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Biomedical subjects

D Vanderschueren

Publications and source records attributed to D Vanderschueren.

At least 19 recordsLinked to original sources
PubMed2006

Calcium and vitamin D in the prevention and treatment of osteoporosis - a clinical update.

Combined calcium and vitamin D supplementation is an essential component of the management of osteoporosis, supported by a strong scientific rationale. The types of individuals who should receive calcium and vitamin D supplements are those: (i) patients with documented osteoporosis receiving antiresorptive or anabolic treatment; (ii) patients receiving glucocorticoids; and (iii) individuals with or at high risk of calcium and/or vitamin D insufficiencies, in particular older women and men. This article describes the evidence base that supports targeting these groups. Benefits are most apparent when 800 IU day(-1) vitamin D is complemented with a dose of 1000-1200 mg day(-1) elemental calcium. Compliance is also key to optimizing clinical efficacy.

Aged↗
PubMed2005

Liver-derived IGF-I is permissive for ovariectomy-induced trabecular bone loss.

INTRODUCTION: Estrogen deficiency results in trabecular bone loss, associated with T-cell proliferation in the bone marrow. Insulin-like growth factor I (IGF-I) is involved in the regulation of both bone metabolism and lymphopoiesis. A major part of serum IGF-I is derived from the liver. The aim of the present study was to investigate the role of liver-derived IGF-I for ovariectomy (ovx)-induced trabecular bone loss. MATERIALS AND METHODS: Mice with adult liver-specific IGF-I inactivation (LI-IGF-I-/-) and wild type mice (WT) were either ovx or sham operated. After 5 weeks, the skeletal phenotype was analyzed by pQCT and microCT. The bone marrow cellularity was analyzed using FACS technique, and mRNA levels were quantified using real-time PCR. RESULTS: Ovx resulted in a pronounced reduction in trabecular bone mineral density (-52%, P < 0.001), number (-45%, P < 0.01) and thickness (-13%, P < 0.01) in WT mice while these bone parameters were unaffected by ovx in LI-IGF-I-/- mice. Furthermore, ovx increased the number of T-cells in the bone marrow of the femur in WT but not in LI-IGF-I-/- mice. Interleukin 7 (IL-7) has been reported to stimulate the formation and function of osteoclasts by inducing the expression of receptor activator of NF-kappaB ligand (RANKL) on T-cells. IL-7 mRNA levels and the RANKL/osteoprotegerin ratio in bone were increased by ovx in WT but not in LI-IGF-I-/- mice. CONCLUSIONS: Liver-derived IGF-I is permissive for ovx-induced trabecular bone loss. Our studies indicate that IGF-I might exert this permissive action by modulation of the number of T-cells and the expression of IL-7, which in turn is of importance for the RANKL/OPG ratio and consequently osteoclastogenesis in the bone marrow.

Acid Phosphatase↗
PubMed2005

Androgens and the skeleton.

Loss of estrogens or androgens causes bone loss by increasing the rate of bone remodeling, and also causes an imbalance between resorption and formation by prolonging the lifespan of osteoclasts and shortening the lifespan of osteoblasts. Conversely, treatment with androgens, as well as estrogens, maintains cancellous bone mass and integrity, regardless of age or sex. Both androgens, via the androgen receptor (AR), and estrogens, via the estrogen receptors (ERs) can exert these effects, but the relative contribution of these 2 pathways remains uncertain. Androgens, like estrogens, stimulate endochondral bone formation at the start of puberty, whereas they induce epiphyseal closure at the end of puberty, thus, they have a biphasic effect. Androgen action on the growth plate is, however, clearly mediated via aromatization into estrogens and interaction with ER alpha. Androgens increase, while estrogens decrease radial growth. This differential effect of the sex steroids may be important because bone strength in males seems to be determined by higher periosteal bone formation and, therefore, greater bone dimensions. Experiments in mice suggest that both the AR and ER alpha pathways are involved in androgen action on radial bone growth. ER beta may mediate growth-limiting effects of estrogens in the female but does not seem to be involved in the regulation of bone size in males. In conclusion, androgens may protect men against osteoporosis via maintenance of cancellous bone mass and expansion of cortical bone. This androgen action on bone is mediated by the AR and ER alpha.

