What factors determine patient adherence to osteoporosis treatment regimens?
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Comment↗
Biomedical subjects
René Rizzoli
Publications and source records attributed to René Rizzoli.
Different responsiveness of alveolar and tibial bone to bone loss stimuli.
UNLABELLED: Mandibular and systemic bone loss are poorly associated. We compared the effect of isocaloric protein undernutrition and/or ovariectomy on BMD and microstructure of mandibular alveolar and proximal tibia sites in adult rats. Mandibular bone was significantly less affected. INTRODUCTION: Whether mandibular bone and axial or peripheral skeleton respond similarly to systemic bone loss remains a subject of controversy. We have previously shown that mechanical loading during mastication influences bone mass and architecture of the mandibular alveolar bone. Isocaloric protein undernutrition and ovariectomy are known to cause bone loss and deterioration of bone microarchitecture at various axial and peripheral skeletal sites. We studied how the mandible, which is subjected to heavy, abrupt, and intermittent forces during mastication, responds to low-protein intake and/or ovariectomy and compared this response to that of the proximal tibia in adult rats. MATERIALS AND METHODS: Forty-four 6-month-old female Sprague-Dawley rats underwent transabdominal ovariectomy (OVX; n=22) or sham operation (n=22) and were pair-fed isocaloric diets containing either 15% or 2.5% casein (sham 15%, n=11; sham 2.5%, n=11; OVX 15%, n=11; and OVX 2.5%, n=11) for 16 weeks. BMD and bone microarchitecture parameters (e.g., bone volume fraction [BV/TV] and trabecular thickness and number) of the mandible and the proximal tibia were measured at the end of the experiment using DXA and microCT. RESULTS: Mandibular alveolar bone was negatively influenced by both protein undernutrition and OVX, but to a significantly lesser extent than the proximal tibia. In sham-operated animals, low-protein intake led to a 17.3% reduction of BV/TV in the mandible and 84.6% in the tibia (p<0.001). In normal protein diet-fed animals, OVX led to a reduction of BV/TV of 4.9% in the mandible but 82% in the tibia (p<0.001). In the mandible, protein undernutrition resulted in thinner trabeculae (p<0.05), whereas OVX led to a reduction of trabecular number (p<0.05). CONCLUSIONS: Mandibular alveolar bone was found to be less sensitive to either protein undernutrition or OVX than the proximal tibia spongiosa. We hypothesize that the mechanical loading of the alveolar process during mastication may protect the alveolar bone from the detrimental effects observed in other skeletal sites, such as the proximal tibia. Morphological and embryological differences between the two skeletal sites might also play a role.
Alveolar Bone Loss↗
Proline-rich motifs in the parathyroid hormone (PTH)/PTH-related protein receptor C terminus mediate scaffolding of c-Src with beta-arrestin2 for ERK1/2 activation.
Parathyroid hormone (PTH) stimulates ERK1/2 through both G-protein signaling and beta-arrestin2-mediated internalization. Beta-arrestin may serve as a scaffold for c-Src. However, the molecular mechanisms for ERK1/2 activation by PTH remain unclear. By using a targeted mutagenesis approach, we investigated the PTH/PTH-related protein receptor (PTH1R) structural determinants for ERK1/2 activation and transcriptional activity in HEK-293 cells. First, ERK1/2 activation was inhibited by PTH1R mutations that specifically abrogate G(q)-protein kinase C signaling without a decrease in cAMP-protein kinase A. Second, PTH1R C-terminal mutations and/or deletions that prevent interaction with beta-arrestin inhibited ERK1/2 activation. Similar results were obtained in HEK-293 cells co-expressing wild-type PTH1R and a dominant-negative beta-arrestin2. Third, the c-Src inhibitor PP2 and a kinase-dead c-SrcK295M mutant co-expressed with wild-type PTH1R both inhibited ERK1/2 activation. Furthermore, c-Src co-precipitated with both PTH1R and beta-arrestin2 in response to PTH. Deleting the PTH1R-proximal C terminus abolished these interactions. However, the need for receptor interaction with beta-arrestin to co-precipitate Src and activate ERK1/2 was obviated by expressing a constitutively active c-SrcY527A mutant, suggesting direct binding of activated Src to PTH1R. Subsequently, we identified and mutated to alanine four proline-rich motifs in the PTH1R distal C terminus, which resulted in loss of both c-Src and arrestin co-precipitation and significantly decreased ERK1/2 activation. These data delineate the multiple PTH1R structural determinants for ERK1/2 activation and newly identify a unique mechanism involving proline-rich motifs in the receptor C terminus for reciprocal scaffolding of c-Src and beta-arrestin2 with a class II G-protein-coupled receptor.
