reduced the bone loss from over 90 percent to less than 50 percent. In ovary-intact rats, however, TAM produced a 31 percent loss of cancellous bone, a deficit associated with a 26 percent reduction in the trabecular number. These results clearly demonstrate an interaction between TAM and ovarian status whereby TAM partially prevents estrogen-deficient bone loss in OVX'd animals but antagonizes selective actions of estrogen on the skeleton of ovary-intact animals.

Analysis of Variance↗
PubMed1996

Leukemia inhibitory factor produces hypercalcemia in rats without altering bone histomorphometry of the tibia.

Leukemia inhibitory factor (LIF) is a single-chain polypeptide that previously was shown in mice to produce hypercalcemia and influence skeletal growth and turnover. We performed dose-response studies to determine if LIF alters the serum calcium or histomorphometry of the tibia in growing male rats. Forty animals were divided into five groups of eight animals each. Recombinant human LIF, 0.01, 0.1, 1, or 10 microg/100 g body wt, or vehicle was administered daily S.C. for 3 weeks. Compared with controls it was found that LIF increased mean serum calcium at the two highest doses (11.4 +/- 0.1 versus 10. 8 +/- 0.1 mg/dl, P = 0.0005 by one-way analysis of variance (ANOVA) but did not alter static or dynamic measurements of histomorphometry or length of the tibia. We conclude that in growing rats, high systemic concentrations of LIF result in hypercalcemia with no changes in bone turnover.

Animals↗
PubMed1996

Demonstration of a lack of racial difference in secretion of growth hormone despite a racial difference in bone mineral density in premenopausal women--a Clinical Research Center study.

We previously found GH secretion to be higher in black than white men. Therefore, we performed studies to determine whether this racial difference in GH secretion also occurs in women. Measurements of GH were obtained at 20-min intervals over 24 h and analyzed by deconvolution in 12 healthy black and 12 healthy white premenopausal women. Bone mineral density (BMD) was determined by dual energy x-ray absorptiometry, and GM allotypes were measured as a genetic marker for race. Racial distribution of the groups, as determined by analysis of GM haplotypes, were typical for black and white American populations. Twenty-four-hour integrated GH concentration, GH secretory burst amplitude, burst frequency, half-duration, mass, and half-life were not different in the two groups. Serum testosterone was modestly, but significantly, greater in the black than in the white women (1.1 +/- 0.1 vs. 0.9 +/- 0.1 nmol/L; P < 0.05). Serum 17 beta-estradiol and insulin-like growth factor (IGF)-binding protein-3 were not different in the two groups. However, the IGF-I/IGF-binding protein-3 molar ratio was significantly greater in the black than the white women (2.0 +/- 0.1 vs. 1.6 +/- 0.1; P < 0.02). The BMD of total body (1.12 +/- 0.02 vs. 1.07 +/- 0.02 g/cm2; P < 0.05) and total hip (0.96 +/- 0.04 vs. 0.86 +/- 0.04 g/cm2, P < 0.05) were greater in the black (n = 13) than in the white (n = 12) women. There was a trend toward greater BMD of the forearm in the black women (0.58 +/- 0.01 vs. 0.56 +/- 0.01 g/cm2; P = 0.06) and no racial difference in the BMD of the spine. When examining all subjects together, the BMD of the total body, trochanter, and spine correlated with total integrated GH secretion. Thus, the racial difference in GH secretion that we had previously found in men does not occur in women despite the higher BMD values at several skeletal sites in black women.

Adult↗
PubMed1995

Effect of oral alendronate on bone mineral density and the incidence of fractures in postmenopausal osteoporosis. The Alendronate Phase III Osteoporosis Treatment Study Group.

