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Biomedical subjects

John P Bilezikian

Publications and source records attributed to John P Bilezikian.

At least 19 recordsLinked to original sources
PubMed2006

Elevations in serum and urinary calcium with parathyroid hormone (1-84) with and without alendronate for osteoporosis.

CONTEXT: The effect of PTH therapy on serum and urinary calcium levels and the risk of hypercalcemia or hypercalciuria has not been formally evaluated. OBJECTIVE: The objective was to examine changes in serum and urinary calcium associated with PTH(1-84) therapy in the PaTH trial and the extent to which a defined algorithm resolved the elevated values. DESIGN, SETTING, PARTICIPANTS, AND INTERVENTION: A total of 178 postmenopausal women were randomized to PTH(1-84) either alone or in combination with alendronate during the first year of the PaTH study. MAIN OUTCOME MEASURE(S): The main outcome measures were fasting serum calcium at baseline and 1, 3, and 12 months and 24-h urinary calcium at baseline and 3 months. RESULTS: In 14% of participants, serum calcium more than 10.5 mg/dl (>2.6 mmol/liter) developed. Following the defined algorithm, 58% of elevated measurements were normal on repeat testing; 38% required discontinuation of calcium and vitamin D supplementation, and one necessitated a decrease in PTH injection frequency to normalize serum calcium. One participant developed transient hypercalcemia between study visits and required hospitalization; the episode resolved with iv hydration and PTH discontinuation. Baseline characteristics associated with the development of hypercalcemia were serum calcium [relative hazards = 1.9 per 0.5 mg/dl (0.12 mmol/liter); 95% confidence interval = 1.1-3.2] and serum 1,25-dihydroxyvitamin D [relative hazard = 1.9 per 10 pg/ml (26 pmol/liter); 95% confidence interval = 1.2-3.1]. Fifteen women (8%) developed hypercalciuria [urinary calcium > 400 mg (100 mmol)/24 h or calcium/creatinine ratio > 0.4]; 80% of cases resolved after discontinuing calcium and vitamin D, 13% without intervention, and one after PTH injection frequency was decreased. Higher baseline urinary calcium excretion was associated with development of hypercalciuria [relative hazard = 1.5 per 50 mg/d (12.5 mmol/d); 95% confidence interval = 1.2-4.0]. Proportions of patients with elevated serum and urinary calcium were similar on single and combination therapy. CONCLUSIONS: The frequency of episodic hypercalcemia or hypercalciuria in the PaTH trial was 21%. Episodes were generally mild, and nearly all cases resolved spontaneously or with discontinuation of calcium and vitamin D. The algorithms used to address hypercalcemia and hypercalciuria in the PaTH trial proved effective in safely resolving clinical episodes of increased urinary or serum calcium and might therefore be helpful to clinicians caring for patients on PTH.

Aged↗
PubMed2006

Official positions of the International Society for Clinical Densitometry and Executive Summary of the 2005 Position Development Conference.

The International Society for Clinical Densitometry (ISCD) convenes a Position Development Conference (PDC) every two years for the purpose of making recommendations on clinically relevant issues in bone densitometry. Topics for consideration are developed by the ISCD Scientific Advisory Committee and the PDC Steering Committee. Clinically relevant questions related to each topic area are assigned to subcommittees for a comprehensive medical literature review and presentation of a report to an international panel of experts. The expert panel includes representatives of the American Society for Bone and Mineral Research (ASBMR) and the International Osteoporosis Foundation (IOF). The recommendations of the PDC expert panel are evaluated by the ISCD Board of Directors, and those that are approved become Official Positions of the ISCD. The Official Positions have subsequently been endorsed by the ASBMR and IOF. The most recent PDC was held July 15-17, 2005, in Vancouver, BC, Canada. Topics considered included technical standardization, vertebral fracture assessment, and application of the 1994 World Health Organization (WHO) criteria to various skeletal sites and to populations other than postmenopausal white women. This report describes the methodology of the 2005 PDC and presents a summary of all ISCD Official Positions.

Absorptiometry, Photon↗
PubMed2006

Standards for performing DXA in individuals with secondary causes of osteoporosis.