Amino Acid Sequence↗
Pamidronate and osteoporosis prevention in liver transplant recipients.
Osteoporosis is a common complication in patients with end-stage liver disease and after orthotopic liver transplantation (LT), with resulting increasing fracture rate. In this study, we investigated the role of treatment with pamidronate in preventing further bone loss after LT. Eighty-five patients with end-stage liver disease were included in the study. Pamidronate 30 mg was given intravenously every 3 months after LT for the duration of 1 year to 43 patients with osteopenia or osteoporosis prior LT. The remainders served as controls. All patients received a supplementation of calcium and vitamin D. Bone mineral density (BMD) at the lumbar spine and the femoral neck, and markers of bone metabolism were measured before and 12 months after LT. Sixty-two BMD were available at 12 months; only paired BMD were evaluated. A significant increase in lumbar spine BMD was observed in pamidronate treated patients. No change was evident in controls. Femoral neck BMD decreased in both treated and untreated patients. Osteocalcin serum levels and deoxypyridinoline urinary excretion were significantly reduced by treatment. Our study suggests that pamidronate decreases bone turnover and is effective in preventing the course of bone loss after LT, however the efficacy, at the dosage regimen employed and in a follow-up of 12 months, appears to be limited to trabecular bone, with no effect on the cortical structure of the femur.
Adult↗
Childhood fractures are associated with decreased bone mass gain during puberty: an early marker of persistent bone fragility?
UNLABELLED: Whether peak bone mass is low among children with fractures remains uncertain. In a cohort of 125 girls followed over 8.5 years, 42 subjects reported 58 fractures. Among those, BMC gain at multiple sites and vertebral bone size at pubertal maturity were significantly decreased. Hence, childhood fractures may be markers of low peak bone mass acquisition and persistent skeletal fragility. INTRODUCTION: Fractures in childhood may result from a deficit in bone mass accrual during rapid longitudinal growth. Whether low bone mass persists beyond this period however remains unknown. MATERIALS AND METHODS: BMC at the spine, radius, hip, and femur diaphysis was prospectively measured over 8.5 years in 125 girls using DXA. Differences in bone mass and size between girls with and without fractures were analyzed using nonparametric tests. The contribution of genetic factors was evaluated by mother-daughter correlations and that of calcium intake by Cox proportional hazard models. RESULTS: Fifty-eight fractures occurred in 42 among 125 girls (cumulative incidence, 46.4%), one-half of all fractures affecting the forearm and wrist. Girls with and without fractures had similar age, height, weight. and calcium intake at all time-points. Before and during early puberty, BMC and width of the radius diaphysis was lower in the fracture compared with no-fracture group (p < 0.05), whereas aBMD and BMAD were similar in the two groups. At pubertal maturity (Tanner's stage 5, mean age +/- SD, 16.4 +/- 0.5 years), BMC at the ultradistal radius (UD Rad.), femur trochanter, and lumbar spine (LS), and LS projected bone area were all significantly lower in girls with fractures. Throughout puberty, BMC gain at these sites was also decreased in the fracture group (LS, -8.0%, p = 0.015; UD Rad., -12.0%, p = 0.004; trochanter, -8.4%, p = 0.05 versus no fractures). BMC was highly correlated between prepuberty and pubertal maturity (R = 0.54-0.81) and between mature daughters and their mothers (R = 0.32-0.46). Calcium intake was not related to fracture risk. CONCLUSIONS: Girls with fractures have decreased bone mass gain in the axial and appendicular skeleton and reduced vertebral bone size when reaching pubertal maturity. Taken together with the evidence of tracking and heritability for BMC, these observations indicate that childhood fractures may be markers for low peak bone mass and persistent bone fragility.
Aging↗
Combined treatment with a beta-blocker and intermittent PTH improves bone mass and microarchitecture in ovariectomized mice.
