DOCSLIB.ORG

Current and Potential Future Drug Treatments for Osteoporosis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Current and Potential Future Drug Treatments for Osteoporosis 700 Annals ofthe Rheumatic Diseases 1996;55:700-714 REVIEW Ann Rheum Dis: first published as 10.1136/ard.55.10.700 on 1 October 1996. Downloaded from Current and potential future drug treatments for osteoporosis Sanjeev Patel Osteoporosis is the most common metabolic ture risk increases by a factor of 1.5 to 3.0.6 bone disease in the developed world and is Other determinants of osteoporotic fracture increasingly recognised as an important public are shown in table 1. health problem.' There is marked worldwide Drugs active on bone can be simplistically variation in its incidence. It is predicted that classified as those that inhibit bone resorption the incidence of hip fractures caused by or those that stimulate bone formation (table osteoporosis will increase, particularly in 2). The effects of these drugs on bone mineral developing countries.2 The human burden of density are summarised in fig 1. Drugs that osteoporosis is considerable, with increased stimulate bone formation lead to a direct morbidity and mortality, especially following increase in bone mineral density, whereas those osteoporotic hip fractures.' The current finan- that inhibit bone resorption result in limited cial burden is substantial, with estimated yearly increases in bone mineral density by costs of £750 million in the UK,' $10 billion in uncoupling bone turnover and allowing forma- the USA, and FF3.7 billion in France.3 The tion to continue in excess of resorption. This ability to measure bone mineral density and leads to an increase in bone mineral density thereby monitor response to intervention has due to filling in of the remodelling space (the been vital in the development ofpharmacologi- remodelling transient).7 It has been suggested cal treatments. In this review I aim to discuss that beyond this increase (5-10%), there is lit- current issues surrounding the use of tle potential for further increases in density, http://ard.bmj.com/ established and newly licensed drugs, as well as giving rise to the term "the remodelling examining agents that are in the early stages of barrier".8 However, more recent evidence sug- development. gests that this may not be the case, and that bone mineral density may continue to increase Background beyond the first year of treatment with The cycle of bone resorption by osteoclasts antiresorptive drugs.9 In addition, decreases in followed by bone formation by osteoblasts is fractures do occur, partly due to increases in on September 25, 2021 by guest. Protected copyright. essential for modelling (resorption followed by bone mineral density leading to increased bone formation at a distant skeletal site resulting in strength as well as to a lower rate of trabecular changes in architecture and growth), and perforation associated with reduced bone remodelling (resorption followed by formation turnover. at the same skeleton site). In the first 20-25 Interventions aimed at decreasing fractures years of life, bone mineral density increases by influencing bone mineral density can either with age until peak density is achieved. It then prevent low mineral density (by maximising remains relatively constant until, in women, the peak density and decreasing rate ofloss ofbone menopause is reached, after which there is a in later life), or they can treat established low phase of rapid oestrogen dependent bone loss mineral density (osteoporosis). There are few for 5-10 years, and then a less rapid phase of data on pharmacological interventions capable age related bone loss. Prospective studies of influencing peak bone mineral density, suggest that the latter may accelerate in the although prospective cohort studies are under very old, particularly at the hip.' In men there way examining several variables including is no rapid phase of bone loss. Whether bone calcium supplements.'01' In established osteo- Osteoporosis Unit, mineral density will decrease below the so porosis, drugs that increase bone formation Department of called fracture threshold in later life is depend- and mass are required; in practice, because of a Rheumatology, St George's Hospital, ent on the absolute magnitude of peak density Table 1 Determinants ofosteoporoticfracture London SW17 OQT, and subsequent rate ofbone loss. Bone mineral United Kingdom density is highly correlated with bone strength Bone mineral density S Patel of variance in bone is Gait and propensity to fall (75-80% strength Geometry (especially at the hip) Correspondence to: explained by bone density)5 and at a given Bone dimensions Dr Sanjeev Patel. skeletal site it predicts future fracture risk. For Bone "quality" deviation which bone Bone architecture Accepted for publication every standard by ? Trochanteric fat (padding) 28 June 1996 mineral density is below peak bone mass, frac- Drug treatments for osteoporosis 701 Table 2 Current andpotentialffuture drug treatments for loss of trabecular connectivity that is seen in osteoporosis severe osteoporosis (fig 2). Ann Rheum Dis: first published as 10.1136/ard.55.10.700 on 1 October 1996. Downloaded from Drugs which suppress bone resorption Hormone replacementt (oestrogens, progestagens, tibolone, Bone resorption inhibitors tamoxifen and derivatives) HORMONE REPLACEMENT THERAPY (HRT) Anabolic steroidst Oestrogen replacement attenuates bone loss Bisphosphonatest Calcitonint that occurs after the menopause and reduces Calcium and vitamin Dt osteoporotic fractures.5 Despite this, and a Activated vitamin Dt Ipriflavonet reduction in coronary heart disease and Integrin antagonists* strokes, compliance is poor.'2 Reasons for this Proton pump inhibitors* are multiple and include the need for monthly Amylin* withdrawal bleeds (at least for non-continuous Drugs which simulate boneformation combined HRT) to prevent uterine cancer, Fluoridet anxiety regarding weight gain, breast Bone growth factors Growth hormone tenderness, and more importantly concern Parathyroid hormone regarding the increased risk of breast cancer. Parathyroid hormone receptor agonists (theoretical)* Previous meta-analyses have suggested a Vitamin D analogues* Zeolite A* relative risk of 1.0 (no increased risk) to as high Stronium salts as 1.6 for breast cancer with HRT.'2 Recent * Not tested on humans. studies do not seem to clarify this issue, show- t Licenced in some countries. ing either no increase in risk,'3 to an increase in risk with longer duration of use and age.'4 20 These differing results could be due to numer- ous factors including methodological design Stimulators of and differing HRT regimens studied in bone formation different populations. Thus whether HRT is suitable for an 10 a individual is dependent on the aim of m treatment and what is in practice a difficult Inhibitors of risk-benefit analysis, with the patient's own 0) bone resorption views and preferences playing a substantial 0o role. That is, treatment benefits such as relief of .C menopausal symptoms and reduction in cardiovascular disease and osteoporotic fractures have to be weighed against side No intervention effects, past medical and family history of -10 L cardiovascular disease, osteoporosis, and 0 1 2 3 breast cancer, as well as other risk factors and http://ard.bmj.com/ Time (years) patient preferences. For the female population, Figure 1 Influence ofvarious treatments on bone mass although more older women die of heart (see textfor details). disease than ofbreast carcinoma, the beneficial effect of HRT on cardiovascular mortality may lack of such agents (apart from fluoride) bone be negated by increased deaths from breast resorption inhibitors are used. However, it cancer. Definitive data may be provided by a should be noted that increasing trabecular long term prospective study examining the net on September 25, 2021 by guest. Protected copyright. thickness by stimulating bone formation or health effects of HRT that is being carried out inhibiting bone resorption does not reverse the in the USA under the auspices of the Women's Health Initiative. The timing and duration of HRT is also controversial. Maximum protection against High CM osteoporosis would be provided by taking life- long HRT from the menopause, although this would have to be weighed against long term side effects, as discussed above. An alternative is to start HRT after a fracture, thus allowing 0 easy identification of patients at risk who may cen\ comply with treatment. However, preventable ._.V\N fractures would occur with this strategy and Low there may be limited response due to extensive Low Normal disruption of bone architecture. A third Bone mineral density possibility is to start HRT many years after the Figure 2 Schematic relations between bone mineral menopause and to continue indefinitely there- density, trabecular connectivity, andfracture risk. As bone after. For example, starting HRT at the age of mineral density decreases from normal (A) to moderate 70-75 years may be adequate intervention to osteoporosis (B), where there is some disruption in reduce fracture since the median trabecular connectivity, fracture risk increases. Treatment at hip rates, age B will restore bone mineral density and reducefracture risk of hip fracture is 80 years and bone density at back to A. However, in severe osteoporosis (C), where bone this site continues to decrease, although mineral density is very low and trabecular connectivity is compliance in this age group is likely to be low disrupted, treatment increases trabecular thickness and bone mineral density (D), but since trabecular connectivity is and many individuals would have
