Search PubMed⌕ Search

Biomedical subjects

P Geusens

Publications and source records attributed to P Geusens.

At least 19 recordsLinked to original sources

Prevalence of rheumatic diseases in a rheumatological outpatient practice.

OBJECTIVE: To assess the prevalence and distribution of rheumatic diseases in a community based rheumatological outpatient practice. METHODS: Rheumatological diagnoses of 3751 consecutive new and returning patients were recorded using a standard diagnosis form. RESULTS: 6264 rheumatological diagnoses were made in 3751 patients, of whom 1097 were newly referred; 69% of all patients were female. Inflammatory joint and spine diseases were diagnosed in 42% of all patients (including 5% with connective tissue diseases), soft tissue rheumatism in 37%, degenerative joint and spine diseases in 36%, and metabolic bone diseases in 17% of all patients. In new patients soft tissue rheumatism was most prevalent (51%), 45% had osteoarthritis, 24% had inflammatory joint and spine disease (including 2% with connective tissue disease), and 13% had metabolic bone disease. One of 10 new patients was diagnosed with definite rheumatoid arthritis. In returning patients the prevalence of inflammatory rheumatic diseases was higher (49%, including 6% with connective tissue diseases). 28% of the returning patients had rheumatoid arthritis. Osteoarthritis was present in 33% and metabolic bone disease in 19% of the returning patients. CONCLUSIONS: Soft tissue rheumatism and degenerative joint and spine diseases are the most common rheumatological diagnoses in newly referred patients visiting a community based rheumatological outpatient practice. Inflammatory rheumatic diseases were most prevalent in returning patients.

Adolescent↗

Effect of risedronate on the risk of hip fracture in elderly women. Hip Intervention Program Study Group.

BACKGROUND: Risedronate increases bone mineral density in elderly women, but whether it prevents hip fracture is not known. METHODS: We studied 5445 women 70 to 79 years old who had osteoporosis (indicated by a T score for bone mineral density at the femoral neck that was more than 4 SD below the mean peak value in young adults [-4] or lower than -3 plus a nonskeletal risk factor for hip fracture, such as poor gait or a propensity to fall) and 3886 women at least 80 years old who had at least one nonskeletal risk factor for hip fracture or low bone mineral density at the femoral neck (T score, lower than -4 or lower than -3 plus a hip-axis length of 11.1 cm or greater). The women were randomly assigned to receive treatment with oral risedronate (2.5 or 5.0 mg daily) or placebo for three years. The primary end point was the occurrence of hip fracture. RESULTS: Overall, the incidence of hip fracture among all the women assigned to risedronate was 2.8 percent, as compared with 3.9 percent among those assigned to placebo (relative risk, 0.7; 95 percent confidence interval, 0.6 to 0.9; P=0.02). In the group of women with osteoporosis (those 70 to 79 years old), the incidence of hip fracture among those assigned to risedronate was 1.9 percent, as compared with 3.2 percent among those assigned to placebo (relative risk, 0.6; 95 percent confidence interval, 0.4 to 0.9; P=0.009). In the group of women selected primarily on the basis of nonskeletal risk factors (those at least 80 years of age), the incidence of hip fracture was 4.2 percent among those assigned to risedronate and 5.1 percent among those assigned to placebo (P=0.35). CONCLUSIONS: Risedronate significantly reduces the risk of hip fracture among elderly women with confirmed osteoporosis but not among elderly women selected primarily on the basis of risk factors other than low bone mineral density.

Aged↗

Risk of new vertebral fracture in the year following a fracture.