Intermittent administration of parathyroid hormone (PTH) induces bone remodeling and renewed bone modeling, resulting in net bone gain. beta-blockers improve trabecular bone architecture in young ovariectomized mice by preventing the inhibition of bone formation and stimulation of bone resorption induced by the adrenergic system. To test the hypothesis that PTH and beta-blockers may exert synergistic effects on the skeleton, 15-week-old ovariectomized mice were either given oral propranolol (PRO) or left untreated for 8 weeks, adding daily hPTH(1-34) (80 microg/kg/day) or vehicle (VEH) during the last 4 weeks. The skeletal response was evaluated using pDXA, microCT, histomorphometry and biochemical markers. PRO significantly attenuated loss of bone mineral density (BMD) at whole body (WB) (-0.1% in PRO vs. -2.4% in VEH, P < 0.05), but not at spine or femur 4 weeks after OVX. Thereafter, PTH increased BMD at all sites in both PRO- and VEH-treated mice (+6.7% to +14%, P < 0.05 to P < 0.0001 vs. VEH). Over 8 weeks, sequential-combined treatment of PRO and PTH significantly improved BMD over PTH alone at WB (+9.1% vs. +4.4% over baseline, respectively, P < 0.005) and spine (+9% vs. -1.7%, respectively, P < 0.05). These effects were paralleled by a decrease in TRACP5b with PRO (P < 0.05 vs. VEH) and an increase in osteocalcin with PTH, irrespective of PRO (P < 0.0001 vs. VEH). Trabecular bone microarchitecture, such as BV/TV, trabecular number and ConnD, was significantly improved by sequential-combined treatment of PRO and PTH compared to PTH alone. At midshaft femur, both PRO and PTH significantly increased cross-sectional area (CSA), but the effects of the two drugs on CSA and cortical thickness were not additive. Dynamic histomorphometry indicated that bone formation was increased by PTH at both cortical and trabecular surfaces, whereas PRO increased osteoblast number and surface on trabecular surfaces. The combined treatment further improved the extent of mineralization and BFR over PTH alone (P < 0.05) at endocortical surfaces and recapitulated the effects of PTH and PRO alone on trabecular surfaces. These results indicate that beta-adrenergic blockade may partially improve the bone remodeling balance induced by estrogen deficiency. In turn, PRO exerted synergistic effects with intermittent PTH on bone mass and cancellous bone architecture. As such, combined therapy of beta-blockers and PTH may be of interest in the treatment of postmenopausal osteoporosis.
Adrenergic beta-Antagonists↗
Glucocorticoid-induced osteoporosis and its treatment.
UNLABELLED: Osteoporosis and fractures are frequent and important consequences of glucocorticoid therapy. Many factors contribute to bone loss during glucocorticoid therapy, such as underlying disease, malnutrition, vitamin D insufficiency, hypogonadism, and low body weight. Bone loss occurs particularly in the first few months of glucocorticoid treatment and affects more cancellous than cortical bone, with reduced bone formation and increased bone resorption. The risk of fracture increases rapidly in patients with glucocorticoid therapy. The existence of a threshold is not well defined but the risk of fracture is increased in patients with higher doses of glucocorticoids. Other effects include altered production of gonadal sex hormones, inhibition of intestinal calcium absorption, and enhancement of renal excretion of calcium. Prevention of glucocorticoid-induced osteoporosis is based on general measures such as calcium and vitamin D supplementation, adequate protein intake, regular physical exercise, and specific therapies. Bisphosphonates, which are potent bone resorption inhibitors, have been shown to increase bone mineral density and to decrease fracture risk, so that they represent the first choice in the prevention of glucocorticoid-induced osteoporosis. Glucocorticoid-induced osteoporosis is a major burden to those whom it affects. It can be prevented provided efficacious preventive measures are introduced early during glucocorticoid treatment. LEVEL OF EVIDENCE: Level V (expert opinion). See the Guidelines for Authors for a complete description of the levels of evidence.
Bone Density↗
Long-term outcome of weekly bisphosphonates.