Load more

Recommended publications
  • Clinico-Biochemical Study on Senile Osteoporosis
    Nagoya ]. med. Sci. 28: 110-125, 1965 CLINICO-BIOCHEMICAL STUDY ON SENILE OSTEOPOROSIS MAsAsHr NAKAGAWA, RErsuKE NATSUME, ToHRU YosHIDA, MrTsUNOBU SaroNO, OsAMU KmA, HrsASHI IwATA, AND HrsASHI HrRAKOH Department of Orthopedic Surgery, Nagoya University School of Medicine (Director: Prof. Masashi Nakagawa) KEIICHI KASAHARA Department of Orthopedic Surgery, Wakayama Medical College Osteoporosis, except that occurring secondarily to known pathogenesis, is termed senile or postmenopausal osteoporosis and arises from a still unknown cause. Primary osteoporosis may occur as a result of adrenal-gonadal imbalance or of calcium deficiency. However since these pathogenetical views are· disagreed with by many other investigators, the cause remains unproven and this clinical diagnosis lacks objective basis. At this stage, determination as to whether senile osteoporosis represents only one aspect of the physiological aging process or is independent pathological entity seems to be of definite clinical interest. In this study total serum hexosamine content in normal subjects was found to increase with advancing age. Especially, the ratio by weight of glucosamine to galactosamine in the sera decreases with increasing age until fourty-nine years of age, but beyond this age limit the ratio significantly increased. On the other hand the ratio of the serum glucosamine to galactosamine was shown to be significantly low in patients with senile osteoporosis as compared with the ratio in normal group of identical age. Also, increased urinary hydroxyproline excretion in senile osteo­ porosis as evidenced in this study appeared to suggest collagen degradation. The present study has found evidences of abnormal mucopolysaccharide metabolism and collagen degradation in osteoporotic patients. These observations suggest that senile osteoporosis, whatever the true cause may be, is an independent pathological entity rather than a simple result of senile metabolic decay.
    [Show full text]
  • Ipriflavone in the Treatment of Postmenopausal Osteoporosis a Randomized Controlled Trial
    ORIGINAL CONTRIBUTION Ipriflavone in the Treatment of Postmenopausal Osteoporosis A Randomized Controlled Trial Peter Alexandersen, MD Context Data on the efficacy and safety of ipriflavone for prevention of postmeno- Anne Toussaint, MD pausal bone loss are conflicting. Claus Christiansen, MD, PhD Objectives To investigate the effect of oral ipriflavone on prevention of postmeno- pausal bone loss and to assess the safety profile of long-term treatment with iprifla- Jean-Pierre Devogelaer, MD, PhD vone in postmenopausal osteoporotic women. Christian Roux, MD, PhD Design and Setting Prospective, randomized, double-blind, placebo-controlled, 4-year Jacques Fechtenbaum, MD, PhD study conducted in 4 centers in Belgium, Denmark, and Italy from August 1994 to July 1998. Carlo Gennari, MD, PhD Participants Four hundred seventy-four postmenopausal white women, aged 45 Jean Yves Reginster, MD, PhD to 75 years, with bone mineral densities (BMDs) of less than 0.86 g/cm2. for the Ipriflavone Multicenter Interventions Patients were randomly assigned to receive ipriflavone, 200 mg 3 times European Fracture Study per day (n = 234), or placebo (n = 240); all received 500 mg/d of calcium. TUDIES OF IPRIFLAVONE, A SYN- Main Outcome Measures Efficacy measures included spine, hip, and forearm BMD thetic isoflavone derivative, have and biochemical markers of bone resorption (urinary hydroxyproline corrected for cre- atinine and urinary CrossLaps [Osteometer Biotech, Herlev, Denmark] corrected for suggested that it inhibits bone re- creatinine), assessed every 6 months. Laboratory safety measures and adverse events sorption and stimulates osteo- were recorded every 3 months. Sblast activity in vitro in cell cultures1,2 and Results Based on intent-to-treat analysis, after 36 months of treatment, the annual in vivo in experimental models of osteo- 3 percentage change from baseline in BMD of the lumbar spine for ipriflavone vs pla- porosis.
