Claude Ribot
University of Toulouse
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Osteoporosis International | 1998
A. M. Schott; C. Cormier; D. Hans; F. Favier; Hausherr E; Patricia Dargent-Molina; P. D. Delmas; Claude Ribot; Jl. Sebert; Gérard Bréart; P.J. Meunier
Abstract: We conducted a population-based cohort study in 7598 white healthy women, aged 75 years and over, recruited from the voting lists. We measured at baseline bone mineral density (BMD g/cm2) of the proximal femur (neck, trochanter and Wards triangle) and the whole body, as well as fat and lean body mass, by dual-energy X-ray absorptiometry (DXA). One hundred and fifty-four women underwent a hip fracture during an average 2 years follow-up. Each standard deviation decrease in BMD increased the risk of hip fracture adjusted for age, weight and centre by 1.9 (95% CL 1.5, 2.3) for the femoral neck, 2.6 times (2.0, 3.3) for the trochanter, 1.8 times (1.4, 2.2) for Wards triangle, 1.6 times (1.2, 2.0) for the whole body, and 1.3 times (1.0, 1.5) for the fat mass. The areas under the receiver operating characteristic (ROC) curves were not significantly different between trochanter and femoral neck BMD, whereas ROC curves of femoral neck and trochanter BMD were significantly better than those for Wards triangle and whole-body BMD.emsp;Women who sustained an intertrochanteric fracture were older (84 ± 4.5 years) than women who had a cervical fracture (81 ± 4.5 years) and trochanter BMD seemed to be a stronger predictor of intertrochanteric ([RR = 4.5 (3.1, 6.5)] than cervical fractures ([RR = 1.8 (1.5, 2.3]).emsp;In very elderly women aged 80 years and more, hip BMD was still a significant predictor of hip fracture but the relative risk was significantly lower than in women younger than 80 years.emsp;In the 48% of women who had a femoral neck BMD T-score less than –2.5, the relative risk of hip fracture was increased by 3, and the unadjusted incidence of hip fracture was 16.4 per 1000 woman-years compared with 1.1 in the population with a femoral neck BMD T-score 5–1.
Calcified Tissue International | 1993
Jean Michel Pouilles; Florence Trémollières; Claude Ribot
SummaryTwo hundred and thirty women aged 45–66 years were divided into three groups according to their menopausal status and were followed to assess the changes in vertebral bone mineral density (BMD). These included 71 premenopausal, 42 perimenopausal, and 117 postmenopausal women. Menopausal status was assessed through menstrual history and plasma concentrations of 17β estradiol and luteinizing hormone. BMD was measured by dual photon absorptiometry between 2 and 5 times over an average period of 27 months, and annual rates of changes were calculated by linear regression. BMD decreased significantly (P<0.0001) in the three groups during the follow-up. Mean (±SD) annual rate of change was-0.79±1.5% for premenopausal,-2.35±1.5% for perimenopausal, and-1.24±1.5% for postmenopausal women. There was no difference in the rates of bone loss between the perimenopausal group and the postmenopausal group within 3 years after menopause (1–2 years:-2.34±2.1%; 2–3 years:-1.9±1.5%). Thereafter, rates decreased exponentially with time since menopause to fall out at the same level as the premenopausal level. These longitudinal data indicate that vertebral bone loss begins before menopause and accelerates sharply during menopause to decline exponentially with time after 3 years.
Journal of Bone and Mineral Research | 2010
Florence Trémollières; Nicolas Drewniak; Jacques Laparra; Claude Ribot; Patricia Dargent-Molina
The aim of this prospective study was (1) to identify significant and independent clinical risk factors (CRFs) for major osteoporotic (OP) fracture among peri‐ and early postmenopausal women, (2) to assess, in this population, the discriminatory capacity of FRAX and bone mineral density (BMD) for the identification of women at high risk of fracture, and (3) to assess whether adding risk factors to either FRAX or BMD would improve discriminatory capacity. The study population included 2651 peri‐ and early postmenopausal women [mean age (± SD): 54 ± 4 years] with a mean follow‐up period of 13.4 years (±1.4 years). At baseline, a large set of CRFs was recorded, and vertebral BMD was measured (Lunar, DPX) in all women. Femoral neck BMD also was measured in 1399 women in addition to spine BMD. Women with current or past OP treatment for more than 3 months at baseline (n = 454) were excluded from the analyses. Over the follow‐up period, 415 women sustained a first low‐energy fracture, including 145 major OP fractures (108 wrist, 44 spine, 20 proximal humerus, and 13 hip). In Cox multivariate regression models, only 3 CRFs were significant predictors of a major OP fracture independent of BMD and age: a personal history of fracture, three or more pregnancies, and current postmenopausal hormone therapy. In the subsample of women who had a hip BMD measurement and who were not receiving OP therapy (including hormone‐replacement therapy) at baseline, mean FRAX value was 3.8% (±2.4%). The overall discriminative value for fracture, as measured by the area under the Receiver Operating Characteristic (ROC) curve (AUC), was equal to 0.63 [95% confidence interval (CI) 0.56–0.69] and 0.66 (95% CI 0.60–0.73), respectively, for FRAX and hip BMD. Sensitivity of both tools was low (ie, around 50% for 30% of the women classified as the highest risk). Adding parity to the predictive model including FRAX or using a simple risk score based on the best predictive model in our population did not significantly improve the discriminatory capacity over BMD alone. Only a limited number of clinical risk factors were found associated with the risk of major OP fracture in peri‐ and early postmenopausal women. In this population, the FRAX tool, like other risk scores combining CRFs to either BMD or FRAX, had a poor sensitivity for fracture prediction and did not significantly improve the discriminatory value of hip BMD alone.