CONTEXT: Vertebral fractures significantly increase lifetime risk of future fractures, but risk of further vertebral fractures in the period immediately following a vertebral fracture has not been evaluated. OBJECTIVE: To determine the incidence of further vertebral fracture in the year following a vertebral fracture. DESIGN AND SETTING: Analysis of data from 4 large 3-year osteoporosis treatment trials conducted at 373 study centers in North America, Europe, Australia, and New Zealand from November 1993 to April 1998. SUBJECTS: Postmenopausal women who had been randomized to a placebo group and for whom vertebral fracture status was known at entry (n = 2725). MAIN OUTCOME MEASURE: Occurrence of radiographically identified vertebral fracture during the year following an incident vertebral fracture. RESULTS: Subjects were a mean age of 74 years and had a mean of 28 years since menopause. The cumulative incidence of new vertebral fractures in the first year was 6.6%. Presence of 1 or more vertebral fractures at baseline increased risk of sustaining a vertebral fracture by 5-fold during the initial year of the study compared with the incidence in subjects without prevalent vertebral fractures at baseline (relative risk [RR], 5.1; 95% confidence interval [CI], 3.1-8.4; P<.001). Among the 381 participants who developed an incident vertebral fracture, the incidence of a new vertebral fracture in the subsequent year was 19.2% (95% CI, 13.6%-24.8%). This risk was also increased in the presence of prevalent vertebral fractures (RR, 9.3; 95% CI, 1.2-71.6; P =.03). CONCLUSION: Our data indicate that women who develop a vertebral fracture are at substantial risk for additional fracture within the next year.

Aged↗

Comparison of bone and total alkaline phosphatase and bone mineral density in postmenopausal osteoporotic women treated with alendronate.

Alendronate therapy in osteoporotic women decreases bone turnover and increases bone mineral density (BMD). Optimal patient management should include verification that each patient is responding to therapy. Markers of bone turnover and BMD have both been proposed for this purpose. We have investigated changes resulting from alendronate therapy with an enzyme immunoassay for bone alkaline phosphatase (BAP) and compared it with total alkaline phosphatase (TAP) and BMD of the lumbar spine, hip, and total body. Subjects were drawn from a multicenter randomized, placebo-controlled trial of alendronate in postmenopausal women with osteoporosis. BAP and TAP levels were measured at baseline and following 3, 6 and 12 months of therapy with either placebo (n = 180) or alendronate 10 mg/day (n = 134). All subjects also received 500 mg/day supplemental calcium. BMD was measured at baseline and following 3, 6, 12, 18, 24 and 36 months of therapy. To compare BAP, TAP and BMD at each site for identifying women that experienced a skeletal effect of alendronate, we calculated least significant change (LSC) values from the long-term intraindividual variability in each placebo-treated woman. Median levels of BAP decreased by 34%, 44% and 43% at 3, 6 and 12 months, respectively, in alendronate-treated women (p < 0.0001 compared with baseline and with placebo). These changes were significantly greater (p < 0.0001) than changes observed for TAP. Following 6 months of alendronate therapy, 90% of the women had experienced a decrease in BAP exceeding the LSC compared with only 71% for TAP. The greatest number of women similarly identified with BMD at any site (i.e. a gain in BMD exceeding the LSC) was 81% for spinal BMD at 36 months. All other sites were less than 70% at 36 months. Short-term changes in BAP and TAP were modestly associated with subsequent changes in BMD at all sites (Spearman's rho -0.22 to -0.52, p < 0.05). Compared with TAP and BMD, BAP testing rapidly and sensitively identified skeletal effects of alendronate thus enabling appropriate drug monitoring of osteoporotic women. Though BAP and TAP changes were modestly predictive of BMD changes, the value of the bone marker tests is their ability to detect rapidly a skeletal effect of therapy.

Aged↗

The autoimmune pathogenesis of rheumatoid arthritis: role of autoreactive T cells and new immunotherapies.

OBJECTIVES: To review the role of T lymphocytes in the pathogenesis of rheumatoid arthritis (RA) and discuss the relevance of the components of the trimolecular complex (synovial T cells, autoantigens, and antigen presenting cells) in the pathogenic autoimmune response in RA. METHODS: Currently available experimental data are combined into a hypothetical pathway that may explain some of the events in the RA process. The literature regarding the potential therapeutic strategies that interfere with specific components of the trimolecular complex and other mediators are discussed briefly. RESULTS: T cells are activated in the peripheral blood, cross the endothelial cell wall, and migrate into the joints. Once in the synovial joints, T cells are reactivated by cross-reactive antigens and clonally expand. Clonally expanded T cells accumulate in the diseased joint and secrete proinflammatory cytokines that attract and activate other cells, such as monocytes and macrophages. Treatment with anti-CD4 monoclonal antibodies or anticytokine agents that prevents antigen presentation and/or T-cell activation were effective in RA. Other therapies, such as T-cell vaccination and T-cell receptor peptide vaccination targeting autoreactive T cells, showed clinical improvement, suggesting a pathogenic role of these lymphocytes in disease progression. CONCLUSION: T cells appear to be actively involved in the pathogenesis of RA, but several parts of the pathway are hypothetical and further research is needed.