    [Show full text]
  • Botanicals in Postmenopausal Osteoporosis
    nutrients Review Botanicals in Postmenopausal Osteoporosis Wojciech Słupski, Paulina Jawie ´nand Beata Nowak * Department of Pharmacology, Wroclaw Medical University, ul. J. Mikulicza-Radeckiego 2, 50-345 Wrocław, Poland; [email protected] (W.S.); [email protected] (P.J.) * Correspondence: [email protected]; Tel.: +48-607-924-471 Abstract: Osteoporosis is a systemic bone disease characterized by reduced bone mass and the deterioration of bone microarchitecture leading to bone fragility and an increased risk of fractures. Conventional anti-osteoporotic pharmaceutics are effective in the treatment and prophylaxis of osteoporosis, however they are associated with various side effects that push many women into seeking botanicals as an alternative therapy. Traditional folk medicine is a rich source of bioactive compounds waiting for discovery and investigation that might be used in those patients, and therefore botanicals have recently received increasing attention. The aim of this review of literature is to present the comprehensive information about plant-derived compounds that might be used to maintain bone health in perimenopausal and postmenopausal females. Keywords: osteoporosis; menopause; botanicals; herbs 1. Introduction Women’s health and quality of life is modulated and affected strongly by hormone status. An oestrogen level that changes dramatically throughout life determines the Citation: Słupski, W.; Jawie´n,P.; development of women’s age-associated diseases. Age-associated hormonal imbalance Nowak, B. Botanicals in and oestrogen deficiency are involved in the pathogenesis of various diseases, e.g., obesity, Postmenopausal Osteoporosis. autoimmune disease and osteoporosis. Many female patients look for natural biological Nutrients 2021, 13, 1609. https:// products deeply rooted in folk medicine as an alternative to conventional pharmaceutics doi.org/10.3390/nu13051609 used as the prophylaxis of perimenopausal health disturbances.
    [Show full text]
  • Nutriceuticals: Over-The-Counter Products and Osteoporosis
    serum calcium levels are too low, and adequate calcium is not provided by the diet, calcium is taken from bone. Osteoporosis: Clinical Updates Long- term dietary calcium deficiency is a known risk Osteoporosis Clinical Updates is a publication of the National factor for osteo porosis. The recommended daily cal- Osteoporosis Foundation (NOF). Use and reproduction of this publication for educational purposes is permitted and cium intake from diet and supplements combined is encouraged without permission, with proper citation. This 1000 mg/day for people aged 19 to 50 and 1200 mg/ publication may not be used for commercial gain. NOF is a day for people older than 50. For all ages, the tolerable non-profit, 501(c)(3) educational organization. Suggested upper limit is 2500 mg calcium per day. citation: National Osteoporosis Foundation. Osteoporosis Clinical Updates. Issue Title. Washington, DC; Year. Adequate calcium intake is necessary for attaining peak bone mass in early life (until about age 30) and for Please direct all inquiries to: National Osteoporosis slowing the rate of bone loss in later life.3 Although Foundation 1150 17th Street NW Washington, DC 20037, calcium alone (or with vitamin D) has not been shown USA Phone: 1 (202) 223-2226 to prevent estrogen-related bone loss, multiple stud- Fax: 1 (202) 223-1726 www.nof.org ies have found calcium consumption between 650 mg Statement of Educational Purpose and over 1400 mg/day reduces bone loss and increases Osteoporosis Clinical Updates is published to improve lumbar spine BMD.4-6 osteoporosis patient care by providing clinicians with state-of-the-art information and pragmatic strategies on How to take calcium supplements: prevention, diagnosis, and treatment that they may apply in Take calcium supplements with food.
    [Show full text]
  • Family Practice Grand Rounds Postmenopausal
    Family Practice Grand Rounds Postmenopausal Osteoporosis and Estrogen Therapy: Who Should Be Treated? Lombardo F. Palma, MD Salt Lake City, Utah DR. LOMBARDO F. PALMA (Robert Wood It is estimated that 25 percent of white women Johnson Foundation Fellow, Department of Fam­ by the age of 65 years and 50 percent by the age of ily and Community Medicine): The objective of 75 years will have vertebral fractures, by far the Grand Rounds today is to discuss the cognitive most common complication in osteoporotic post­ process by which the family physician can make a menopausal women. Hip fractures have also been rational decision about estrogen therapy in post­ related to osteoporosis, and they are at least two menopausal women. I will briefly present some times more frequent in women than in men, de­ facts about osteoporosis, the physiology of meno­ pending on the age group.1 In the United States pause and subsequent bone demineralization, the there are about 200,000 hip fractures a year at an characteristics of women at risk of developing estimated cost of over one billion dollars, and 75 osteoporosis, and the therapeutic alternatives, as percent of those are probably due to osteoporosis. well as their risks and benefits. Then we will open Hip fractures are related to a high death rate in the the discussion. elderly (16 percent die within six months).1 This is a public health issue, as there are about four mil­ lion women in the United States who are sympto­ matic from osteoporotic fractures. From the Department of Family and Community Medicine, Menopause is the result of a sharp decline in the University of Utah Medical Center, Salt Lake City, Utah.