UNLABELLED: Bisphosphonates currently are the preferred therapy for treating osteoporosis. Treatment with potent bisphosphonates such as alendronate or risedronate decreases biochemical markers of bone turnover and increases bone mineral density. These changes are associated with significant reductions in vertebral and nonvertebral fracture risk. Clinical trial data with up to 10 years of followup shows these agents are effective and well tolerated for long-term periods. Daily administration is effective and generally well tolerated. However, once weekly doses are more convenient, which may enhance long-term compliance and lead to more successful outcomes. The pharmacokinetics and mechanism of action predict the short-term and long-term skeletal effects and safety profile of once-weekly doses of bisphosphonates are similar to daily doses. These predictions are supported by authors of trials of up to 2 years who report once-weekly doses are therapeutically equivalent to daily doses in terms of BMD and biochemical markers of bone remodeling. Once-weekly bisphosphonate doses have safety and tolerability profiles as good as daily doses and are comparable with the placebo. LEVEL OF EVIDENCE: Therapeutic study, Level V (expert opinion). See the Guidelines for Authors for a complete description of the levels of evidence.
Bone Density↗
Long-term experience with alendronate in the treatment of osteoporosis.
Osteoporosis is characterised by increased bone turnover, low bone mass and impaired bone microarchitecture, leading to increased fracture risk. Effective anticatabolic therapies decrease fracture risk by reducing the rate of bone turnover, thereby maintaining bone microarchitecture and increasing bone mineral density. At present, potent oral bisphosphonates, such as alendronate (FOSAMAX; Merck & Co.), are preferred for the treatment of osteoporosis. Long-term clinical trial data demonstrate that alendronate is effective and generally well tolerated. Results from head-to-head studies and meta-analyses suggest that alendronate is more effective than certain other anticatabolic agents in the treatment of patients with osteoporosis.
Aged↗
Low protein intake is associated with impaired titanium implant osseointegration.
UNLABELLED: Low protein intake is highly prevalent among orthopaedic elderly patients. We studied the effects of an isocaloric low protein diet on the resistance to pull-out of titanium rods implanted into rats proximal tibia. Isocaloric low protein intake impairs titanium implant osseointegration, with a decreased strength needed to completely loose the implant and altered bone microarchitecture in its vicinity. INTRODUCTION: Low protein intake is highly prevalent among elderly patients in orthopaedic wards and could retard fracture healing. It was previously shown that reduced protein intake decreases bone strength. Whether dietary protein intake could influence titanium implant osseointegration is unknown. We studied the effects of an isocaloric low protein diet on the resistance to pull-out of titanium rods implanted into rats proximal tibia. MATERIALS AND METHODS: Forty-eight 11-month-old female rats were fed isocaloric diets containing 2.5% (low protein) or 15% (normal protein) casein from 2 weeks before the implantation of a 1-mm-diameter cylindrical titanium rod in the proximal metaphysis of each tibia. Four, 6, and 8 weeks after implantation, the tibias were removed for microCT histomorphometry to quantify bone-to-implant contact and bone trabecular microarchitecture around the implant. Resistance to implant pull-out was tested by recording the maximal force necessary to completely loosen the implant. RESULTS: Pull-out strength was significantly lower in rats fed an isocaloric low protein diet by 6 and 8 weeks after implantation (-43%, p < 0.001 and -42%, p < 0.001, respectively) compared with rats fed a normal protein diet. Bone-to-implant contact was significantly lower in the low protein group 8 weeks after implantation (p < 0.05). Bone-to-implant contact and pull-out strength were correlated (r2= 0.57, p < 0.0001). BV/TV around the implant was 19.9 +/- 2.2% (SE) versus 31.8 +/- 3.3% (p < 0.05) at 6 weeks and 20.1 +/- 1.9% versus 29.8 +/- 3.2% (p < 0.05) at 8 weeks after implantation in the low protein and normal protein intake groups, respectively. Trabecular thickness was 96.2 +/- 3.7 versus 113.0 +/- 3.6 microm (p < 0.01) at 6 weeks and 101.4 +/- 2.7 versus 116.2 +/- 3.3 microm (p < 0.01) at 8 weeks in the corresponding groups. In a structure model index analysis, there was a significant shift to a more rod-like pattern in the low protein diet groups. All these changes were associated with lower plasma IGF-I levels. CONCLUSIONS: Isocaloric low protein intake impairs titanium implant osseointegration, with decreased strength needed to completely loosen the implant and altered bone microarchitecture in the vicinity of the implant.
Animals↗
[Osteoporosis: a controlled epidemic?].
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Disease Outbreaks↗
Recommendations for an update of the current (2001) regulatory requirements for registration of drugs to be used in the treatment of osteoporosis in postmenopausal women and in men.
