Prospective 10‐year study of the determinants of bone density and bone loss in normal postmenopausal women, including the effect of hormone replacement therapy

Wu, Fiona; Ames, Ruth; Clearwater, Judy; Evans, Margaret C.; Gamble, Greg; Reid, Ian R.

doi:10.1046/j.1365-2265.2002.01534.x

Cited by 84 publications

(46 citation statements)

References 39 publications

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“…(13). In contrast with the studies mentioned above, no association between the levels of endogen testosterone in each study group (normal, osteopenia, osteoporosis) and BMDs of any site of the body (lumbar or femoral) was found in the present study.…”

Section: Discussioncontrasting

confidence: 99%

Serum testosterone does not affect bone mineral density in postmenopausal women

Arpacı

Sağlam

Cuhaci

et al. 2015

Arch. Endocrinol. Metab.

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Objective: The purpose of the present study was to investigate the correlation between serum testosterone levels and bone mineral density (BMD) in postmenopausal women. Materials and methods: The study group was made up of postmenopausal women admitted to our tertiary center. Serum calcium, phosphorus, albumin, parathyroid hormone (PTH), thyrotropin (TSH), 25-OH vitamin D, and total testosterone concentrations were measured. Subjects were categorized into three groups regarding bone mineral density (BMD) values: normal (n = 22), osteopenia (n = 21), and osteoporosis (n = 21). Subjects were also categorized into three groups according to serum testosterone levels: low testosterone (n = 10), normal testosterone (n = 42), and high testosterone (n = 12). Results: No significant difference was found for serum testosterone, TSH, calcium, phosphorus, albumin, PTH, and 25-hydroxyvitamin D levels among patients with normal BMD, osteopenia, and osteoporosis (p > 0.05). Lumbar spine, total femur, femoral neck, trochanteric, intertrochanteric, and Ward's triangle BMD values were similar for the different testosterone levels (p > 0.05). Conclusion: There was no correlation between serum testosterone levels and patient age, body-mass index, or any measured BMD values. Given the findings in our study, which failed to demonstrate a statistically significant relationship between testosterone and BMD, adjustment of other risk factors for osteoporosis might have a more distinctive effect in this setting. Arch Endocrinol Metab. 2015;59(4):292-6

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Section: Discussioncontrasting

confidence: 99%

Serum testosterone does not affect bone mineral density in postmenopausal women

Arpacı

Sağlam

Cuhaci

et al. 2015

Arch. Endocrinol. Metab.

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“…The same group reported that BMD was dependent on both fat and lean mass in premenopausal women; however, male BMD was related only to lean mass [15]. Furthermore, baseline fat mass and changes in fat mass were predictive of changes in BMD over 10 years in postmenopausal women [21]. Another study on 921 African-American, Asian, Latino, and Caucasian women 20 to 25 years old found that fat mass was positively correlated with BMD at all skeletal sites [22].…”

Section: Discussionmentioning

confidence: 96%

Fat mass is negatively associated with bone mineral content in Koreans

et al. 2011

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“…Each female was then given 1 g of calcium orally at bedtime, in the form of calcium citrate, and a first-void fasting urine sample collected. Urinary calcium and creatinine concentrations were measured using standard methods [19]. …”

Section: Methodsmentioning

confidence: 99%

Mutational Analysis of CLC-5, Cofilin and CLC-4 in Patients with Dent’s Disease

Reed²,

Williams³

et al. 2009

Nephron Physiol

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Background/Aims: Dent’s disease is caused by mutations in the chloride/proton antiporter, CLC-5, or oculo-cerebro-renal-syndrome-of-Lowe (OCRL1) genes. Methods: Eighteen probands with Dent’s disease were investigated for mutations in CLC-5 and two of its interacting proteins, CLC-4 and cofilin. Wild-type and mutant CLC-5s were assessed in kidney cells. Urinary calcium excretion following an oral calcium challenge was studied in one family. Results: Seven different CLC-5 mutations consisting of two nonsense mutations (Arg347Stop and Arg718Stop), two missense mutations (Ser244Leu and Arg516Trp), one intron 3 donor splice site mutation, one deletion-insertion (nt930delTCinsA) and an in-frame deletion (523delVal) were identified in 8 patients. In the remaining 10 patients, DNA sequence abnormalities were not detected in the coding regions of CLC-4 or cofilin, and were independently excluded for OCRL1. Patients with CLC-5 mutations were phenotypically similar to those without. The donor splice site CLC-5 mutation resulted in exon 3 skipping. Electrophysiology demonstrated that the 523delVal CLC-5 mutation abolished CLC-5-mediated chloride conductance. Sixty percent of women with the CLC-5 deletion-insertion had nephrolithiasis, although calcium excretion before and after oral calcium challenge was similar to that in unaffected females. Conclusions: Three novel CLC-5 mutations were identified, and mutations in OCRL1, CLC-4 and cofilin excluded in causing Dent’s disease in this patient cohort.

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Prospective 10‐year study of the determinants of bone density and bone loss in normal postmenopausal women, including the effect of hormone replacement therapy

Cited by 84 publications

References 39 publications

Serum testosterone does not affect bone mineral density in postmenopausal women

Serum testosterone does not affect bone mineral density in postmenopausal women

Fat mass is negatively associated with bone mineral content in Koreans

Mutational Analysis of CLC-5, Cofilin and CLC-4 in Patients with Dent’s Disease

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