Relationship between whole plasma calcitonin levels, calcitonin secretory capacity, and plasma levels of estrone in healthy women and postmenopausal osteoporotics.

Reginster, Jean‐Yves; Deroisy, Rita; Albert, Adelin; Denis, Danielle; Lecart, Marie-Paule; Collette, Julien; Franchimont, P

doi:10.1172/jci113950

Cited by 62 publications

(11 citation statements)

References 19 publications

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“…Hereby, women comprise an individually varying discontinuous annual bone loss of 1-5% per year for the first 10-15 years after menopause. 12,14 Thereafter, bone loss seems to decrease further but to a smaller extent.…”

Section: Bone Physiology and Pathophysiologymentioning

confidence: 99%

Cancer Treatment-Induced Bone Loss in women with breast cancer

Hadji

2015

BoneKEy Reports

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Osteoporosis is one of the most frequent diseases in postmenopausal women, leading to an increased fracture risk due to the physiologic loss of the bone protective effects of estrogen. Hereby, several risk factors for fracture such as prevalent fracture, low bone mineral density (BMD), age, low body mass index, family history, tendency to falls, smoking, use of SSRIs, glucocorticoid use etc. have been identified. In addition, the further reduction in endogenous estrogens with chemotherapy (CHT), GnRH analoga or aromatase inhibitors (AIs) continuously increases fracture risk. Breast cancer (BC) on the other hand is the most frequent cancer type in women. Recent reports indicate a continuous increased incidence, whereas mortality, due to early diagnosis and treatment improvements, is decreasing. Dependent on specific tumor characteristics, radiation, CHT, antibody treatment as well as endocrine treatment have been included into the adjuvant clinical treatment setting. Some but not all of these cancer-specific treatments interfere with bone turnover, leading to an accelerated bone loss referred to as cancer treatment-induced bone loss (CTIBL). Whereas CHT leads to an unspecific increase in bone resorption, AI reduces residual serum endogenous estrogen level and is associated with a decrease in BMD and increased fracture risk. Independent of the type of AI administered, bone loss is 2-3-fold increased compared with healthy, age-matched postmenopausal controls. Therefore, several guidelines have emerged to help managing CTIBL in women with BC including strategies to identify and treat those at highest risk for fractures. This review summarizes the current knowledge on CTIBL and fracturing risk and indicates preventative strategies.

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Section: Bone Physiology and Pathophysiologymentioning

confidence: 99%

Cancer Treatment-Induced Bone Loss in women with breast cancer

Hadji

2015

BoneKEy Reports

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“…The effect of estrogens in patients with osteoporosis was to increase serum PTH levels (27)(28)(29) which was postulated to be secondary to an estrogen induced hypocalcemia (27,29), whilst the effect on calcitonin levels was variable (30,31 ) possibly due to the insensitivity of calcitonin immunoassays (32). Our results, together with the earlier in vitro reports of a direct effect of estrogens on PTH and calcitonin secretion (16)(17)(18)(19), indicate that the effect of estrogens to increase PTH and calcitonin levels is a direct effect ofestrogens on the parathyroid and C cells, respectively.…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptors and biologic response in rat parathyroid tissue and C cells.

Naveh-Many¹,

Almogi²,

Livni³

et al. 1992

J. Clin. Invest.

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“…hot flushes, mucosal atrophy) caused by physiologically decreased plasma levels of estriol, bone health is majorly impacted. Although individually varying, healthy postmenopausal women experience a gradual bone loss of 1% per year [13,14]. …”

Section: From Pathophysiology and Evidence To Guidelinesmentioning

confidence: 99%

Breast Cancer and Osteoporosis - Management of Cancer Treatment-Induced Bone Loss in Postmenopausal Women with Breast Cancer

Kalder

Hadji

2014

Breast Care

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The incidence of breast cancer (BC) in postmenopausal women is continuously rising. Due to early diagnosis and various treatment designs, the long-term clinical outcome has improved. Frequent settings are chemotherapy as well as endocrine treatment. Both have proven to interfere with bone health resulting in cancer treatment-induced bone loss (CTIBL). Whereas chemotherapy is associated with increased bone resorption, aromatase inhibitor (AI) therapy reduces residual estrogen and is associated with decreased bone mineral density. Independent of the AI administered, the loss of bone mineral density is twice as high compared to healthy postmenopausal women. As a consequence of CTIBL, both chemotherapy and AI treatment can lead to a significantly increased fracture risk. Therefore, several guidelines have emerged for the management of CTIBL in women with BC, including strategies to identify and treat those at high risk for fractures. Further research on tracking guideline adherence examining the feasibility and practicability of guideline implementation to bridge the gap between determined scientific best evidence and applied best practice is needed to adjust these guidelines in the future.

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Relationship between whole plasma calcitonin levels, calcitonin secretory capacity, and plasma levels of estrone in healthy women and postmenopausal osteoporotics.

Cited by 62 publications

References 19 publications

Cancer Treatment-Induced Bone Loss in women with breast cancer

Cancer Treatment-Induced Bone Loss in women with breast cancer

Estrogen receptors and biologic response in rat parathyroid tissue and C cells.

Breast Cancer and Osteoporosis - Management of Cancer Treatment-Induced Bone Loss in Postmenopausal Women with Breast Cancer

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