Androgens↗
PubMed2004

Coping with infertility: a body-mind group intervention programme for infertile couples.

BACKGROUND: The recognition of the distressing character of infertility diagnosis and treatment has led to the development of several psychosocial interventions for infertile couples. At the Leuven University Fertility Centre, a body-mind marital group intervention was developed to help infertile couples cope with the distress related to infertility. METHODS AND RESULTS: This treatment programme was originally adapted from a mind-body approach, but integrated concepts and techniques from body-oriented therapy, art therapy and multi-family group therapy. In this paper, the therapeutic foundations, treatment goals and practical implications of the mind-body marital group intervention are outlined. Further, the treatment procedure is explained in detail and illustrated by clinical vignettes. CONCLUSIONS: Although the first clinical impressions about the usefulness of the body-mind group programme in fertility clinics seem promising, further research is needed to assess its effectiveness.

Adaptation, Psychological↗
PubMed2004

Preventing osteoporotic fractures with antiresorptive therapy: implications of microarchitectural changes.

Prospective studies have demonstrated that low bone mass correlates well with increased risk of osteoporotic fractures at various skeletal sites. Trials have likewise confirmed that enhancing bone mass with antiresorptive therapy reduces fracture incidence in individuals at risk. However, correlation of bone mineral density (BMD) increases with therapeutic risk reduction has proved less consistent than correlation of BMD decreases with greater fracture risk in the untreated. Indeed, various analyses have indicated that - even during treatment with potent bisphosphonates like alendronate and risedronate - BMD changes from baseline account for <30% of the reduction in vertebral fractures in treated women. It is clearly, therefore, that factors other than BMD are involved in the reduction of fracture risk achieved by antiresorptive therapies. According to recent micro-computed tomography imaging and other studies, antiresorptive therapy can help rebuild the microarchitecture of bone as well as strengthen the materials that go into it. When treating individuals with osteoporosis, these microarchitectural changes contribute to the reduction of fracture risk achieved by antiresorptive therapies.

Bone Density↗
PubMed2004

Primary hyperparathyroidism: diagnosis and management in the older individual.

As more and more cases of primary hyperparathyroidism are being detected by screening for serum calcium concentration, the majority of patients are older individuals who are asymptomatic or have symptoms which are difficult to ascribe to hyperparathyroidism. Long-term follow-up has provided evidence that most asymptomatic patients who do not undergo parathyroidectomy will not develop symptomatic complications. Some asymptomatic patients, however, have progression of disease over time. These observations and the lack of reliable predictors of the rate of progression in most patients reinforce the need for careful monitoring in elderly individuals who do not undergo surgery. Biannual measurements of serum calcium concentrations and annual measurements of urinary calcium excretion and bone mineral density should be performed in all patients who are managed conservatively. In elderly patients with symptomatic or complicated primary hyperparathyroidism, parathyroidectomy results in biochemical cure and increased bone density, both at the lumbar spine and the femoral neck, and should be considered. Criteria for surgery include significant hypercalcemia (>1 mg/dl above the upper limit of normal), marked hypercalciuria (>400 mg per day), low bone density, unexplained renal insufficiency and an episode of acute primary hyperparathyroidism. Consideration of parathyroidectomy should also be given to elderly patients with primary hyperparathyroidism who are vitamin D deficient. Radionuclide scanning has become the initial non-invasive study of choice when parathyroid gland localization is necessary before parathyroidectomy; this is generally for fragile patients and reoperative cases. In a subset of older individuals, surgery may not be an option because of coexisting medical problems even though surgical indications are present.

Aged↗
PubMed2002

[A 35-year-old man with gynaecomastia as the first symptom of hyperthyroidism].