    [Show full text]
  • Ipriflavone: an Important Bone-Building Isoflavone
    Ipriflavone: An Important Bone-Building Isoflavone Kathleen A. Head, N.D. Abstract Ipriflavone, an isoflavone synthesized from the soy isoflavone daidzein, holds great promise in the prevention and treatment of osteoporosis and other metabolic bone diseases. It has been widely studied in humans and found effective for inhibiting bone resorption and enhancing bone formation, the net result being an increase in bone density and a decrease in fracture rates in osteoporotic women. While ipriflavone appears to enhance estrogen’s effect, it does not possess intrinsic estrogenic activity, making it an attractive adjunct or alternative to conventional hormone replacement therapy. Preliminary studies have also found ipriflavone effective in preventing bone loss associated with chronic steroid use, immobility, ovariectomy, renal osteodystro- phy, and gonadotrophin hormone-releasing hormone agonists. In addition, it holds prom- ise for the treatment of other metabolic diseases affecting the bones, including Paget’s disease of the bone, hyperparathyroidism, and tinnitus caused by otosclerosis. (Altern Med Rev 1999;4(1):10-22) Introduction Ipriflavone (chemical structure: 7-isopropoxyisoflavone), derived from the soy isoflavone, daidzein, holds great promise for osteoporosis prevention and treatment (see Figure 1). Ipriflavone (IP) was discovered in the 1930s but has only recently begun to be embraced by the medical community in this country. Over 150 studies on safety and effective- ness, both animal and human, have been conducted in Italy, Hungary, and Japan. As of 1997, 2,769 patients had been treated a total of 3,132 patient years.1 Pharmacokinetics IP is metabolized mainly in the liver and excreted in the urine. Food appears to enhance its absorption.
    [Show full text]
  • PRODUCT MONOGRAPH Pr Zoledronic Acid
    PRODUCT MONOGRAPH Pr Zoledronic Acid - A (zoledronic acid injection) 5 mg/100 mL solution for intravenous infusion Bone Metabolism Regulator Sandoz Canada Inc. Date of Revision: 145 Jules-Léger June 01, 2016 Boucherville, QC, Canada J4B 7K8 Control No. : TBD Zoledronic Acid – A Page 1 of 62 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION ............................................................ 3 SUMMARY PRODUCT INFORMATION ........................................................................... 3 INDICATIONS AND CLINICAL USE ................................................................................. 3 CONTRAINDICATIONS ....................................................................................................... 4 WARNINGS AND PRECAUTIONS ..................................................................................... 4 ADVERSE REACTIONS ..................................................................................................... 10 DOSAGE AND ADMINISTRATION ................................................................................. 25 OVERDOSAGE ..................................................................................................................... 27 ACTION AND CLINICAL PHARMACOLOGY............................................................... 27 STORAGE AND STABILITY ............................................................................................. 30 SPECIAL HANDLING INSTRUCTIONS .......................................................................... 30
    [Show full text]
  • Free PDF Download
    European Review for Medical and Pharmacological Sciences 2018; 22: 4669-4676 Ipriflavone promotes osteogenesis of MSCs derived from osteoporotic rats A.-G. GAO1,2, Y.-C. ZHOU2, Z.-J. HU2, B.-B. LU2 1Department of Orthopedics, The First Affiliated Hospital Of Soochow University, Suzhou, China 2Department of Orthopedics, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi, China Abstract. – OBJECTIVE: To explore whether celerated bone resorption, bone mass decrease, Ipriflavone could prevent postmenopausal oste- microstructure destruction and bone fragility oporosis (PMOP) and improve bone quality via elevation, thus eventually leading to high risk of promoting osteogenesis of bone marrow-de- fracture5. Therefore, PMOP is a serious problem rived mesenchymal stem cell (MSCs). 6 MATERIALS AND METHODS: MSCs were ex- that poses a great challenge in public health . In tracted from rats and identified using flow cy- recent years, hormone replacement therapy and tometry. Osteogenic specific genes and adipo- calcitonin intervention are the main treatments genic specific genes in MSCs were detected by for PMOP7. However, the long-term use of es- quantitative Real-time polymerase chain reac- trogen significantly increases the prevalence of tion (qRT-PCR). The effect of Ipriflavone on os- endometrial cancer and breast cancer8. Besides, teogenesis was detected by CCK-8 (cell count- the long-term use of calcitonin injection is incon- ing kit-8) assay, ALP activity detection, alizarin 3 red staining and Western blot, respectively. Fur- venient and expensive . Currently, Ipriflavone has thermore, ovariectomized PMOP rat model was been well recognized since it could effectively constructed. The effects of Ipriflavone on osteo- prevent PMOP9,10.
