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F Trémollières

Publications and source records attributed to F Trémollières.

At least 19 recordsLinked to original sources
PubMed2006

[Raloxifene in postmenopausal women].

Since the diffusion of the WHI's trial and MWS results, which reported a negative risk/benefit balance of hormone therapy, the management of postmenopausal women has deeply changed over the last 2-3 years. In particular, for the prevention of osteoporosis, the use of other efficient agents tends now to be more widely recommended rather than estrogens. The SERMs with raloxifene are new molecules that have estrogen agonist effects on bone and estrogen antagonist or neutral effects on endometrial and breast tissue. The efficacy of raloxifene to inhibit postmenopausal bone loss as well as to reduce the incidence of vertebral fractures has been demonstrated in women at high risk for osteoporosis through a large randomized placebo-controlled trial involving several thousands of postmenopausal women (MORE trial). Furthermore, the extraskeletal effects of raloxifene might represent an advantage for a global management approach of postmenopausal women, although to date, its exclusive indication is namely the prevention of osteoporosis. However, the estrogen antagonist effects of raloxifene on breast tissue as well as its good safety profile with regard to both the endometrium and the risk of heart diseases are likely to make raloxifene of particular interest for women around the age of 60 years old. Adverse events associated with raloxifene only included an increase in the absolute risk of venous thromboembolism in a comparable manner as with estrogen therapy. Also, its lack of efficacy in reducing hot flushes or preventing vaginal dryness may limit its use in young symptomatic postmenopausal women. Also, its lack of reimbursement in women with no prior fragility fracture must be taken into account.

Bone Density Conservation Agents↗
PubMed1999

[Hormone replacement therapy in the prevention of osteoporosis. Evolution of therapeutic methods].

ESTABLISHED FACTS: Many studies have evidenced that hormone replacement therapy can help prevent post-menopausal osteoporosis and osteoporotic fractures in menopaused women. Thanks to recent advances in pharmacology, hormone replacement therapy can now closely mimic ovarian physiology and thus eliminate most of the contraindications related to metabolic disorders. UNRESOLVED QUESTIONS: The need for prolonged treatment to reach optimal efficacy raises the problems of safety and compliance. This is particularly true for the prevention of fractures of the femoral neck which usually occur in older women, suggesting it could be useful to revisit the estrogen strategy. NEW COMPOUNDS: The action of selective estrogen receptor modulators (SERM) depends on the target organ. They have an estrogen agonist effect on bone and lipid metabolism but no such effect on the uterus. SERMs could offer new therapeutic opportunities for the prevention of post-menopausal osteoporosis.

Adolescent↗
PubMed1996

[Vertebral bone loss in perimenopause. Results of a 7-year longitudinal study].

OBJECTIVES: Rapid bone loss after menopause is generally recognized although the exact chronology of the events, particularly in relation to onset of amenorrhea, remains poorly understood. We assessed bone loss in perimenopausal women over a 7-year period. METHODS: Twenty-one women with an uneventful past history were enrolled before menopause and followed until menopause had been completely established. Vertebral bone density was measured by biphotonic absorptiometry annually over two 2-year periods. Individual variations in bone density were calculated according to onset of menopause. RESULTS: Bone loss in the vertebral body increased during the two years preceding menopause (-1.6 +/- 1.5% per year), reached a peak during the first three post-menopausal years (-2.4 +/- 1.6% per year), and then fell off (-1.2 +/- 1.4% per year). CONCLUSION: Bone loss was independent of calcium intake and appeared to be related mainly to characteristic hormone changes during the perimenopausal period. These findings raise the question as to the need and means of prevention.

Absorptiometry, Photon↗
PubMed1996

Variability of vertebral and femoral postmenopausal bone loss: a longitudinal study.

The rate of postmenopausal bone loss varies considerably between individuals and it has been suggested that about 1 in 3 women loses significant amount of bone mineral in the forearm. The rate of vertebral and femoral bone loss was determined by dual-energy X-ray absorptiometry throughout two consecutive 22-month periods, in 93 healthy women who had passed a natural menopause 6-60 months earlier. In all cases the bone changes were normally distributed, ranging from -6.9% to +2.8% per year in the spine and from -7% to +4.8% per year in the femur. No significant relationship was found between the two fractional rates of bone loss. When the women were stratified into three groups according to their individual rate of bone loss, we found that only 20%-47% retained their first classification during the second period of follow-up. In particular, less than 10% of the women showed a rapid rate of bone loss throughout the study. We conclude that spontaneous vertebral and femoral bone loss exhibit a great variability within the first postmenopausal years and that only a small minority of women sustain a fast rate of bone loss over several years. These results raise the question as to whether the evaluation of individual rates of bone loss at menopause might be useful in the identification of women at higher risk of osteoporosis.