This document addresses skeletal health assessment in individuals with secondary causes of osteoporosis. Recommendations are based on consensus of the Canadian Panel of the International Society for Clinical Densitometry and invited international experts. Bone mineral density (BMD) testing in these populations is performed in conjunction with careful evaluation of the disease state contributing to bone loss and increased fragility fracture risk, as well as assessment of other contributing risk factors for fracture. The presence of secondary causes of bone loss may further increase the risk of fracture independently of BMD and may necessitate earlier pharmacologic intervention. Dual-energy X-ray absorptiometry is indicated in the initial workup of secondary causes of osteoporosis. The BMD fracture risk relationship is not known for individuals with chronic renal failure (CRF). The BMD testing in this population may be normal in the presence of skeletal fragility, and quantitative bone histomorphometry is better at evaluating skeletal status than BMD in CRF. Dual-energy X-ray absorptiometry is a valuable tool in assessing skeletal health in individuals with secondary causes of osteoporosis.

Absorptiometry, Photon↗
PubMed2006

The use of parathyroid hormone in the treatment of osteoporosis.

Anabolic skeletal agents have recently broadened our therapeutic options for osteoporosis. By directly stimulating bone formation, they reduce fracture incidence by improving bone qualities in addition to increasing bone mass. Teriparatide [recombinant human parathyroid hormone(1-34)], the only anabolic agent currently approved in the United States for osteoporosis, has emerged as a major therapeutic approach to selected patients with osteoporosis. Teriparatide is approved for both postmenopausal women and men with osteoporosis who are at high risk for fracture. With the use of this anabolic agent, bone density and bone turnover increase, microarchitecture improves, and bone size is beneficially altered. The incidence of vertebral and nonvertebral fractures is reduced with teriparatide use. Combination therapy with parathyroid hormone and an antiresorptive does not appear to offer definitive advantages over the use of PTH or an antiresorptive alone, although recent ideas about combining these agents may offer new insights. In order to maintain increases in bone density acquired during PTH therapy, it is important to follow its use with an antiresorptive agent.

Anabolic Agents↗
PubMed2006

Combination/sequential therapies for anabolic and antiresorptive skeletal agents for osteoporosis.

In this paper, we focus upon the use of anabolic skeletal therapy for the treatment of postmenopausal and other forms of osteoporosis. The only anabolic skeletal agent currently available is a recombinant bioactive fragment of parathyroid hormone, PTH(1-34), known as teriparatide. The full length molecule, human PTH(1-84) is being investigated at this time as are other PTH molecules. Teriparatide improves bone quality by actions on bone turnover, bone density, bone size, and microarchitecture. In postmenopausal women with osteoporosis, teriparatide reduces the incidence for vertebral and nonvertebral fractures. In individuals who have been treated previously with an antiresorptive agent, the subsequent actions of teriparatide on bone density are delayed transiently if bone turnover is markedly suppressed. Combination therapy with teriparatide or PTH(1-84) and an antiresorptive does not appear, at this time, to offer advantages over the use of PTH or an antiresorptive alone. To maintain the gains in bone density with PTH, it is important to follow its use with an antiresorptive agent.

Anabolic Agents↗
PubMed2006

Pseudohypoparathyroidism: a rare cause of bilateral slipped capital femoral epiphysis.

Pseudohypoparathyroidism (PHP) type 1b is a rare childhood disorder characterized by renal resistance to parathyroid hormone (PTH) resulting in biochemical hypoparathyroidism but with skeletal sensitivity to PTH. We describe a patient with PHP type 1b who we believe is one of the youngest reported patients with bilateral slipped capital femoral epiphyses (SCFE).

Child, Preschool↗
PubMed2006

The diagnosis and management of asymptomatic primary hyperparathyroidism.