Arthritis, Rheumatoid↗

Bone turnover, joint damage and bone mineral density in early rheumatoid arthritis treated with combination therapy including high-dose prednisolone.

OBJECTIVES: Exploration of bone metabolism changes at different levels of disease activity, both with and without oral corticosteroid therapy, and prediction of changes in joint damage and bone density from the observed changes in markers of bone turnover. METHODS: Data analysis from a randomized clinical trial with 155 rheumatoid arthritis (RA) patients; median age 50 yr, early and active disease (diagnosis < 2 yr); one group treated with a combination of sulphasalazine (SSZ; 2000 mg/day), methotrexate (MTX; 7.5 mg/week) and prednisolone (initially 60 mg/day, tapered in six weekly steps to 7.5 mg/day), the other group with SSZ alone. Prednisolone and MTX were tapered and stopped after weeks 28 and 40, respectively, while SSZ was continued. Urine and serum samples were collected at baseline and weeks 16, 28, 40 and 56. Measurements of urinary pyridinoline (PYD) and deoxypyridinoline (DPD) and serum alkaline phosphatase (tAP) and osteocalcin (OC) were performed, as well as standard clinimetry and bone densitometry. RESULTS: Over time and in both treatment groups, bone formation and bone resorption markers showed a pattern similar to erythrocyte sedimentation rate (ESR): a significant decrease compared with baseline and a larger decrease with combined treatment at weeks 16 and 28. PYD excretion, tAP, OC, and joint damage scores were significantly lower in the combined treatment group. Changes in bone density (of spine and hips) did not significantly differ between treatment groups. Mainly cumulative ESR explained progression of joint damage. CONCLUSIONS: Prednisolone and disease-modifying anti-rheumatic drug therapy in patients with early and active RA are both independently associated with decreased levels of urinary excretion of bone collagen resorption markers PYD and DPD. Markers of bone formation and resorption closely followed changes in ESR in both treatment groups. Reduced bone resorption together with reduced bone formation-initially at a somewhat faster pace-resulted in less bone turnover and explain the observed (non-significant and partially reversible) extra bone loss in the lumbar spine associated with prednisolone (combined treatment).

Adult↗

Recovery from severe glucocorticoid-induced osteoporosis in an adolescent boy.

An 18-yr-old boy presented with extreme back pain as the result of multiple vertebral fractures. At age 16 he had developed a tumor of the mesencephalon. A ventriculoperitoneal shunt was established surgically. One year later, he developed progressive neurologic deficits in his upper and lower limbs with an increase in the size of the tumor. He was treated by irradiation and high doses of glucocorticoids. Although the neurologic deficits progressively improved, he developed severe back pain resulting in complete immobilization for 3 mo in spite of neurologic recovery. Multiple vertebral fractures were diagnosed by X-ray. Bone density was extremely low (Z-score of -5.5 in the spine and -3.1 in the femoral neck). The patient was treated with calcium and vitamin D, calcitonin, bisphosphonates, physiotherapy, and progressive mobilization. Glucocorticoids were decreased and could be stopped as the neurologic deficits fully recovered. After 1 yr of treatment with intermittent i.v. pamidronate, bone density had increased by 40% in the spine and by 25% in the femoral neck despite growth arrest. He progressively recovered from back pain and is now, at age 20, fully ambulant, studying mechanical engineering, without neurologic sequelaes and free of glucocorticoids. Magnetic resonance imaging revealed that the tumor had disappeared. This case proves that treatment of symptomatic glucocorticoid-induced osteoporosis during puberty can be rewarding, even when multiple and invalidating vertebral fractures already exist.

Adolescent↗

Review of risedronate in the treatment of osteoporosis.