A 35-year-old man suffered painful bilateral gynaecomastia for 2 months due to serious Graves' hyperthyroidism. During treatment with propylthiouracil and levothyroxine, the plasma concentrations of thyroid hormone, sex hormones and sex hormone-binding globulin normalised and the gynaecomastia disappeared. Gynaecomastia occurs in 30 to 40% of men diagnosed with Graves' hyperthyroidism. However, gynaecomastia as a presenting symptom of this autoimmune disease is uncommon.

Adult↗
PubMed2002

The estrogen receptor ligand ICI 182,780 does not impair the bone-sparing effects of testosterone in the young orchidectomized rat model.

Testosterone (T) can affect bone metabolism not only directly, but also via its metabolites, estrogen or dihydrotestosterone, produced by enzymes present in bone. Therefore, the aim of this study was to investigate whether the high-affinity estrogen receptor ligand ICI 182,780 (ICI) impaired the bone-protective action of T in 3-month-old orchidectomized (Orch) rats, studied during an experimental period of 3 months. As expected, Orch significantly decreased trabecular bone volume in the proximal tibial metaphysis (-52%), as measured by histomorphometry, and had a similar negative effect on volumetric bone mineral density (BMD) in the distal femoral metaphysis (-53%), as assessed by peripheral quantitative computed tomography (pQCT). The loss of bone induced by Orch was completely prevented by T administration. Moreover, the Orch-associated increases of biochemical markers of bone turnover (serum osteocalcin, urinary deoxypyridinoline, and calcium excretion) did not occur when Orch rats received T. Administration of ICI in combination with T did not impair this bone-sparing effect. Cortical bone parameters (as determined by pQCT), body weight gain, and body composition (as measured by dual-energy X-ray absorptiometry) were not affected by T or ICI in combination with T. Furthermore, no differences were observed in serum concentrations of insulin-like growth factor-I or glucose homeostasis. In conclusion, ICI does not impair the long-term bone-protective effects of T in orchidectomized male rats, suggesting that testosterone can mediate its effect on the male skeleton directly via the androgen receptor. The absence of effects on body growth via the growth hormone--insulin-like growth factor-I axis may be a possible explanation for the lack of skeletal effects of this selective estrogen receptor antagonist.

Animals↗
PubMed2002

Evidence from the aged orchidectomized male rat model that 17beta-estradiol is a more effective bone-sparing and anabolic agent than 5alpha-dihydrotestosterone.

This study was designed to evaluate the impact of estrogen versus androgen action on orchidectomy (ORX)-induced bone loss and associated changes in body composition. During an experimental period of 4 months, aged (12-month-old) ORX rats were treated with 17beta-estradiol (E2; 0.75 microg/day) or different doses of the nonaromatizable androgen 5alpha-dihydrotestosterone (DHT; 45, 75, and 150 microg/day, respectively), via subcutaneous (sc) silastic implants. Low doses of DHT and E2 inhibited the ORX-induced rise of bone turnover markers (serum osteocalcin and urinary deoxypyridinoline [DPD]) to a similar extent. High-dose DHT prevented the ORX-induced decrease of trabecular bone density but had no significant effect on cortical thinning as assessed by peripheral quantitative computed tomography (pQCT). This bone-sparing action of DHT occurred at the expense of hypertrophy of the ventral prostate and seminal vesicles. On the other hand, E2 restored both trabecular bone density and cortical thickness in ORX rats and even prevented age-related bone loss. In contrast to DHT, E2 increased lean body mass and inhibited the ORX-associated increase of fat mass, as measured by DXA. Administration of E2 was associated with increased serum concentrations of insulin-like growth factor (IGF) I and decreased circulating levels of leptin. We conclude that, in the aged ORX rat model, E2 is more effective in preventing ORX-induced bone loss than DHT. Additionally, E2 has anabolic effects on muscle tissue and prevents the ORX-related increase of fat mass. Overall, these data suggest that androgen action on bone and body composition is dependent on stimulation of both androgen receptors (ARs) and estrogen receptors (ERs).

Aging↗
PubMed2001

Testosterone prevents orchidectomy-induced bone loss in estrogen receptor-alpha knockout mice.