Classical primary hyperparathyroidism--a disease of 'bones, stones, and psychic groans'--is a rarity in the US, although it is still seen in some parts of the world. Today, most patients with primary hyperparathyroidism are asymptomatic. This change in clinical profile is not merely because of improved detection techniques, and patients with primary hyperparathyroidism who lack symptoms, if left untreated, rarely develop the 'classical' features that were common previously. Indeed, currently available data suggest that there is, today, a disorder with different, yet characteristic, effects on the end-organs of the hyperparathyroid process. In this review, the features of the skeletal, renal, neuropsychologic, cardiovascular, and gastrointestinal manifestations of 'asymptomatic' primary hyperparathyroidism will be discussed. The considerable body of data that has emerged since the recognition of the new clinical profile of primary hyperparathyroidism has allowed a reconsideration of standards of care for this disease. These data were reviewed and incorporated into new clinical guidelines at the 2002 NIH workshop on asymptomatic primary hyperparathyroidism. These recommendations highlight both what is known about the disease, and important areas that need investigation. Continued interest in the skeletal, cardiovascular, and neuropsychiatric manifestations of the disease, and therapeutic trials of medical approaches for its management, will further refine our current understanding, and could lead to additional modifications in the approach to patients with this common endocrine disorder.

Bone Diseases↗
PubMed2006

Asymptomatic primary hyperparathyroidism.

Primary hyperparathyroidism is a common disorder of mineral metabolism characterized by incompletely regulated, excessive secretion of parathyroid hormone from one or more of the parathyroid glands. In adults with the disease, a single, benign adenoma is seen approximately 80 percent of the time, with multiple gland involvement comprising most of the remaining patients. Very rarely, a parathyroid cancer is responsible but it is seen in less than 0.5 percent of patients with primary hyperparathyroidism. In this article, we will review important clinical and diagnostic features of asymptomatic primary hyperparathyroidism as well as considerations for surgical or medical management of the disease.

Biomarkers↗
PubMed2006

Anabolic skeletal therapy for osteoporosis.

Antiresorptive agents for osteoporosis are a cornerstone of therapy, but anabolic drugs have recently widened our therapeutic options. By directly stimulating bone formation, anabolic agents reduce fracture incidence by improving bone qualities besides increasing bone mass. In this article, we review the role of anabolic treatment for osteoporosis. The only anabolic agent currently approved in the United States for osteoporosis, teriparatide [recombinant human parathyroid hormone(1-34)], has clearly emerged as a major approach to selected patients with osteoporosis. Teriparatide increases bone density and bone turnover, improves microarchitecture, and changes bone size. The incidence of vertebral and nonvertebral fractures is reduced. Teriparatide is approved for both postmenopausal women and men with osteoporosis who are at high risk for fracture. Other potential anabolic therapies for osteoporosis, including other forms of parathyroid hormone, strontium ranelate, growth hormone, and insulin-like growth factor-1, are also reviewed in this article.

Bone Density↗
PubMed2006

Update on osteoporosis therapy.

Osteoporosis is a skeletal disorder characterized by compromised bone strength that predisposes a person to increased fracture risk. Fractures are often associated with increased morbidity, higher mortality, loss of function and even psychological consequences. Pharmacotherapeutic interventions (e.g., bisphosphonates, selective estrogen receptor modulators, calcitonin, and teriparatide) in women with postmenopausal osteoporosis provide substantial reduction in fracture risk over and above risk reduction with calcium and vitamin D supplementation alone. The importance of nutritional support along with an appropriate exercise regimen, avoiding smoking and excessive alcohol use is to be emphasized along with the pharmacologic approach to osteoporosis. Despite the effectiveness of therapy with pharmacologic agents, most patients who start therapy do not remain on treatment for more than 1 year.

Accidental Falls↗
PubMed2006

Anabolic Agents for Osteoporosis : What is Their Likely Place in Therapy?

Antiresorptive agents for osteoporosis are a cornerstone of therapy, but anabolic drugs have recently widened our therapeutic options. By directly stimulating bone formation, anabolic agents reduce fracture incidence by improving other bone qualities in addition to increasing bone mass. Teriparatide (human parathyroid hormone[1-34]) has clearly emerged as a major approach for selected patients with osteoporosis. Teriparatide increases bone mineral density and bone turnover, improves bone microarchitecture, and changes bone size. The incidence of vertebral and non-vertebral fractures is reduced. Teriparatide is approved in many countries throughout the world for the treatment of both postmenopausal women and men with osteoporosis who are at high risk for fracture. Another anabolic agent, strontium ranelate, may both promote bone formation and inhibit bone resorption. Clinical trials support the use of strontium ranelate as a treatment for postmenopausal osteoporosis and have shown that strontium ranelate reduces the frequency of vertebral and non-vertebral fractures. Other potential anabolic therapies for osteoporosis, including other forms of parathyroid hormone, growth hormone, and insulin-like growth factor-I, have been examined, although less data are currently available on these approaches.