Risedronate (Actonel, Procter & Gamble and Aventis) is a novel, orally administered pyridinyl bisphosphonate. Preclinical studies have shown that risedronate is a potent inhibitor of osteoclasts. Risedronate inhibited bone resorption and increased bone density in the spine and hip. Prospective, randomised, placebo-controlled trials (RCTs) in patients with postmenopausal osteoporosis (PMO) have demonstrated that risedronate decreased the risk of vertebral fractures by up to 49% and of non-vertebral fractures by up to 39% over 3 years in postmenopausal women with one or more prevalent vertebral fractures. This reduction of the risk for vertebral fractures was significant from the first year of treatment (risk reduction up to 65%). Risedronate was the first bisphosphonate to be studied in a large RCT with prevention of hip fracture as the primary end point. In this study, risedronate reduced the risk of hip fracture by 40% in elderly women with low hip bone density and one clinical risk factor for hip fracture and by 60% in women with low bone density and a prevalent vertebral fracture at baseline. Risedronate was also effective in the prevention and treatment of bone loss in glucocorticoid-induced osteoporosis (GIO), with a positive effect on vertebral fractures within the first year. Risedronate was well-tolerated with a safety profile comparable to placebo in all clinical studies. Patients with a previous or current history of upper GI illness or who were taking NSAIDs or aspirin were not excluded from these studies. Importantly, the upper GI safety profile of risedronate was shown to be similar to that of placebo in endoscopic studies. There was no evidence of acute-phase reactions or primary mineralisation defects. The most appropriate dose of risedronate was 5 mg/day.

Clinical Trials, Phase III as Topic↗

High prevalence of thoracic vertebral deformities and discal wedging in ankylosing spondylitis patients with hyperkyphosis.

OBJECTIVE: To study the prevalence of deformities of vertebrae and intervertebral discs in patients with ankylosing spondylitis (AS) in relation to fixed hyperkyphosis of the spine. METHODS: Altogether 50 patients (15 women, 35 men) with AS were studied. Hyperkyphosis was measured by the occiput to wall distance (OWD). Anterior (Ha), mid- (Hm), and posterior height (Hp) of the vertebrae and intervertebral discs were measured on lateral radiographs of the thoracic (Th5-Th12) and lumbar spine (L1-L5). Vertebral shapes were analyzed according to McCloskey, et al. Wedging of discs was calculated as Ha/Hp. Hyperkyphosis was defined as OWD > 1 cm. RESULTS: In the thoracic spine, the prevalence of vertebral deformities was higher in patients with hyperkyphosis (n = 38) compared to patients without hyperkyphosis (n = 12) (45% vs 8%; p = 0.01). The prevalence of thoracic vertebral deformities in patients with hyperkyphosis differed little between men and women (39% vs 58%; p > 0.10) and among patients above and below the age of 45 years (50% vs 33%; p > 0.10). Patients with one or more deformed thoracic vertebrae had a higher mean OWD than patients without deformed vertebrae (12 +/- 7 vs 7 +/- 6 cm; p < 0.01). The total sum of deformities of the thoracic vertebrae and discs explained 43% of the variance of the age adjusted OWD (p < 0.001). Deformities of lumbar vertebrae and discs did not contribute to hyperkyphosis. CONCLUSION: In patients with AS and hyperkyphosis, deformities of the thoracic vertebrae occur frequently and, together with wedging of the thoracic discs, contribute significantly to fixed hyperkyphosis of the spine.

Adult↗

Algodystrophy.

Algodystrophy is a clinical syndrome characterized by intense locoregional pain, vasomotor and trophic changes and delayed recovery, mostly occurring after trauma or surgery. The variety of nomenclature reflects the spectrum of clinical presentations and the uncertain pathophysiology. Although most patients recover, it can result in persistent disability in some patients. The diagnosis is based mostly on clinical signs. The specificity and sensitivity of additional technical investigations, such as radionuclide scintigraphy and X-ray, is variable. Algodystrophy progresses in several stages, from an inflammation-like clinical picture to recovery or sequels. The management is mainly supportive and can be difficult in some patients, especially in persistent chronic cases or when recognized at a late stage. Management is based on the results of limited prospective controlled studies. There is a need for a better understanding of the pathophysiology and for prospective clinical studies about the natural course and the effect of treatment.