Atherosclerosis | 1999
Florence Trémollières; Colette Cauneille; Claude Ribot
This study aimed to assess the relationship between menopause and various risk factors for coronary heart diseases (CHD) in a large sample of French women aged 45 65 years. One thousand six hundred and eighty-four consecutive healthy women who received a systematic check-up in our Menopause Unit were included in this study. All the women answered a computer-assisted questionnaire which comprised 156 items, 72 questions being exclusively related to the identification of familial and personal cardio-vascular risk factors. Biological measurements were performed to evaluate lipid-lipoprotein profile and fasting glucose levels. Women, none of whom were treated with hormonal replacement therapy, were classified as postmenopausal according to the date of their last menses and levels of serum FSH and estradiol (n = 1200). Perimenopausal women were further subdivided into two subgroups according to the regularity of their menstrual cycles and FSH levels (early (n = 143) and late (n = 341) perimenopause). 12% (n = 205) of the women were currently receiving lipid-lowering drugs (84.4% postmenopausal vs. 15.6% perimenopausal). When all women were considered, menopause was associated with a higher prevalence of hypertension and hypercholesterolemia (serum total cholesterol level > 250 mg/dl + LDL cholesterol level > 160 mg/dl). This higher prevalence in postmenopausal women was also found when the analysis was restricted to women aged 45 55 years, which rather suggests an effect of menopause than of age. Of the women not receiving hypolipidemic treatments, postmenopausal women had significantly higher serum levels of total cholesterol, LDL , VLDL cholesterol, triglycerides and apolipoprotein B and lower levels of HDL cholesterol than perimenopausal women. Multivariate analysis indicated that these effects were independent of age, body mass index and years since menopause. The prevalence of other metabolic disturbances was much more lower. On average, perimenopausal women had significantly less CHD risk factors than postmenopausal women (P < 0.0001). Fifty-two per cent of the perimenopausal women had none of the risk factors studied as compared with 39% of the postmenopausal women (P < 0.0001). This study shows that menopause was associated with a higher prevalence of risk factors for CHD.
Calcified Tissue International | 1993
Jean Michel Pouilles; Florence Trémollières; Claude Ribot
SummaryThe aim of our study was to compare the results provided by the measurement of vertebral and femoral bone mineral density (BMD) for assessing the individual risk of osteoporosis as defined by either low BMD and/or rapid bone loss. Vertebral and femoral BMD were measured twice at a mean interval of 21 months in 85 normal, early post-menopausal women who had passed a natural menopause 6 months to 3 years previously. According to the measurement site, 36% (spine), 29% (femoral neck), 35% (Wards triangle), and 25% (trochanter) fall in the “at risk” category, defined by a BMD value of 1 SD or more below the normal values for premenopausal women. Based on vertebral BMD, 39–48% of the women at risk had a normal femoral BMD. On the other hand, 24–37% of the women classified at risk based on femoral BMD maintained a low risk at the vertebral level. The annual rate of bone loss was significantly greater for the Wards triangle (-2.7±3.8%) and femoral neck (-2.1±2.5%) than for the spine (-1.5±2.1%) and trochanter (-1.5±3.4%). There was a significant relationship between the rate of loss measured at the spine and femoral levels (r=0.34–0.58). Among the 21 women with a rapid vertebral bone loss, 48–67% had a low bone loss at the femoral level and vice versa. The ratio between mean rate of loss and the precision of the measurement sites was greater for the spine (1.6) compared with the femur (1.1–0.71). Our results indicate that vertebral and femoral BMD measurements produce discordant results in assessing the individual risk for osteoporosis.