BACKGROUND: Postmenopausal osteoporosis is a serious health problem, and additional treatments are needed. METHODS: We studied the effects of oral alendronate, an aminobisphosphonate, on bone mineral density and the incidence of fractures and height loss in 994 women with postmenopausal osteoporosis. The women were treated with placebo or alendronate (5 or 10 mg daily for three years, or 20 mg for two years followed by 5 mg for one year); all the women received 500 mg of calcium daily. Bone mineral density was measured by dual-energy x-ray absorptiometry. The occurrence of new vertebral fractures and the progression of vertebral deformities were determined by an analysis of digitized radiographs, and loss of height was determined by sequential height measurements. RESULTS: The women receiving alendronate had significant, progressive increases in bone mineral density at all skeletal sites, whereas those receiving placebo had decreases in bone mineral density. At three years, the mean (+/- SE) differences in bone mineral density between the women receiving 10 mg of alendronate daily and those receiving placebo were 8.8 +/- 0.4 percent in the spine, 5.9 +/- 0.5 percent in the femoral neck, 7.8 +/- 0.6 percent in the trochanter, and 2.5 +/- 0.3 percent in the total body (P < 0.001 for all comparisons). The 5-mg dose was less effective than the 10-mg dose, and the regimen of 20 mg followed by 5 mg was similar in efficacy to the 10-mg dose. Overall, treatment with alendronate was associated with a 48 percent reduction in the proportion of women with new vertebral fractures (3.2 percent, vs. 6.2 percent in the placebo group; P = 0.03), a decreased progression of vertebral deformities (33 percent, vs. 41 percent in the placebo group; P = 0.028), and a reduced loss of height (P = 0.005) and was well tolerated. CONCLUSIONS: Daily treatment with alendronate progressively increases the bone mass in the spine, hip, and total body and reduces the incidence of vertebral fractures, the progression of vertebral deformities, and height loss in postmenopausal women with osteoporosis.

Aged↗
PubMed1995

Effect of growth hormone on bone: bone mineral density, trabecular bone volume, and alkaline phosphatase improve or are restored in the dwarf rat treated with growth hormone.

Studies were performed to determine whether serum total alkaline phosphatase (SAP), an index of bone formation; body weight; total body bone mineral density (BMD), measured by dual-energy X-ray absorptiometry; and tibial trabecular bone volume (TBV), measured by histomorphometry, are reduced in 2-week-old female sexually immature Lewis dwarf (dw/dw) rats (DW-CT, n = 9) with isolated growth hormone (GH) deficiency and, if so, whether recombinant human GH (rhGH), 200 micrograms/day subcutaneously for 4 weeks (DW-GH, n = 7), restores them. Studies were also performed to determine if 30% dietary restriction in 2-week-old female Lewis rats (LW-DR, n = 11) alters SAP, body weight, total BMD, or TBV compared with pair-fed controls (LW-CT, n = 7) given an ad libitum diet. Mean SAP (91 +/- 5 versus 109 +/- 5 U/l), body weight (102 +/- 11 versus 140 +/- 10 g), total BMD (88.5 +/- 0.3 versus 101.4 +/- 2.0 mg/cm2), and TBV (19.0 +/- 1.0 versus 27.0 +/- 1.4%) were significantly lower in DW-CT than in LW-CT animals, p < 0.05. In DW-GH, rhGH significantly increased mean SAP (130 +/- 7 U/l), body weight (133 +/- 10 g), total BMD (92.7 +/- 1.3), and TBV (24.0 +/- 1.9) compared with DW-CT animals. Compared with LW-CT rats, mean body weight and TBV were not different, but mean SAP was significantly higher (p < 0.01) and mean total BMD was significantly lower (p < 0.003) in DW-GH rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1995

Demonstration that bone mineral density of the lumbar spine, trochanter, and femoral neck is higher in black than in white young men.

The incidence of osteoporosis and fractures of the hip and spine is lower in black than in white subjects. To determine whether bone mass is increased in black men and to assess the influence of body weight and age, bone mineral density (BMD) of the lumbar spine, trochanter, and femoral neck was measured by dual-photon absorptiometry in 59 normal white men and 40 black men between the ages of 20 and 50 years. Body weight and age were not different from each other in the two groups. BMD of the midradius was measured by single-photon absorptiometry. Multivariate regression was used for independent analysis of each group and for analysis of the two groups together. After adjusting for body weight, age was inversely related to BMD of the femoral neck in both blacks and whites and of the trochanter in blacks. When body weight was analyzed independently of age, it was a positive predictor for BMD of the midradius of black men and of the femoral neck in white men. Despite the racial differences in age and weight on BMD, there were no significant interactions between race and age or race and weight when the data from black and white men were combined. Race had a highly significant effect on BMD of the lumbar spine, trochanter, and femoral neck midradius, and BMD was higher in blacks than in whites at these sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1995

Prednisone inhibits formation of cortical bone in sham-operated and ovariectomized female rats.