Bone and Bones↗

Skewed T-cell receptor variable gene usage in the synovium of early and chronic rheumatoid arthritis patients and persistence of clonally expanded T cells in a chronic patient.

OBJECTIVE: Autoreactive T cells may contribute to the pathogenesis of rheumatoid arthritis (RA). We studied the T-cell receptor (TCR) V-gene repertoire in the blood and synovium of early and chronic RA patients using polymerase chain reaction-enzyme-linked immunosorbent assay to evaluate possible differences between these patient groups. RESULTS: Over-represented TCR V genes were observed in the synovium, but not in the blood of all RA patients (n = 38). The number of over-represented V genes was higher in the synovium of chronic RA patients (n = 31) than in that of early RA patients (n = 7). The V-gene profile was different among patients, and similar in the two knees for patients with bilateral synovitis (n = 5). The clonal composition of over-represented TCR BV genes in a patient with early RA and a patient with chronic RA was further studied by CDR3 region sequence analysis. A high level of clonal diversity was found in the joints and the blood of the early RA patient, suggesting a polyclonal T-cell expansion. In the chronic RA patient, predominant clonal expansions were observed in the blood and synovium, and some expanded clones were still present 2 yr later. CONCLUSIONS: The observation of similar T-cell populations in both joints in patients with bilateral synovitis and the persistence of clonally expanded T cells for more than 2 yr in the joints of a chronic RA patient may indicate a pathogenic role for these cells in the disease process.

Amino Acid Sequence↗

Influence of physical mobility and season on 25-hydroxyvitamin D-parathyroid hormone interaction and bone remodelling in the elderly.

OBJECTIVE: To investigate influences of physical mobility and season on 25-hydroxyvitamin D-intact parathyroid hormone (iPTH) interaction in the elderly. DESIGN: We examined 188 frail institutionalized elderly at the expected nadir of their serum vitamin D concentrations (winter). This group was compared with 309 healthy ambulatory elderly at the expected time of maximum vitamin D repletion (summer), to accentuate the influences of season and physical activity. METHODS: Serum concentrations of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, iPTH and urinary deoxypyridinoline (DPD) were measured. RESULTS: Vitamin D metabolites were significantly lower in the institutionalized elderly (P<0.0001), with an 82.5% prevalence of vitamin D deficiency (25-hydroxyvitamin D <12ng/ml) in institutionalized elderly in wintertime and 15.5% in ambulatory elderly in summertime. Overall, median iPTH did not differ between groups. However, median iPTH secretion in the presence of low vitamin D serum concentrations (5-30ng/ml) was greater in ambulatory elderly. This could be explained by lower mobility status being correlated with greater serum calcium concentrations (r=0.24, P=0.02 in women; r=0.35, P=0. 001 in men) and greater urinary excretion of DPD (r=0.41, P=0.0001 in women; r=0.42, P=0.0002 in men), independent of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and iPTH. CONCLUSIONS: These data support the hypothesis that immobility, even in the presence of vitamin D deficiency, acts as an overriding influence on bone metabolism by promoting bone resorption (measured as urinary DPD) and increasing serum calcium independent of iPTH. Therefore mobility status may substantially affect 25-hydroxyvitamin D threshold values and the degree to which patients benefit from vitamin supplementation.

Aged↗

A pooled data analysis on the use of intermittent cyclical etidronate therapy for the prevention and treatment of corticosteroid induced bone loss.