To examine the role of the estrogen receptor-alpha (ERalpha) during male skeletal development, bone density and structure of aged ERalphaKO mice and wild-type (WT) littermates were analyzed and skeletal changes in response to sex steroid deficiency and replacement were also studied. In comparison to WT, ERalphaKO mice had smaller and thinner bones, arguing for a direct role of ERalpha to obtain full skeletal size in male mice. However, male ERalphaKO mice had significantly more trabecular bone as assessed both by pQCT and histomorphometry, indicating that ERalpha is not essential to maintain cancellous bone mass. Six weeks following orchidectomy (ORX), both WT and ERalphaKO mice showed high-turnover osteoporosis as revealed by increases in serum osteocalcin and decreases in trabecular (-38% and -58% in WT and ERalphaKO, respectively) and cortical bone density (-5% and -4% in WT and ERalphaKO, respectively). Administration of testosterone propionate (T, 5 mg/kg/day) completely prevented bone loss both in ERalphaKO and in WT mice. As expected, estradiol (E2, 60 microg/kg/day) replacement did not prevent cancellous bone loss in ORX ERalphaKO mice. However, E2 stimulated bone formation at the endocortical surface in ORX ERalphaKO, suggesting that osteoblasts may respond to nonERalpha-mediated estrogen action. In conclusion, although functional ERalpha may play a significant role during male skeletal development, this receptor does not seem essential for androgen-mediated skeletal maintenance in older male mice.

Animals↗
PubMed2001

Renal function, cytogenetic measurements, and sexual development in adolescents in relation to environmental pollutants: a feasibility study of biomarkers.

BACKGROUND: Human exposure to chemicals is normally monitored by measurement of environmental pollutants in external media. We investigated whether biomarkers in adolescents can show exposure to, and health effects of, common environmental pollutants. METHODS: We recruited 200 17-year-old adolescents (120 girls) from a rural control area and from two suburbs polluted by a lead smelter and two waste incinerators. We measured biomarkers of exposure and of effect in blood and urine samples, and obtained questionnaire data. School doctors measured testicular volume and staged sexual maturation. FINDINGS: Internal exposure was mostly within current standards. Concentrations of lead and cadmium in blood, PCBs (polychlorinated biphenyls) and dioxin-like compounds in serum samples, and metabolites of VOCs (volatile organic compounds) in urine were higher in one or both suburbs than in the control area. Children who lived near the waste incinerators matured sexually at an older age than others, and testicular volume was smaller in boys from the suburbs than in controls. Biomarkers of glomerular or tubular renal dysfunction in individuals were positively correlated with blood lead. Biomarkers of DNA damage were positively correlated with urinary metabolites of PAHs (polycyclic aromatic hydrocarbons) and VOCs. Interpretation Biomarkers can be used to detect environmental exposure to pollutants and measure their biological effects before overt disease develops. Our findings suggest that current environmental standards are insufficient to avoid measurable biological effects.

Adolescent↗
PubMed2001

Primary hyperparathyroidism: pathophysiology, diagnosis and indications for surgery.

There is little debate about the primacy of surgery in the management of symptomatic or complicated primary hyperparathyroidism. Rather, the question has been what to do about the many patients with nonclassical disease. Recent prospective data have confirmed that patients with asymptomatic primary hyperparathyroidism who are not surgical candidates for parathyroidectomy appear to do well when they are managed conservatively. On average, these patients remain stable, with little progression to the more serious manifestations of hyperparathyroidism over 10 years. It would seem, therefore, that the overall population of older patients with mild asymptomatic primary hyperparathyroidism can be safely followed without intervention. A certain proportion of cases do progress, however, so surveillance is necessary. Individual patients can have worsening hypercalcemia or hypercalciuria, and in a small percentage of patients, bone density may decrease over time. In most patients, deferral of surgery is not a one-time decision, but rather one that is reviewed and reconsidered in conjunction with meticulous monitoring.

Bone Density↗
PubMed2000

Skeletal effects of estrogen deficiency as induced by an aromatase inhibitor in an aged male rat model.

