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Biomedical subjects

C Ribot

Publications and source records attributed to C Ribot.

At least 19 recordsLinked to original sources
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↗
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

Can we detect women with low bone mass using clinical risk factors?

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.

Bone Density↗
PubMed1995

Effect of menopause on femoral and vertebral bone loss.

The aim of this study was to investigate the effect of menopause on bone loss in the proximal femur and the lumbar spine. The rates of change in bone mineral density (BMD) were measured longitudinally by dual X-ray absorptiometry (DXA) at the femoral neck (FN), Ward's triangle (WT), and trochanter (TR) together with the lumbar spine in 81 healthy postmenopausal women (45-65 years of age) who had passed a natural menopause, 6 months to 12 years before. A significant correlation between the rate of change and interval since menopause was evidenced. The best fit of the data was a binomial function of interval since menopause at the spine, FN, and WT and a simple linear regression at TR level. At each skeletal site, the rate of bone loss (mean +/- SD) was significantly different (p<0.05) and twice as high in women who were between 6 months and 2 years postmenopausal at enrollment (FN, -1.82 +/- 1.1%; WT, -2.43 +/- 1.7%; TR, -1.12 +/- 1.7%) than in those who were beyond 5 years of menopause (FN, -0.48 +/- 0.8%; WT, -0.68 +/- 2.1% TR, 0.41 +/- 1.2%). A poor correlation (r = 0.39 - 0.42, p<0.001) was found between the rate of vertebral and that of femoral postmenopausal bone loss. This study demonstrates that menopause is associated with a rapid and transient bone loss in BMD of the proximal femur, which declines with time after 3 years. These data suggest that therapy should be initiated as early as possible after menopause to prevent bone loss.

Absorptiometry, Photon↗
PubMed1995

[Sex steroids and bone tissue].

The precise mechanism of action of sexual steroids in the regulation of bone tissue is still poorly understood. Besides the indirect action via the production of calciotropic hormones, the fact that receptors respond to oestrogens as well as to androgens and progesterone is evidence that sexual steroids have a direct action in regulating bone activity. The anti-osteoclastic action of oestrogens, via the modulation in osteoblastic production of different substances such as interleukin-1 and -6, TGF beta, GM-CSF which inhibit osteoclastogenesis and bone resorption activity, is well documented. More recently, the direct role in osteoclast inhibition was suggested by the observation that osteoclasts carry oestrogen receptors. Likewise, certain in vivo and in vitro data suggest that oestrogens could also have a positive effect on bone formation regulation. For androgens, currently available data show that in vitro stimulation of bone formation, with increased proliferation and cell differentiation, could be mediated by TGF beta. The role of progesterone is more recently known. In vivo, progesterone increases cell growth and IFGF-II secretion by non-transformed human osteoblasts. The number of potential mechanisms which have already been demonstrated suggest the complexity of sex hormone regulation which leads to the final situation of physiological calcium sparing in the skeleton while maintaining skeletal structure.

Bone and Bones↗
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↗
PubMed1994

Influence of early age at menopause on vertebral bone mass.

Menopause leads to rapid bone loss, mainly as a result of estrogen deficiency superimposed on the age-related linear bone loss. The influence of age at menopause on bone loss is unclear, although early menopause is widely considered a risk factor for osteoporosis. Vertebral bone mineral density (BMD) was measured in 1667 women divided into five groups according to hormonal status and age at menopause. Menopausal status was an independent predictor of BMD in a multiregression analysis, along with current age, years since menopause (YSM), weight, and height. For the same chronologic age (55 years), women with early menopause had a 15% lower BMD and a higher YSM than women whose menopause occurred later ("normal" menopause). After adjusting for the interval since menopause, postmenopausal women with early menopause were found to have lower vertebral BMD than postmenopausal women with normal menopause. Finally, after the age of 60, 66% of the women with early menopause had a BMD that was below the fracture threshold compared to 18% of the women with normal menopause. The results of this cross-sectional study suggest that early menopause is associated with a quantitatively higher bone loss than in women with menopause of later onset and thus constitutes a risk factor for osteoporosis.

