Oestrogen Replacement Therapy for Prevention of Osteoporosis after Oophorectomy

Aitken, J. M.; Hart, D.M.; Lindsay, Robert

doi:10.1136/bmj.3.5879.515

Cited by 234 publications

(45 citation statements)

References 30 publications

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“…This might be interpreted as indicating that 'routine' replacement is not sufficient to optimize bone mineral content and prevent fractures. However, the impact of the years of untreated hypogonadism on the fracture frequency must be considered, as it is well known that untreated hypogonadism is a major reason for osteopenia and fractures in both men (14,15) and women (16,17). On average, the patients had about 4 years of untreated hypogonadism, which might contribute to some osteopenia.…”

Section: Discussionmentioning

confidence: 99%

Increased fracture frequency in adult patients with hypopituitarism and GH deficiency

Rosén

Wilhelmsen²,

Landin‐Wilhelmsen

et al. 1997

European Journal of Endocrinology

259

137

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Fracture frequency was studied in 107 hypopituitary patients with GH deficiency (GHD) (69 men, mean age 53 years, range 18-74 and 38 women, mean age 54 years, range 31-73). Routine hormonal replacement therapy was given, except GH. Five male patients and 15 female patients with untreated hypogonadism were allocated to a separate group. The mean duration of hypopituitarism was 13.4 years. The prevalence of a history of fractures was assessed using questionnaires. A subsample of the Göteborg WHO MONICA Project was used as a reference population (n ¼ 323).The total fracture frequency was threefold higher (P<0.001) in patients (24.1%) compared with controls (8.7%) (odds ratio 3.49) (1.85-6.56; 95% confidence intervals). In men (n ¼ 64) the fracture frequency was 25.0%, compared with 7.8% among the controls (P<0.001). In women (n ¼ 23) the fracture frequency was 21.7%, compared with 9.5% among the controls (P ¼ 0.08). The odds ratios for fracture frequency were 3.97 (1.81-8.40; 95% confidence intervals) and 2.64 (0.89-7.81; 95% confidence intervals) in men and women respectively.In conclusion, adult hypopituitary patients with GHD had a threefold increased fracture frequency compared with controls. Further studies are needed to ascertain whether long-term recombinant human GH treatment can reduce the fracture rate in hypopituitary patients with GHD. European Journal of Endocrinology 137 240-245

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Section: Discussionmentioning

confidence: 99%

Increased fracture frequency in adult patients with hypopituitarism and GH deficiency

Rosén

Wilhelmsen²,

Landin‐Wilhelmsen

et al. 1997

European Journal of Endocrinology

259

137

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“…17 Table 5 shows that among matched case-control 1 pairs the risk of hip fracture had a greater reduction if estrogen exposure was begun within three years of menopause rather than three or more years after menopause. This was not shown with matched case-control 2 pairs.…”

Section: Estrogen Exposurementioning

confidence: 99%

“…"-' 5 It also appears that time of initiation, and length and continuity of estrogen drug therapy influence rate and amount of bone loss. [16][17][18][19] Until recently, however, the effect of estrogen drug treatment in preventing the clinical outcomes of osteoporosis, such as hip fractures, had not been investigated. A recent study of medical records showed no significant protective effect of conjugated estrogen exposure of six months or longer upon the hip and distal radius fracture experience of 157 matched case-control pairs of postmenopausal females.…”

mentioning

confidence: 99%

The risk of hip fracture in postmenopausal females with or without estrogen drug exposure.

Johnson¹,

Specht²

1981

Am J Public Health

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“…Ovarian hormone deficiency is the most important risk factor for postmenopausal osteoporosis (1,2). Bone loss also occurs in premenopausal women following ovariectomy (OVX) (3) or treatment with gonadotrophin-releasing hormone agonists (4).…”

mentioning

confidence: 99%

Estrogen regulates the rate of bone turnover but bone balance in ovariectomized rats is modulated by prevailing mechanical strain

Westerlind

Wronski

Ritman

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

176

141

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Estrogen deficiency induced bone loss is associated with increased bone turnover in rats and humans. The respective roles of increased bone turnover and altered balance between bone formation and bone resorption in mediating estrogen deficiency-induced cancellous bone loss was investigated in ovariectomized rats. Ovariectomy resulted in increased bone turnover in the distal femur. However, cancellous bone was preferentially lost in the metaphysis, a site that normally experiences low strain energy. No bone loss was observed in the epiphysis, a site experiencing higher strain energy. The role of mechanical strain in maintaining bone balance was investigated by altering the strain history. Mechanical strain was increased and decreased in long bones of ovariectomized rats by treadmill exercise and functional unloading, respectively. Functional unloading was achieved during orbital spacef light and following unilateral sciatic neurotomy. Increasing mechanical loading reduced bone loss in the metaphysis. In contrast, decreasing loading accentuated bone loss in the metaphysis and resulted in bone loss in the epiphysis. Finally, administration of estrogen to ovariectomized rats reduced bone loss in the unloaded and prevented loss in the loaded limb following unilateral sciatic neurotomy in part by reducing indices of bone turnover. These results suggest that estrogen regulates the rate of bone turnover, but the overall balance between bone formation and bone resorption is inf luenced by prevailing levels of mechanical strain.Ovarian hormone deficiency is the most important risk factor for postmenopausal osteoporosis (1, 2). Bone loss also occurs in premenopausal women following ovariectomy (OVX) (3) or treatment with gonadotrophin-releasing hormone agonists (4). Estrogen replacement therapy prevents bone loss in postmenopausal and ovariectomized women, suggesting that 17␤-estradiol is the gonadal hormone that is essential for normal bone balance.The mechanism for the skeletal effects of estrogen are incompletely understood but have been the subject of intense study in laboratory animal models (5). The rat has proven to be especially useful. OVX and gonadotrophin-releasing hormone agonists result in bone loss in rats, and these changes are prevented by estrogen treatment (6-9). These observations suggest similar skeletal mechanisms of action of estrogen in rats and humans. Furthermore, the skeletal changes in rats in response to partial estrogen agonists have accurately predicted the differential responses of pre-and postmenopausal women to tamoxifen treatment (10, 11).The bone loss in postmenopausal women and ovariectomized women and rats is associated with elevated bone turnover (6,(12)(13)(14). However, the bone loss is not uniform; cancellous bone is at a greater risk than cortical bone (7,14,15). In addition, there is site specificity in the loss of cancellous bone. For example, cancellous bone is lost more rapidly from the proximal tibial metaphysis than from vertebral bodies (16). Also, bone is preferenti...

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Oestrogen Replacement Therapy for Prevention of Osteoporosis after Oophorectomy

Cited by 234 publications

References 30 publications

Increased fracture frequency in adult patients with hypopituitarism and GH deficiency

Increased fracture frequency in adult patients with hypopituitarism and GH deficiency

The risk of hip fracture in postmenopausal females with or without estrogen drug exposure.

Estrogen regulates the rate of bone turnover but bone balance in ovariectomized rats is modulated by prevailing mechanical strain

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