Clinical Rheumatology | 1994
Michel Laroche; Jean Michel Pouilles; Claude Ribot; P. Bendayan; J. J. Bernard; H. Boccalon; B. Mazieres
SummaryIn a previous study, the authors demonstrated that in 17 men with ischaemic atherosclerotic disease the bone mineral density (BMD) of the femoral neck was lower than in matched control subjects. The patients with arterial disease were thinner and were heavier smokers than the controls. Osteoporosis and arterial disease of the lower limbs were perhaps due to common risk factors: tobacco consumption and a low body build index. In order to demonstrate the direct effect of atherosclerosis on bone mineral content (BMC), the authors studied by dual-energy X-ray absorptiometry the BMC of both legs in 18 men presenting symptomatic arterial disease of the lower limbs quantified by measurement of distal systolic indexes by doppler ultrasonography.The mean BMC of the leg more severely affected by arterial disease was significantly lower than the mean BMC of the leg less affected by arterial disease (512±76 g versus 495±80 g: p=0.003). In 13 of the 18 patients, the BMC was lower in the leg more severely affected by arterial disease; in 4 of 18 the difference between the BMC of the left and right legs was less than 1%, and in a single patient the BMC was higher in the leg more affected by arterial disease.Arterial disease of the lower limbs could lead to bone mineral loss.
Osteoporosis International | 2001
Florence Trémollières; Claude Ribot
Abstract: This study aimed to assess the changes in vertebral bone mineral density (BMD) after cessation of hormone replacement therapy (HRT) in postmenopausal women who had been treated on a long-term basis. Fifty healthy postmenopausal women who had been followed both during the course of HRT and after cessation of treatment in our menopause clinic were included in this study. All women had started HRT within the first 3 years after the postmenopause and had received HRT (either 1.5 mg/day of 17β-estradiol given percutaneously or 50 μg/day of 17β-estradiol given as a transdermal patch, combined in all women with natural progesterone or a 19-norprogesterone derivative) for a mean 5 ± 2.4 years. In all women, vertebral BMD was assessed during the course of HRT up to the last 6 months before estrogen withdrawal, then at least once within the first 18 months after cessation of treatment. Of the initial population, 30 women were additionally reviewed later on and up to 8 years after cessation of treatment (mean duration of follow-up for the whole population: 3.9 ± 1.7 years). Rates of changes in vertebral BMD were compared with those determined in a group of healthy untreated women who had been followed within the first years of postmenopause during the same time period as the study population. In the study group, bone loss was found to accelerate within the first 2 years after HRT withdrawal and the annual rate of loss was identical to that which occurs within the first 2 years of postmenopause in untreated women (−1.64%± 1.3% vs −1.52 ± 0.9%, NS). Beyond this first 2-year time period, the annual rate of bone loss decreased as a function of time following cessation of treatment, as was observed following the menopause in untreated women (between 3 and 5 years: −0.83%+ 1.35% in the study group vs −0.70%± 0.8% in the control group, NS). On average, 3 years after cessation of HRT mean vertebral BMD when expressed as a Z-score was significantly higher (−0.13 vs −0.89, p<0.01) than at baseline, before HRT was started, which suggested a lasting beneficial effect on bone mass. However, even though our findings do not support the hypothesis that bone loss might continue to be accelerated several years after cessation of treatment we cannot fully address the question as to whether any residual benefit on bone mass over a longer period of time may be observed. In conclusion, the pattern of bone loss observed after cessation of estrogen therapy was found to be comparable to that which occurs in younger women within the first years after the menopause. Such a pattern needs to be kept in mind when the decision to stop HRT is taken, especially in women who were given HRT to prevent osteoporosis. The issue of assessing their risk of fracture several years after cessation of treatment thus needs to be addressed.
The American Journal of Medicine | 1995
Claude Ribot; Florence Trémollières
The magnitude of osteoporosis, the established relationship between low bone mass and the risk of fracture, and the availability of preventive treatment suggest that the early detection of women with low bone mass is justified. The feasibility of population screening using bone mass measurements remains controversial. Another approach is the use of clinical risk factors to detect women at high risk. However, several studies have demonstrated that the assessment of risk factor status does not appear to be an efficient tool for the identification of perimenopausal women with low bone mass. The poor performance of the prediction models might be explained in part by unmeasured factors, especially genetic factors, which are an important determinant of bone mass. On the other hand, the clinical usefulness of clinical risk factors needs to be more precisely evaluated, especially in the detection of women at high risk for hip fracture.
Advances in Nutritional Research | 1994
Claude Ribot; Florence Trémollières
There are many data indicating that osteoporotic fractures, and particularly hip fractures, are less frequent in obese subjects. Overweight and obese women have a higher bone mass after menopause than women of the same age who are not overweight, and thus in all probability have a slower bone loss. This protective effect appears to be related both to mechanical factors and to estrogen synthesis in adipose tissue.
Osteoporosis International | 1996
Florence Trémollières; Claude Ribot
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.