Absorptiometry, Photon↗
PubMed1994

The effect of obesity on postmenopausal bone loss and the risk of osteoporosis.

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.

Adult↗
PubMed1994

Comparison of the bone mineral content of the lower limbs in men with ischaemic atherosclerotic disease.

In 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.

Adult↗
PubMed1994

[Autocrine regulation of cell proliferation and secretion of insulin-like growth factor I (IGF-I) in osteoblastic cell line MC3T3-E1].

Bone cells maintained in culture produce different growth factors which modulate cell growth via a mechanism of auto/paracrine regulation. IGF-1 is abundantly produced by murine bone cells where it acts as a mitogenic agent. The aim of this work was to study the effect of IGF-II, TGF beta 1, basic FGF (FGFb) and PDGF on cell growth and production of IGF-1 in the murine osteoblastic clonal cell line MC3T3-E1. IGF-1 was assayed by RIA after elimination of the IGF binding proteins. After 24th of treatment in culture conditions without serum, incorporation of [3H] methylthymidine increased significantly in MC3T3-E1 treated with IGF-II, FGFb and PDGF. The effect was dose-dependent. At low cell density (2.5 X 10(4) cemm/cm2) and after 24 h treatment, IGF-II at 10 ng/ml led to a 220% increase in IGF-I production in MC3T3-E1 cells (9.5 +/- 1.5 vs 4.2 +/- 0.44 ng/micrograms protein, p < 0.001) while TGF beta 1, FGFb and PDGF at 1 ng/ml led to a significant decrease (65, 95 and 85% respectively) in IGF-I (TGF beta 1: 1.5 +/- 0.3 ng/micrograms; FGBb: 0.21 +/- 0.04 ng/micrograms; PDGF: 0.66 +/- 0.1 ng/micrograms; p < 0.001). Production of IGF-I was controlled by a dose-dependent relationship and varied as a function of incubation time and cell density. IGF-II led to an increase in mRNA coding for IGF-1 as early as the first hour after IGF-II addition with a maximal effect at 6 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Estrogens, progestins and the bone].

Estrogens are the most effective agents in the prevention of post-menopausal osteoporosis, as witnessed by numerous epidemiological and clinical studies. They inhibit bone resorption by complex mechanisms, modulating the action of calciotropic hormones and facilitating the production by bone cells of proteinic factors (cytokines, bone growth factor). Recent studies suggest that estrogens might also stimulate bone formation directly. Moreover, synthetic progestins are thought to have a trophic effect on bone tissue. The effectiveness and excellent metabolic tolerance of the available compounds should widen the indications of replacement therapy in postmenopause.

Drug Therapy, Combination↗
PubMed1993

The effects of menopause on longitudinal bone loss from the spine.

Two 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 17 beta 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.

Absorptiometry, Photon↗
PubMed1993

Spine and femur densitometry at the menopause: are both sites necessary in the assessment of the risk of osteoporosis?

The 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 postmenopausal women who had passed a natural menopause 6 months to 3 years previously. According to the measurement site, 36% (spine), 29% (femoral neck), 35% (Ward's 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 Ward's 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).(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1993

Risk factors for hip fracture. MEDOS study: results of the Toulouse Centre.

The development of preventive strategies for hip fractures requires better identification of risk factors. The MEDOS study was designed to study prospectively the incidence of hip fracture in 14 centres from six countries and characterise risk factors. At one centre (Toulouse), data were gathered from questionnaires completed by 386 cases of hip fracture aged over 50 years and 848 age- and sex-matched controls over a 12-month period. Of the 935 variables of the MEDOS questionnaire, 235, grouped into 56 items, were statistically analysed. Odds ratios (and 95% confidence intervals) were estimated for each variable from a multiple stepwise logistic regression model. The population comprised 19.2% men and 80.8% women, with a mean age of 80 +/- 8.8 years; 80% were living in an urban area and 76% with their family. Of the 17 significant variables, moderate excess weight and a high nutritional intake of calcium were associated with a decreased risk of hip fracture. Loss of autonomy, a higher height than normal (> 1SD), and a history of previous fractures significantly increased the risk of fracture. Interestingly, all these variables accounted for only 18% of the risk of hip fracture.

Aged↗