Prednisone inhibits bone formation and causes bone loss. To investigate possible mechanisms and sites, the effects of sham operation, ovariectomy, and prednisone were determined on bone and mineral metabolism in 7-week-old growing female rats. Forty animals were divided into groups of 10 each. Sham operation and ovariectomy were performed. One week later, pellets containing 5 mg prednisone or drug free were implanted S.C. at the back of the neck. Four weeks later, animals were sacrificed and tibiae were removed for histomorphometric analysis of the middiaphysis and proximal metaphysis. In both sham-operated and ovariectomized rats, prednisone (1) reduced weight gain (P < 0.02) and did not alter uterine weight; (2) lowered serum magnesium (Mg) (P < 0.001) and did not change serum calcium (Ca), phosphate (P), 25-hydroxyvitamin D (25OHD), or 1,25-dihydroxyvitamin D [1,25(OH)2D]; (3) produced striking increases in calcified cartilage, reduced cross-sectional area (P < 0.05) and cortical area (P < 0.01) and did not change medullary area of the tibial diaphysis; (4) lowered periosteal and endocortical bone formation and apposition rates; and (5) increased mean cancellous bone area (P < 0.05) and cancellous bone perimeter (P < 0.01) of the tibial metaphysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Alendronate treatment of the postmenopausal osteoporotic woman: effect of multiple dosages on bone mass and bone remodeling.

BACKGROUND: The effects of the aminobisphosphonate alendronate sodium on bone mass and markers of bone remodeling were investigated. PATIENTS AND METHODS: In a multicenter, randomized, double-blind, placebo-controlled, 2-year study, 188 postmenopausal women, aged 42 to 75 years, with low bone mineral density (BMD) of the lumbar spine were randomly assigned to 1 of 6 daily treatment groups: placebo for 2 years, alendronate 5 or 10 mg for 2 years, alendronate 20 or 40 mg for 1 year followed by placebo for 1 year, or alendronate 40 mg for 3 months followed by 2.5 mg for 21 months. All subjects were given 500 mg/d of elemental calcium as calcium carbonate. RESULTS: At each dose, alendronate produced significant reductions in markers of bone resorption and formation, and significantly increased bone mass at the lumbar spine, hip, and total body, as compared with decreases (significant at lumbar spine) in subjects receiving placebo. In the 10-mg group, mean urinary deoxypyridinoline/creatinine had declined by 47% at 3 months, and mean serum osteocalcin by 53% at 6 months. Mean changes in BMD over 24 months with 10 mg alendronate were +7.21% +/- 0.49% for the lumbar spine, +5.27% +/- 0.70% for total hip, and +2.53% +/- 0.68% for total body (each P < 0.01) compared to changes of -1.35% +/- 0.61%, -1.20% +/- 0.64% and -0.31% +/- 0.44% at these sites, respectively, with placebo treatment. Progressive increases in BMD of both lumbar spine and total hip were observed in the second year of treatment with 10 mg alendronate (both P < 0.05). CONCLUSION: Alendronate, a potent inhibitor of bone resorption, reduces markers of bone remodeling and significantly increases BMD at the lumbar spine, hip, and total body, and is well tolerated at therapeutic doses (5 or 10 mg daily) in the treatment of osteoporosis in postmenopausal women.

Adult↗
PubMed1995

25-Hydroxyvitamin D3 reverses alteration of the vitamin D-endocrine system in blacks.

BACKGROUND: Previous findings indicated that serum 25-hydroxyvitamin D and urinary calcium are decreased and serum immunoreactive parathyroid hormone, serum 1,25-dihydroxyvitamin D, and urinary cyclic adenosine 3',5'-monophosphate are increased in normal black compared to normal white subjects. Studies were carried out to determine if alteration of the vitamin D-endocrine system in blacks is reversed by oral supplementation with 25-hydroxyvitamin D3. PATIENTS AND METHODS: Eight normal young adult black men and women were admitted two times to a metabolic ward for 2.5 days and studied after no treatment and again after treatment for 1 week with oral 25-hydroxyvitamin D3, 40 to 60 micrograms/d. Six of the subjects underwent a postcontrol study after discontinuation of treatment. RESULTS: 25-Hydroxyvitamin D3 treatment significantly increased serum 25-hydroxyvitamin D and urinary calcium and reduced serum 1,25-dihydroxyvitamin D and urinary cyclic adenosine 3',5'-monophosphate, an index of function of parathyroid hormone. In a postcontrol study, values for serum 25-hydroxyvitamin D, serum 1,25-dihydroxyvitamin D, and urinary calcium had returned to control values. CONCLUSIONS: The results provide evidence that reduction of serum 25-hydroxyvitamin D contributes to or accounts for alteration of the vitamin D-endocrine system in black subjects.