OBJECTIVE: To conduct a pooled data analysis in a group of patients defined by sex, menopausal status, and underlying disease in order to examine the effect of intermittent cyclical etidronate in the prevention and treatment of corticosteroid induced osteoporosis. METHODS: We selected 5 randomized, placebo controlled studies that examined the efficacy of intermittent cyclical etidronate therapy in which the raw data were available for analysis. Three were prevention studies and 2 treatment studies. The primary outcome was the difference between treatment groups in the percentage change from baseline in lumbar spine bone density. Secondary outcomes included the difference between treatment groups in the percentage change from baseline in femoral neck and trochanter bone density, and vertebral fracture rates. RESULTS: Results are separately pooled for the prevention and treatment studies. The prevention studies had significant mean differences (95% CI) between groups in mean percentage change from baseline in lumbar spine, femoral neck, and trochanter bone density of 3.7 (2.6 to 4.7), 1.7 (0.4 to 2.9), and 2.8% (1.3 to 4.2) after one year of treatment, in favor of the etidronate group. The treatment studies displayed a mean difference between groups in mean percentage change from baseline in lumbar spine bone density of 4.8 (2.7 to 6.9) and 5.4% (2.5 to 8.4) after one and 2 years of therapy. In the prevention studies, a reduced fracture incidence was observed in the etidronate group compared with the placebo group (relative risk 0.50; CI 0.21 to 1.19). CONCLUSION: Etidronate therapy was effective in preventing bone loss in the prevention studies and in preventing or slightly increasing bone mass in the treatment studies. A fracture benefit was observed in postmenopausal women treated with etidronate in the prevention studies.

Adult↗

Identification of overrepresented T cell receptor genes in blood and tissue biopsies by PCR-ELISA.

The analysis of T cell receptor variable (TCR V) gene repertoires in blood or tissues may provide important information when studying immunopathological mechanisms. The overexpression of a TCR gene may indicate the expansion of the corresponding T cell subset. In autoimmune diseases, clonally expanded T cell subsets in the affected organs may represent pathogenic lymphocytes. We describe a simple, rapid and sensitive method to determine the TCR AV and BV gene repertoire using a PCR-ELISA method. RNA is extracted from lymphocytes, transcribed to cDNA, which is then used as a template for PCR with 19 different TCR AV gene and 20 BV gene specific primers as the forward primer, and a digoxigenin (DIG) labeled AC/BC primer as the reverse primer. The DIG labeled PCR amplicons are hybridized with a fluorescein isothiocyanate (FITC) labeled TCR C region specific probe. Finally, the amplicons are quantified by ELISA using anti-FITC coated microtiter plates, and an anti-DIG conjugated peroxidase. Although PCR-ELISA cannot accurately quantify the expression level of a given TCR gene, overrepresented TCR V genes are easily identified by comparing the relative expression levels of each individual V gene in the total V gene repertoire. We demonstrate that this technique can be used to determine TCR profiles in blood and tissue samples containing as few as 50,000 T cells. In combination with CDR3 fragment size analysis, this method is an efficient tool to identify clonally expanded T cell subsets in the synovial biopsies of rheumatoid arthritis patients.

Arthritis, Rheumatoid↗

Perspectives on bone mechanical properties and adaptive response to mechanical challenge.

The bones of the human skeleton serve a mechanical function besides providing a reservoir for calcium and hematopoietic homeostatis. When mechanically challenged, they usually respond and adapt; failure to do so can result in fracture. The mechanical behavior of bone is determined by bone mass and its material properties and by its geometry and architecture. Therefore, in vivo noninvasive measurements of bone mass, geometry, and structure can predict bone strength and are usually employed as a useful-if not always reliable-way to estimate bone fragility, whereas direct bone biomechanical testing in vitro can provide detailed information about mechanical strength. Because bone strains are likely to be regulators of bone mass and strength, exercise protocols designed to counteract the effects of osteoporosis should load the target bone with repeated high peak forces and high strain rates or high impacts on a long-term basis. Such a protocol creates varied strain distributions throughout the bone structure, producing short, repeated strains on the bone in directions to which it is unaccustomed. Exercise in this manner can maintain and perhaps increase bone mass and improve mechanical properties and neuromuscular competency, reducing skeletal fragility and the predisposition to falls.

Adaptation, Physiological↗

Lack of association between estrogen receptor genotypes and bone mineral density, fracture history, or muscle strength in elderly women.