Bone Density↗
PubMed1995

[Hormone replacement therapy and early and late prevention of postmenopausal osteoporosis].

Osteoporosis is one of the main features of the ageing process and the cost of health care for osteoporosis-related fractures and their complications is a major incentive for prevention, particularly in developed countries with a continuously ageing population. The earliest strategies for prevention in menopaused women were based on the anti-osteoclastic effect of hormone replacement therapy. Several epidemiological studies have provided proof of its efficacy showing that in treated populations, there is a significant reduction in osteoporosis-related fractures of about 50%, whatever the site of fracture. Although the effects of hormone replacement therapy in the prevention of post-menopausal osteoporosis have been well established, three problems remain. First, what is the degree of efficacy if replacement therapy is started late? Second, what is the effect in patients who have already suffered an osteoporotic fracture? Third, and most importantly, what is the optimal duration of treatment for effective prevention in a given population particularly at risk of hip fracture? These questions suggest new strategies for preventive hormone replacement are needed.

Aged↗
PubMed1995

[Influence of body weight variations on the rate of bone loss at the beginning of menopause].

Numerous data suggest, at any age, a clear relationship between body weight and Bone Mineral Density (BMD). On the other hand, the effects of individual changes in body weight on BMD are still poorly understood. Fourty four normal women of normal weight, who had passed a natural menopause 6 months to 5 years earlier, were followed during a mean period of time of 40 months. They all underwent three BMD measurements by Dual X-Ray Absorptiometry and a clinical examination. There was a significant correlation (p < 0.05) between the changes in weight and the changes in BMD at the vertebral (r = 0.31) and femoral (r = 0.30) levels. This association remained significant after adjustment for physical characteristics, age, years since menopause and initial BMD values. Moreover, the subgroup of women who gained more than one kilogram during the follow-up had a rate of bone loss which was about twice less than that in the rest of the group. This longitudinal study shows that changes in body weight are able to influence the rate of postmenopausal bone loss through mechanisms that are still discussed.

Body Weight↗
PubMed1995

[Anti-estrogens and bone tissue].

Anti-oestrogens are a class of non-steroid compounds with, depending on the tissue, oestrogen-antagonist or oestrogen-agonist actions resulting from different mechanisms, especially by binding to oestrogen receptors. These compounds are commonly called anti-oestrogens because of their extensive use in treating breast cancer. Tamoxifen, the first of these complex compounds, has a partial agonist effect on the endometrium and also affects bone and lipid metabolism. Currently, our knowledge of anti-oestrogen action on bone is based on experimental work and a few clinical trials with tamoxifen. The animal studies show that tamoxifen has a preventive effect against bone hyper-remodelling resulting form ovariectomy in the rat. Most of the clinical studies, including the most recent, show that tamoxifen has no deleterious effect, and possibly even a moderate protective effect against bone loss, in menopaused women. This effect on bone tissue, together with lowered plasma cholesterol levels, has led to the development of other compounds with a bone and lipid agonist effect and secondary effects limited to endometrial hyperplasia. Third generation compounds include droloxifen keoxifen (or raloxifen) currently under investigation. This research should lead to wider indications for anti-oestrogens in the prevention of the effects of post-menopause oestrogen deficiency, particularly in patients with contraindications for oestrogen therapy.

Animals↗
PubMed1994

[Effect of menopause on vertebral bone mass. A longitudinal study].