Anabolic Agents↗
PubMed2006

Position Development Conference of the International Society for Clinical Densitometry. Vancouver, BC, July 15-17, 2005.

Every 2 years the International Society for Clinical Densitometry (ISCD) organizes a position development conference at which a panel of experts reviews topics of interest in the field of bone densitometry and proposes Official Positions of the ISCD. In July 2005, the most recent conference was held in Vancouver, Canada, during which 4 topics were discussed: (1) Cross-calibration of dual energy x-ray absorptiometry (DXA) systems, (2) Vertebral fracture assessment, (3) World Health Organization (WHO) classification of bone density for populations other than postmenopausal women, and (4) WHO classification for varying skeletal sites. The Official Positions reached at this conference enumerated in this report have been published in The Journal of Clinical Densitometry, and can be found at www.iscd.org.

Absorptiometry, Photon↗
PubMed2005

Clinical review: Rare causes of hypercalcemia.

CONTEXT: Although hypercalcemia is usually caused by primary hyperparathyroidism or malignancy, a number of other conditions can be important to consider. This review considers unusual causes of hypercalcemia that are generally not found in reviews on this subject. EVIDENCE ACQUISITION: Articles describing rarely reported associations between hypercalcemia and unusual causes were identified through a computer search of the terms hypercalcemia/etiology and through the references listed in those articles. We grouped the 58 different reports into categories defined by a presumed etiology: increased levels of 1,25-dihydroxyvitamin D or PTHrP, occult milk-alkali syndrome, and undefined mechanisms. Reports in infants and children are listed separately, as are reports of pseudohypercalcemia, situations that are not truly hypercalcemic because the ionized calcium is normal. EVIDENCE SYNTHESIS: In some situations, as this review points out, a number of unusual causes of hypercalcemia are important to consider. The search for an elusive cause of hypercalcemia is best accomplished by the most likely potential mechanism. An orderly search in this manner is likely to reveal the underlying cause. CONCLUSIONS: That so many patients have been described with rare and usually poorly understood causes of hypercalcemia highlights our incomplete understanding of calcium metabolism in humans and suggests additional areas in which directed clinical investigation might improve our knowledge of the normal metabolism of calcium.

Calcitriol↗
PubMed2005

One year of alendronate after one year of parathyroid hormone (1-84) for osteoporosis.

BACKGROUND: Since the use of parathyroid hormone as a treatment for osteoporosis is limited to two years or less, the question of whether antiresorptive therapy should follow parathyroid hormone therapy is important. We previously reported results after the first year of this randomized trial comparing the use of full-length parathyroid hormone (1-84) alone, alendronate alone, or both combined. In the continuation of this trial, we asked whether antiresorptive therapy is required to maintain gains in bone mineral density after one year of therapy with parathyroid hormone (1-84). METHODS: In the data reported here, women who had received parathyroid hormone (1-84) monotherapy (100 microg daily) in year 1 were randomly reassigned to one additional year with either placebo (60 subjects) or alendronate (59 subjects). Subjects who had received combination therapy in year 1 received alendronate in year 2; those who had received alendronate monotherapy in year 1 continued with alendronate in year 2. Bone mineral density at the spine and hip was assessed with the use of dual-energy x-ray absorptiometry and quantitative computed tomography (CT). RESULTS: Over two years, alendronate therapy after parathyroid hormone therapy led to significant increases in bone mineral density in comparison with the results for placebo after parathyroid hormone therapy, a difference particularly evident for bone mineral density in trabecular bone at the spine on quantitative CT (an increase of 31 percent in the parathyroid hormone-alendronate group as compared with 14 percent in the parathyroid hormone-placebo group). During year 2, subjects receiving placebo lost substantial bone mineral density. CONCLUSIONS: After one year of parathyroid hormone (1-84), densitometric gains appear to be maintained or increased with alendronate but lost if parathyroid hormone is not followed by an antiresorptive agent. These results have clinical implications for therapeutic choices after the discontinuation of parathyroid hormone.

Aged↗