Osteoporosis Management in Younger Premenopausal Women
Osteoporosis Management in Younger Premenopausal Women
The purpose of this review is to describe the available evidence for osteoporosis treatments in young and premenopausal women. A review of articles evaluating the treatment or prevention of osteoporosis in young (age less than 50 years) or premenopausal women was conducted. Several trials evaluating the treatment of anorexia nervosa and use of hormone therapy in those women, the use of bisphosphonates in women undergoing chemotherapy for breast cancer and the use of bisphosphonates, teriparatide and vitamin D in women with glucocorticoid-induced osteoporosis are described. Limited data were found to support the treatment of osteoporosis in women with idiopathic osteoporosis or cystic fibrosis, or after kidney transplant. The evidence for treatment of osteoporosis in premenopausal women is not nearly as robust as that for postmenopausal osteoporosis. Although fracture risk in the premenopausal population is low, women with secondary osteoporosis may benefit from treatment with various agents, depending upon the condition.
Osteoporosis in younger women results from either a low peak bone mass, increased bone loss prior to menopause or both. Peak bone mass is reached by 30 years of age with 90% of the development completed by 18 years of age. For most women, bone mass remains stable until menopause, when the loss of estrogen in conjunction with aging is associated with a decline in bone mineral density (BMD). Family history, gender and race are responsible for the majority of peak bone mass; however, diet and exercise behaviors are responsible for up to 25%. Peak bone mass variations are genetic in 60–70% of cases. Osteoporosis is a disease of the bone, with effects including decreased BMD and increased risk of fractures, especially at the spine, hip and wrist. The loss of bone results from an imbalance in bone formation by osteoblasts and bone resorption by osteoclasts. Most treatments for osteoporosis aim to adjust this imbalance. In the case of premenopausal osteoporosis, secondary causes are responsible for at least half of cases. Secondary causes are listed in Table 1. In the Michigan Bone Health Study, over 600 premenopausal women followed for 6 years showed varied changes in lumbar spine (LS) BMD but a 1.6% decrease in femoral neck (FN) BMD starting in a woman's mid 20s. Risk factors for low BMD in premenopausal women include low body weight, amenorrhea, lack of physical activity, smoking, low dietary calcium or vitamin D, personal or family history of fracture, pregnancy and Caucasian or Asian race. Minimal bone loss is noted during pregnancy and breastfeeding; however, this loss is usually corrected shortly after pregnancy and breastfeeding are complete.
Healthy premenopausal women experience a 0.25–1% loss in BMD annually after reaching peak bone mass (commonly at the FN); however, no link has been established between this gradual loss in BMD and fracture risk in healthy women. Low Z-scores (2.5 standard deviations below other young females) are seen in 0.5% of premenopausal women. In Spanish women 20–44 years of age, 0.34% will have osteoporosis at the LS and 0.17% will have osteoporosis at the FN based on BMD alone. Overall, 50–90% of premenopausal women have a secondary cause for osteoporosis (e.g., eating disorders or glucocorticoid use, among others), with the remaining women diagnosed with idiopathic osteoporosis. Fracture risk in premenopausal women with osteoporosis remains low due to the small baseline fracture risk in younger women. The incidence of fractures in females under the age of 35 years is more difficult to detect due to the low incidence of three fractures per 100,000 patient-years but is noted to increase to 21 per 100,000 patient-years in women aged 35–44 years. Premenopausal fractures are associated with a 1.5- to 3-fold increase in the risk of postmenopausal fractures. Fracture risk is doubled or tripled once a loss of 10% in BMD has occurred; however, treatments resulting in a 5% increase in BMD may decrease fracture risk.
Premenopausal women referred to a bone disease referral program at a tertiary medical center were evaluated for secondary versus idiopathic osteoporosis. A retrospective review of all premenopausal women referred for fracture or low bone mass over 1 year (n = 61) was conducted, and 39% were found to have idiopathic osteoporosis, while 49% of the 29 women with a history of low-trauma fracture had idiopathic osteoporosis. This is consistent with other measures in premenopausal women. Low-trauma fracture was defined as that occurring due to a fall from standing height or less, with the exception of digit or skull fracture. Over half of the women (57%) reported a family history of osteoporosis. Secondary osteoporosis was due to amenorrhea in 34%, anorexia nervosa (AN) in 16%, glucocorticoid use in 13% and celiac disease in 10%. Premenopausal women with secondary osteoporosis had lower BMD at the spine (Z-score: -2.39 vs -1.58; p = 0.001) and hip than those with idiopathic osteoporosis, indicating a greater need for treatment in those women with secondary causes. Of the women referred due to a fracture, 28% did not have a low BMD. Bisphosphonates were used by 47% of women with low BMD but no history of fracture and by 50% of women with idiopathic osteoporosis, which may indicate overuse of osteoporosis treatments in this population. Therefore, a need to clarify the role of osteoporosis treatments in younger, premenopausal women is needed.
The purpose of this review is to describe the available evidence for osteoporosis treatments in young and premenopausal women (Table 2).