OBJECTIVE: We evaluated bone loss in women during the peri and post-menopausal period in order to determine the exact effect of menopause on vertebral bone density and biochemical markers of bone remodelling. METHODS: One hundred fifty-seven women who consulted for menopause and who did not wish to receive substitution therapy were enrolled. Menopause was defined as amenorrhoea > or = 1 year and serum 17-beta oestradiol < or = 20 pg/ml and luteinizing hormone > 30 IU/ml. Precocious or surgical menopauses were excluded. Two groups were formed according to the hormone pattern: a peri-menopausal group (n = 32, mean age 51.2 +/- 2.9 years) and a post-menopausal group (n = 125, mean age 54.3 +/- 3.7, menopause 1 to 11 years at entry). Bone density was measured by biphonotonic absorptiometry and blood chemistry was performed with routine laboratory methods. All tests were repeated at successive consultations and mean follow-up was 32 +/- 12 months. RESULTS: Annual rate of bone loss was during peri-menopause (-1.8 +/- 1.7%) and the first 4 years of menopause (-1.6 +/- 1.6%), then decreased significantly beyond 4 years. Mean bone loss from 5 to 10 years menopause (-0.60 +/- 1%). Initial serum calcium, phosphorus, alkaline phosphatase and osteocalcine levels were significantly higher during post-menopause than during peri-menopause (P < 0.05). The urinary calcium/creatinine ratio was comparable between the two periods and decrease after 4 years of menopause. CONCLUSION: This longitudinal study indicated that increased vertebral bone loss begins early during peri-menopause and is temporary since it does not continue beyond 5 years. It is important to consider these findings when developing strategy for the prevention of menopausal osteoporosis.

Bone Density↗
PubMed1994

[Bone involvement in endocrinopathies].

Progress in bone densitometry, particularly biphotonic absoptiometry, has made it possible to better identify the effects of endocrinopathies on bone. Both cortical and trabecular bone structures can be evaluated quantitatively and topographically revealing important information on the pathophysiology of bone loss. Sex hormones play a major role in the regulation of bone mineralization and hypogonadism, whatever the origin, can lead to deleterious effects. Bone loss is known to be significative in high performance female athletes with amenorrhoea; long-term consequences are not yet determined, but stress fractures have been reported in up to 50%. Other hypogonadisms leading to bone demineralization include anorexia nervosa, chronic intake of gonadotrophin releasing hormone analogues and anti-oestrogens, and hyperprolactinism. Hyperthyroidism leads to a negative calcium balance and demineralization with remodelling, predominantly in cortical bone. In hypothyroid states a 10% bone loss is observed in vertebrae. In both cases, bone densitometry should be performed in order to evaluate the effect of treatment. The deleterious effect of spontaneous or iatrogenic hypercortisism is well known, leading to spontaneous wedge fractures of the vertebrae due to predominating trabecular bone loss. The mechanism of action of corticosteroids on bone metabolism is complex, but the major effect is an inhibition of osteoblast maturation. Recovery may be possible, but no large long-term series have yet been reported. Hyperparathyroidism and acromegaly also affect bone mineralization. The information provided by bone densitometry is essential to properly manage patients with endocrinopathies affecting bone mineralization.

Acromegaly↗
PubMed1994

[Effect of early menopause by ovariectomy on bone loss].

OBJECTIVES: Early menopause is a well-known risk factor for osteoporosis. It could be an aggravating factor when induced ovariectomy. This study was conducted to compare vertebral bone density and biochemical markers of bone remodelling in patients with spontaneous and induced early and "normal" menopause. METHODS: The main biochemical markers of bone remodelling (serum calcium, albumin, alkaline phosphatase, osteocalcin and urinary calcium/creatinine) together with bone density (L2-L4) were measured in 55 women (age 46-77 at inclusion) with spontaneous (n = 16) or surgically induced (n = 39) early menopause (before age 40) and in 227 women (age at inclusion 47-67 years) with normal menopause (after 40 years) either spontaneous (n = 136) or surgically induced (n = 91). RESULTS: At equivalent ages, vertebral bone density was 7 to 12% lower (p < 0.05) in women with early menopause than in women menopaused after 40. However, the serum levels of alkaline phosphatase and osteocalcin as well as the Nordin index were similar in the two groups. After adjusting for the duration of menopause, women with early menopause did not have a higher bone density than their "normal" menopause counterparts despite their younger age (9 years younger). No differences were observed between spontaneous and surgically induced menopause. CONCLUSION: These results suggest that bone loss is more rapid or more long lasting after precocious menopause. Surgically induced menopause does not appear to aggravate bone loss independently of age. Effective prevention of this hormone dependent bone loss is required.

Age Factors↗