The PvuII polymorphism of the estrogen receptor (ESR) gene and its relation to bone mineral density (BMD), fracture history, and muscle strength was studied in 313 postmenopausal (76 +/- 5 years) women of Caucasian origin, of whom 142 had suffered from a fragility fracture after the age of 50 years (14 with fracture of the hip, 38 of the spine, 45 of the wrist, and 85 of other bones). The ESR genotype distribution was similar in women with and without a history of fragility fracture (PP 21%, Pp 43%, pp 36% compared with PP 18%, Pp 47%, pp 35%). We did not find a correlation between the ESR genotypes and BMD at the lumbar spine, the femoral neck, or the proximal forearm. No association was found with grip or quadriceps strength. We further evaluated the relationship between the vitamin D receptor (VDR) and ESR haplotypes and BMD in a random subgroup of 270 elderly women. No differences were found in women with the BBpp versus the bbPP haplotype in the femoral neck (mean difference +/- SD, in Bbpp compared with bbPP groups: -0.05 +/- 0.15 g/cm2), the spine (0.01 +/- 0.13 g/cm2), or the forearm (0.04 +/- 0.08 g/cm2). The significant association of quadriceps strength with VDR genotypes (25% lower in BB compared with bb genotype, p < 0.05) was not influenced by ESR haplotypes. We conclude that in elderly Caucasian women the PvuII ESR polymorphism is not associated with osteoporosis, fracture history, nor muscle strength and does not influence the association of bone density and muscle strength with polymorphism of the VDR.

Aged↗

Bone mineral density and biomechanical properties of spine and femur of ovariectomized rats treated with naproxen.

Prostaglandins have been reported to mediate the effects of ovariectomy on bone loss. We studied the effect of naproxen, an inhibitor of production of prostaglandins, on ovariectomy-induced bone loss. One hundred forty female Wistar rats 4.5 months of age were divided into groups of baseline, sham operation (sham), sham treated with naproxen at 10 mg/kg per day (in food), and ovariectomy treated with naproxen or estrogen as intramuscular injection of estradiol at 0.2 mg/kg body weight per week. They were killed 3, 6, and 9 months postsurgery. Bone mineral density (BMD) of the lumbar spine (L1-4), femoral neck, midshaft, and distal metaphysis was determined using dual-energy X-ray absorptiometry (DXA) in vitro. The compressive test of the L1 vertebral body and torsional test of the left femur were performed. The right femoral neck and femoral midshaft were processed undecalcified for determining cross-sectional moments of inertia. Naproxen treatment partially prevented ovariectomy-induced loss or less gain in BMD, in a significant manner, in the femoral neck cortical area, and also in L1 compressive strength and stiffness. Estrogen fully prevented these ovariectomy-induced effects. Naproxen showed no effect on ovariectomy-induced improvement in femoral torsional strength and stiffness and cross-sectional moments of inertia. No statistically significant difference was found between naproxen-treated sham rats and untreated sham rats. The data suggest that naproxen partially prevents ovariectomy-induced osteopenia.

Absorptiometry, Photon↗

Cyclical etidronate increases bone density in the spine and hip of postmenopausal women receiving long term corticosteroid treatment. A double blind, randomised placebo controlled study.

OBJECTIVE: To study the effect of cyclic etidronate in secondary prevention of corticosteroid induced osteoporosis. METHODS: A double blind, randomised placebo controlled study comparing cyclic etidronate and placebo during two years in 37 postmenopausal women receiving long term corticosteroid treatment, mainly for polymyalgia rheumatica (40% of the patients) and rheumatoid arthritis (30%). Bone density was measured in the lumbar spine, femoral neck, and femoral trochanter. RESULTS: After two years of treatment there was a significant difference between the groups in mean per cent change from baseline in bone density in the spine in favour of etidronate (p = 0.003). The estimated treatment difference (mean (SD)) was 9.3 (2.1)%. Etidronate increased bone density in the spine (4.9 (2.1)%, p < 0.05) whereas the placebo group lost bone (-2.4 (1.6)%). At the femoral neck there was an estimated difference of 5.3 (2.6)% between the groups (etidronate: 3.6% (1.4)%, p < 0.05, placebo: -2.4 (2.1)%). The estimated difference at the trochanter was 8.2 (3.0) (etidronate: 9.0 (1.5)%, p < 0.0001, placebo: 0.5 (2.3)%). No significant bone loss occurred in the hip in placebo treated patients. CONCLUSIONS: Cyclic etidronate is an effective treatment for postmenopausal women receiving corticosteroid treatment and is well tolerated.

Aged↗