Administration, Oral↗
PubMed1995

Greater secretion of growth hormone in black than in white men: possible factor in greater bone mineral density--a clinical research center study.

To determine why blacks have a higher bone mineral density (BMD) and lower incidence of osteoporosis and fractures than whites, we investigated whether the secretion of GH is higher in black than in white men. Measurements of GH were obtained at 20-min intervals over 24 h and analyzed by deconvolution. BMD was determined by dual energy x-ray absorptiometry in 16 normal black and 17 normal white men, aged 20-40 yr. The 24-h integrated GH concentration 942 +/- 174 vs. 602 +/- 104 micrograms/L; P = 0.0495) and GH secretory burst amplitude (0.499 +/- 0.163 vs. 0.169 +/- 0.027 micrograms/L.min; P = 0.0482) were higher in black than in white men. GH burst frequency, half-duration, mass, and half-life were not different in the 2 groups. The serum 17 beta-estradiol level (162 +/- 12 vs. 108 +/- 11 pmol/L; P = 0.0011) was higher, and the serum insulin-like growth factor-binding protein 3 level (2.2 +/- 0.1 vs. 2.8 +/- 0.1 microgram/mL; P = 0.0001) was lower in black than in white men. BMD values for total body (1.22 +/- 0.02 vs. 1.14 +/- 0.02 g/cm2; P = 0.0041), forearm (0.69 +/- 0.01 vs. 0.66 +/- 0.01 g/cm2; P = 0.0211), trochanter (0.91 +/- 0.03 vs. 0.77 +/- 0.03 g/cm2; P = 0.0003), and femoral neck (1.08 +/- 0.03 vs. 0.93 +/- 0.03 g/cm2; P = 0.0007) were higher in black than in white men. Thus, serum 17 beta-estradiol level, GH secretion, and BMD values for the total body, forearm, trochanter, and femoral neck are greater in black than in white men. As estrogen is known to increase GH secretion and GH to increase bone mass, increases in circulating 17 beta-estradiol may contribute to the higher GH secretion and bone mass in black men.

Absorptiometry, Photon↗
PubMed1994

Diclofenac sodium inhibits bone resorption in postmenopausal women.

BACKGROUND: The results of experimental studies with animals indicated that prostaglandins stimulate bone resorption, that skeletal production of prostaglandin E2 is enhanced by ovariectomy and is diminished by 17 beta-estradiol, and that the nonsteroidal anti-inflammatory drug (NSAID) naproxyn prevents bone loss after ovariectomy. Studies were carried out to investigate the effects of the NSAID diclofenac sodium on bone and mineral metabolism in premenopausal women and to compare the effects of diclofenac sodium and conjugated estrogens on bone and mineral metabolism in postmenopausal women. PATIENTS AND METHODS: Ten healthy premenopausal women and 17 healthy postmenopausal women were studied while not being treated and again after 4 weeks of treatment with diclofenac sodium, 150 mg per day in divided doses (both groups), and conjugated estrogens, 0.625 mg per day (postmenopausal women). Cross-linked N-telopeptides of type I collagen were measured in the urine as an index of bone resorption. The postmenopausal women were separated into two groups, responders and nonresponders, based on their response to conjugated estrogens as assessed by linear discriminant analysis for groups. Conjugated estrogens lowered urinary N-telopeptides of type I collagen in responders, but not in nonresponders. RESULTS: Urinary cross-linked N-telopeptides were higher in the eight postmenopausal women responders than in the nine postmenopausal nonresponders or in the premenopausal women, and were not altered by diclofenac sodium in premenopausal women. In the eight postmenopausal women with higher rates of bone resorption, diclofenac sodium and conjugated estrogens significantly lowered both urinary calcium concentration and urinary cross-linked N-telopeptides. The effects of the two drugs were comparable. CONCLUSION: The preliminary results demonstrate that, at the dose used, diclofenac sodium is almost as effective as conjugated estrogens for decreasing bone loss in postmenopausal women. Further studies will be needed to determine whether diclofenac sodium can prevent postmenopausal bone loss.

Adult↗