Aromatization of androgens into estrogens may be important for maintenance of the male skeleton. To address this hypothesis, we evaluated the skeletal effects of selective estrogen deficiency as induced by the aromatase inhibitor vorozole (Vor), with or without 17beta-estradiol (E(2)) administration (1.35 microg/day), in aged (12-month-old) male rats. A baseline group was killed at the start of the experiment (Base). The control group (Control), the group treated with vorozole alone (Vor), the group treated with E(2) alone (E(2)), or the group with a combination of both (Vor + E(2)) were killed 15 weeks later. Vorozole significantly increased serum testosterone (T) and reduced serum E(2) compared with Control. Body weight gain and serum insulin-like growth factor-I (IGF-I) were also lower in Vor, whereas significant weight loss and decrease of serum IGF-I occurred as a result of E(2) administration. Bone formation as assessed by serum osteocalcin was unaffected but osteoid surface in the proximal metaphysis of the tibia was increased in Vor-treated rats. Bone resorption as evaluated by urinary deoxypyridinoline excretion was increased in Vor. Biochemical parameters of bone turnover were reduced significantly in all E(2) treated rats. Premature closure of the growth plates and decreased osteoid and mineralizing surfaces were also observed in E(2) and Vor + E(2). Apparent bone density of lumbar vertebrae and femur, as measured by dual-energy X-ray absorptiometry (DXA), was significantly reduced in Vor. Vorozole decreased femoral bone density mainly in the distal femur (trabecular and cortical region). This decrease of bone density was not present in E(2) and Vor + E(2). Similar findings were observed when bone density was assessed by peripheral quantitative computed tomography (pQCT); that is, trabecular density of the distal femur, the proximal tibia, and the distal lumbar vertebra were all lower in Vor. This decrease in density was not observed in all E(2)-treated animals. In conclusion, administration of the aromatase inhibitor, vorozole, to aged male rats induces net trabecular bone loss in both the appendicular and axial skeleton, despite a concomitant increase in serum testosterone. E(2) administration is able to prevent this trabecular bone loss in vorozole-treated animals.

Aging↗
PubMed2000

Trazodone: a double-blind, placebo-controlled, randomized study of its effects in patients with erectile dysfunction without major organic findings.

UNLABELLED: This study examined the efficacy of trazodone 200 mg/day in patients with erectile dysfunction (ED) without major organic findings. PATIENTS AND METHODS: Thirty-four patients with ED without major organic findings entered a double-blind, placebo-controlled, randomized two-centre trial comparing placebo and trazodone 200 mg/day. After a 2 week treatment-free, baseline period eligible patients entered a 4 week treatment-phase. Nocturnal erectile activity was measured before and after treatment by Rigiscan Plus. Sexual desire, quality of partner relation and depressive symptomatology were assessed with the derogatis sexual functioning inventory (DSFI), the dyadic adjustment scale (DAS) and the Hamilton depression rating scale (HDRS), respectively. Sexual function during the study period was assessed with patient diaries. Compliance was measured by trazodone serum concentrations. There were no significant differences between trazodone and placebo in total erection duration, change in sexual desire, report of morning erections or psychometric scales, except for the HDRS. Trazodone serum levels indicated that half of the patients were not compliant. In conclusion, Trazodone 200 mg/day has no effect on sexual function in men with ED without major organic findings and non-compliance was an important issue in the present study.

Adolescent↗
PubMed2000

Androgens and osteoporosis.

Androgen receptors are present in relevant numbers in osteoblasts. Stimulation of androgen receptors in osteoblastic bone marrow stromal cells inhibits the differentiation of osteoclasts in the bone marrow cavity. Androgens not only inhibit osteoclastogenesis but also increase cortical bone formation mainly by stimulating periosteal bone formation. Clinically, androgen action is crucial for the gain of bone mass during puberty and the maintenance of bone mass after puberty. Therefore, androgen replacement is necessary in hypogonadal men. However, the role of androgen replacement in partial androgen deficiency still remains unclear. Thus far, only testosterone has established its role in androgen replacement. However, further clinical and basic research should better define the selective role of androgen versus oestrogen receptor stimulation in male skeletal homeostasis.