Recent advances in the understanding of the epidemiology of osteoporosis suggest that certain parts of the current European guidelines for the registration of drugs in osteoporosis might be no longer substantiated. The object of this review is to provide the European regulatory authorities with an evidence-based working document providing suggestions for the revision of the "Note for guidance for the approval of drugs to be used in postmenopausal osteoporosis" (CPMP/EWP/552/95). Following an extensive review of the literature (1990-2004), the Group for the Respect of Ethics and Excellence in Science (GREES) organized a workshop including European regulators, academic scientists and representatives of the pharmaceutical industry. The outcomes of this meeting reflect the personal views of those who attended and should not, in any case, be seen as an official position paper of any regulatory agency. The group identified a certain number of points that deserve discussion. They mainly relate to the nature of the indication being granted to new chemical entities (treatment of osteoporosis in women at high risk of fracture instead of prevention and treatment of osteoporosis), the requirements of showing an anti-fracture efficacy on all or on major nonvertebral fractures (instead of the hip), the duration of pivotal trials (2 years instead of 3) and the possibility of considering bridging studies for new routes of administration, new doses or new regimens of previously approved drugs. The group also recommends that an indication could be granted for the treatment of osteoporosis in males on the basis of a placebo-controlled study, with bone mineral density changes after 1 year as the primary endpoint, for medications approved in the treatment of osteoporosis in women at high risk of fractures.
Female↗
Primary hyperparathyroidism: can parathyroid carcinoma be anticipated on clinical and biochemical grounds? Report of nine cases and review of the literature.
BACKGROUND: Parathyroid carcinoma (PC) mimics benign primary hyperparathyroidism (PHP), but the diagnosis of PC is seldom available at the time of the first operation. Because PC is plagued by recurrences usually beyond cure, one may wonder whether some of these could be prevented by more extensive resections initially, i.e., if the diagnosis of PC were available at that time. METHODS: Over a 25-year period, 311 consecutive patients with PHP underwent operation in our department: 302 had benign disease (adenomas or hyperplasias), and 9 had PC. Several clinical parameters, serum calcium and parathyroid hormone (PTH) levels, and the weight of the parathyroid tumor removed were compared in both groups. Receiver operating characteristic curves and logistical regression analyses were used to distinguish PC from benign PHP. RESULTS: Eight of 9 patients with PC had symptoms, versus 238 (79%) of 302 with benign PHP (not significant). In the PC subgroup, serum calcium and PTH levels and the tumor weights of the parathyroid glands removed were significantly higher than in the benign PHP cohort, even if these three parameters were regularly flawed by low positive predictive values (14%, 20%, and 15%, respectively). CONCLUSIONS: Serum calcium, PTH levels, and tumor weights were significantly greater in the PC subgroup, even if not invariably in a discriminatory way. However, when PTH is <4 times the upper limit of normal and tumor weight is <1.9 g, the probability of PC is nil.
Adult↗
Pamidronate prevents bone loss and decreased bone strength in adult female and male rats fed an isocaloric low-protein diet.
UNLABELLED: Isocaloric dietary protein deficiency is associated with decreased BMD and bone strength as well as depressed somatotroph and gonadotroph axis. Inhibition of increased bone resorption by the bisphosphonate pamidronate in rats fed an isocaloric low-protein diet fully prevents bone loss and alteration of bone strength. INTRODUCTION: Isocaloric dietary protein deficiency is associated with decreased BMD and bone strength as well as depressed somatotroph and gonadotroph axis. This negative bone balance is the consequence of increased bone resorption and decreased bone formation. Whether inhibition of bone resorption could prevent low-protein diet-induced bone loss and alteration of biomechanics is not known. MATERIALS AND METHODS: The effect of the bisphosphonate pamidronate was studied in 5.5-month-old female or 6-month-old male rats pair-fed a control (15% casein) or an isocaloric low-protein (2.5% casein) diet for 19 and 26 weeks, respectively. Pamidronate (0.6 mg/kg) was given subcutaneously 5 days/month for 4 months in female rats or for 5 months in male rats. BMD, microarchitecture, and bone strength were measured at the level of the proximal and midshaft tibia. Urinary deoxypyridinoline excretion, serum osteocalcin, and IGF-I were also measured. RESULTS: The increase in bone resorption in female rats (+100%) and in male rats (+33%) fed a low-protein diet was prevented by pamidronate treatment. The reduced osteocalcin levels observed in rats fed a low-protein diet were further decreased in both female (-34%) and male (-30%) rats treated with pamidronate. The bone turnover decrease induced by pamidronate prevented bone strength reduction, trabecular bone loss, microarchitecture, and BMD alterations induced by the isocaloric low-protein diet. Similar effects were observed at the level of the midshaft tibia. Significant decrease of plasma IGF-I was observed in rats fed a low-protein diet independently of the pamidronate treatment. CONCLUSION: In conclusion, inhibition of increased bone resorption in rats fed an isocaloric low-protein diet fully prevents bone loss and alteration of bone strength.