Abstract and Introduction
Abstract
The purpose of this review is to describe the available evidence for osteoporosis treatments in young and premenopausal women. A review of articles evaluating the treatment or prevention of osteoporosis in young (age less than 50 years) or premenopausal women was conducted. Several trials evaluating the treatment of anorexia nervosa and use of hormone therapy in those women, the use of bisphosphonates in women undergoing chemotherapy for breast cancer and the use of bisphosphonates, teriparatide and vitamin D in women with glucocorticoid-induced osteoporosis are described. Limited data were found to support the treatment of osteoporosis in women with idiopathic osteoporosis or cystic fibrosis, or after kidney transplant. The evidence for treatment of osteoporosis in premenopausal women is not nearly as robust as that for postmenopausal osteoporosis. Although fracture risk in the premenopausal population is low, women with secondary osteoporosis may benefit from treatment with various agents, depending upon the condition.
Introduction
Osteoporosis in younger women results from either a low peak bone mass, increased bone loss prior to menopause or both. Peak bone mass is reached by 30 years of age with 90% of the development completed by 18 years of age. For most women, bone mass remains stable until menopause, when the loss of estrogen in conjunction with aging is associated with a decline in bone mineral density (BMD). Family history, gender and race are responsible for the majority of peak bone mass; however, diet and exercise behaviors are responsible for up to 25%. Peak bone mass variations are genetic in 60–70% of cases. Osteoporosis is a disease of the bone, with effects including decreased BMD and increased risk of fractures, especially at the spine, hip and wrist. The loss of bone results from an imbalance in bone formation by osteoblasts and bone resorption by osteoclasts. Most treatments for osteoporosis aim to adjust this imbalance. In the case of premenopausal osteoporosis, secondary causes are responsible for at least half of cases. Secondary causes are listed in Table 1. In the Michigan Bone Health Study, over 600 premenopausal women followed for 6 years showed varied changes in lumbar spine (LS) BMD but a 1.6% decrease in femoral neck (FN) BMD starting in a woman's mid 20s. Risk factors for low BMD in premenopausal women include low body weight, amenorrhea, lack of physical activity, smoking, low dietary calcium or vitamin D, personal or family history of fracture, pregnancy and Caucasian or Asian race. Minimal bone loss is noted during pregnancy and breastfeeding; however, this loss is usually corrected shortly after pregnancy and breastfeeding are complete.
Healthy premenopausal women experience a 0.25–1% loss in BMD annually after reaching peak bone mass (commonly at the FN); however, no link has been established between this gradual loss in BMD and fracture risk in healthy women. Low Z-scores (2.5 standard deviations below other young females) are seen in 0.5% of premenopausal women. In Spanish women 20–44 years of age, 0.34% will have osteoporosis at the LS and 0.17% will have osteoporosis at the FN based on BMD alone. Overall, 50–90% of premenopausal women have a secondary cause for osteoporosis (e.g., eating disorders or glucocorticoid use, among others), with the remaining women diagnosed with idiopathic osteoporosis. Fracture risk in premenopausal women with osteoporosis remains low due to the small baseline fracture risk in younger women. The incidence of fractures in females under the age of 35 years is more difficult to detect due to the low incidence of three fractures per 100,000 patient-years but is noted to increase to 21 per 100,000 patient-years in women aged 35–44 years. Premenopausal fractures are associated with a 1.5- to 3-fold increase in the risk of postmenopausal fractures. Fracture risk is doubled or tripled once a loss of 10% in BMD has occurred; however, treatments resulting in a 5% increase in BMD may decrease fracture risk.
Premenopausal women referred to a bone disease referral program at a tertiary medical center were evaluated for secondary versus idiopathic osteoporosis. A retrospective review of all premenopausal women referred for fracture or low bone mass over 1 year (n = 61) was conducted, and 39% were found to have idiopathic osteoporosis, while 49% of the 29 women with a history of low-trauma fracture had idiopathic osteoporosis. This is consistent with other measures in premenopausal women. Low-trauma fracture was defined as that occurring due to a fall from standing height or less, with the exception of digit or skull fracture. Over half of the women (57%) reported a family history of osteoporosis. Secondary osteoporosis was due to amenorrhea in 34%, anorexia nervosa (AN) in 16%, glucocorticoid use in 13% and celiac disease in 10%. Premenopausal women with secondary osteoporosis had lower BMD at the spine (Z-score: -2.39 vs -1.58; p = 0.001) and hip than those with idiopathic osteoporosis, indicating a greater need for treatment in those women with secondary causes. Of the women referred due to a fracture, 28% did not have a low BMD. Bisphosphonates were used by 47% of women with low BMD but no history of fracture and by 50% of women with idiopathic osteoporosis, which may indicate overuse of osteoporosis treatments in this population. Therefore, a need to clarify the role of osteoporosis treatments in younger, premenopausal women is needed.
The purpose of this review is to describe the available evidence for osteoporosis treatments in young and premenopausal women (Table 2).
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