Androgens↗
PubMed2000

Osteoporosis and osteoporotic fractures in men: a clinical perspective.

The lifetime risk of any fracture of the hip, spine or distal forearm in men aged 50 years has been estimated to be 13%, compared with 40% in women. Although the overall incidence of osteoporosis is less in men than in women, the disease still represents an important public health problem. In particular, hip fractures are associated with substantial mortality and morbidity, even more so than in women. In male patients presenting with osteoporotic fractures, major causes of skeletal fragility, such as hypogonadism, glucocorticoid excess, primary hyperparathyroidism and alcohol abuse, can often be identified. In as many as 50% of osteoporotic men, however, no aetiology can be found: these men suffer from a syndrome commonly referred to as idiopathic osteoporosis, which is presumably related to some type of osteoblast dysfunction. Recent evidence indicates that the loss of skeletal integrity in ageing men may be partially related to endocrine deficiencies, including vitamin D, androgen and/or oestrogen deficiency. While the consequences of vitamin D or oestrogen deficiency in women have been well established, the skeletal impact of these (partial) age-related deficiencies in men remains to be clarified. Osteoporosis in elderly men is a multifactorial disease, as it is in women. The prevention of osteoporosis should therefore focus not only on increasing the bone strength, but also on decreasing the risk of falls. However, the prevention and therapy of osteoporotic disorders in men are virtually unexplored. To date, the use of specific osteoporotic drugs in osteoporotic men is still based on reasonable but untested assumptions.

Endocrine System Diseases↗
PubMed2000

An aged rat model of partial androgen deficiency: prevention of both loss of bone and lean body mass by low-dose androgen replacement.

The aim of this study was to evaluate the effects of different doses of androgen replacement, both on body composition and bone, in an aged male orchidectomized rat model. Testosterone was administered by 0.5, 1, and 2.5-cm sc SILASTIC implants (release of, respectively, 11.5, 23, and 55 microg/day) to aged (12 months old, +/- 550 g) male orchidectomized Wistar rats during a 15-week experimental period. T 0.5 only partially prevented decrease of ventral prostate and seminal vesicle weight, compared with an intact group that received an empty implant (Intact). The 1-cm implant (T 1) completely prevented decrease of both seminal vesicles and ventral prostate weight. The 2.5-cm implant (T 2.5) was clearly supraphysiological, as demonstrated by significant hypertrophy of both androgen-sensitive organs. Serum testosterone was lower in T 0.5 and T 1 (0.38 +/- 0.06 ng/ml and 0.92 +/- 0.06 ng/ml, respectively) and higher in T 2.5 (2.4 +/- 0.28. ng/ml), compared with both Intact (1.6 +/- 0.23 ng/ml) and the baseline group(1.6 +/- 0.11 ng/ml). As expected, orchidectomized rats that received an empty SILASTIC implant had significantly lower bone mineral content (-7.9%), apparent density (-5.7%), and lean body mass (-10.8%), as measured by dual-energy x-ray absorptiometry, without significant changes in body weight and fat mass, compared with Intact. Also, cancellous (-50.3%) and cortical (-1.8%) volumetric density, as measured by peripheral quantitative computed tomography, were decreased in the tibia. Bone turnover, as measured by serum osteocalcin and urinary deoxypyridinoline excretion, was increased in orchidectomized rats that received an empty SILASTIC implant. T 0.5 prevented all changes, not only in bone mineral content, density, and turnover but also in lean body mass. Moreover, there were no significant differences, for all these parameters, between the different doses of testosterone replacement. In conclusion, low-dose androgen replacement does not lead to lower bone mineral density, higher bone turnover, and lower lean body mass in aged male rats, whereas complete androgen deficiency does. Therefore, the threshold concentration of testosterone necessary for prevention of both bone and lean body mass loss in aged male rats is clearly lower than for prostate and seminal vesicles.

Aging↗