Amino Acids↗
Vertebral fracture risk reduction with risedronate in post-menopausal women with osteoporosis: a meta-analysis of individual patient data.
BACKGROUND AND AIMS: The effect of risedronate, a potent pyridinyl bisphosphonate, on vertebral fractures in post-menopausal women was evaluated in randomized, placebo-controlled clinical trials. These trials included two large vertebral fracture studies that used time-to-event methods to evaluate the effects of treatment on fracture risk, thereby allowing both the occurrence and the timing of fractures to be considered. METHODS: We used individual patient data (IPD) and time-to-event methods to perform a meta-analysis of the anti-fracture efficacy of risedronate (2.5 or 5 mg daily) in osteoporotic women enrolled in five double-blind, placebo-controlled clinical trials. Women were included in the analysis if, at baseline, they had either at least one prevalent vertebral fracture or a femoral neck bone mineral density (BMD) T-score of less than -2.5, were at least 1 year post-menopausal, and had had vertebral fracture assessments (N = 3331). RESULTS: Risedronate 5 mg daily reduced the risk of radiographically defined vertebral fracture by 64% (95% CI, 46 to 76%, p < 0.001) in the first year of treatment and 45% (95% CI, 31 to 57%, p < 0.001) in 3 years. The numbers of patients who needed to be treated with risedronate 5 mg to prevent one new vertebral fracture over 1 and 3 years were 21 and 13, respectively. Comparable findings were observed in sub-populations defined on the basis of either prevalent vertebral fracture without regard to femoral neck BMD, or femoral neck BMD without regard to vertebral fracture status. Risedronate significantly reduced the incidence of clinical (symptomatic) vertebral fractures in the first 6 months of treatment (p < 0.001). CONCLUSIONS: This meta-analysis, based upon five trials and using IPD and time-to-event statistical methods, provides a more precise estimate of the effect of risedronate in reducing vertebral fracture risk in postmenopausal osteoporotic women than a meta-analysis using summary statistics from the literature.
Bone Density↗
Treatment of patients with postmenopausal osteoporosis is worthwhile. The position of the International Osteoporosis Foundation.
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Aged↗
A rapid self-administered food frequency questionnaire for the evaluation of dietary protein intake.
BACKGROUND: Dietary calcium and proteins are important determinants of bone health. Among the various methods to evaluate dietary intakes, food frequency questionnaires provide a self-administered, quick and simple estimation of dietary intakes. OBJECTIVES: To validate a simple, rapid, self-administered food frequency questionnaire for the estimation of dietary protein intake. DESIGN AND METHODS: A self-administrable food frequency questionnaire comprising 20 items was developed. The accuracy of dietary protein evaluation by this questionnaire was verified by comparing it to the results of a diary performed over a 4-day-period in 29 normal healthy subjects (mean age+/-SD, 40.1+/-12.3), and to the mean of three last 24-h recalls, administered at 6-week intervals in 43 healthy men (mean age+/-SD, 51.2+/-5.1). RESULTS: As compared with the values from both reference methods, the slope coefficient of linear regression analysis was statistically different from zero, but the percent of variance explained by the frequency questionnaire results amounted to 35% (diary) and 18% (24-h recall), respectively. Bland and Altman graphs as well as the Pitman's test did not show any difference in variability between the reference methods and the new food frequency questionnaire. This indicates a reliable estimate of group average dietary protein intakes. CONCLUSION: This rapid, self-administered food frequency questionnaire could be a useful tool for the evaluation of dietary protein intakes in groups of subjects.
Adult↗
Transient diplopia after parathyroidectomy for hyperparathyroidism in chronic haemodialysed patients.
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Acute Disease↗