    [Show full text]
  • [Product Monograph Template
    PRODUCT MONOGRAPH Pr ZOLEDRONIC ACID INJECTION 5 mg / 100 mL zoledronic acid (as zoledronic acid monohydrate) Solution for intravenous infusion Bone Metabolism Regulator Manufacturer: Dr. Reddy’s Laboratories Limited Bachupally 500 090 – INDIA Imported/Distributed By: Date of Revision: August 1, 2019 Dr. Reddy’s Laboratories Canada Inc. Mississauga, ON L4W 4Y1 Canada Submission Control Number: 228238 1 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION ..................................................................... 3 SUMMARY PRODUCT INFORMATION .................................................................................... 3 INDICATIONS AND CLINICAL USE ......................................................................................... 3 CONTRAINDICATIONS ............................................................................................................... 4 WARNINGS AND PRECAUTIONS ............................................................................................. 4 ADVERSE REACTIONS ............................................................................................................. 10 DRUG INTERACTIONS.............................................................................................................. 24 DOSAGE AND ADMINISTRATION ......................................................................................... 25 OVERDOSAGE ............................................................................................................................ 27 ACTION AND CLINICAL
    [Show full text]
  • Bone Health in Estrogen-Free Contraception
    Osteoporosis International (2019) 30:2391–2400 https://doi.org/10.1007/s00198-019-05103-6 REVIEW Bone health in estrogen-free contraception P. Hadji1,2 & E. Colli3 & P.-A. Regidor 4 Received: 11 May 2019 /Accepted: 18 July 2019 /Published online: 24 August 2019 # International Osteoporosis Foundation and National Osteoporosis Foundation 2019 Abstract Estrogens and progestogens influence the bone. The major physiological effect of estrogen is the inhibition of bone resorption whereas progestogens exert activity through binding to specific progesterone receptors. New estrogen-free contraceptive and its possible implication on bone turnover are discussed in this review. Insufficient bone acquisition during development and/or accelerated bone loss after attainment of peak bone mass (PBM) are 2 processes that may predispose to fragility fractures in later life. The relative importance of bone acquisition during growth versus bone loss during adulthood for fracture risk has been explored by examining the variability of areal bone mineral density (BMD) (aBMD) values in relation to age. Bone mass acquired at the end of the growth period appears to be more important than bone loss occurring during adult life. The major physiological effect of estrogen is the inhibition of bone resorption. When estrogen transcription possesses binds to the receptors, various genes are activated, and a variety modified. Interleukin 6 (IL-6) stimulates bone resorption, and estrogen blocks osteoblast synthesis of IL- 6. Estrogen may also antagonize the IL-6 receptors. Additionally, estrogen inhibits bone resorption by inducing small but cumu- lative changes in multiple estrogen-dependent regulatory factors including TNF-α and the OPG/RANKL/RANK system.
    [Show full text]
  • Clinical Practice Guidelines AMERICAN ASSOCIATION OF
    Clinical Practice Guidelines AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS/ AMERICAN COLLEGE OF ENDOCRINOLOGY CLINICAL PRACTICE GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS— 2020 UPDATE Pauline M. Camacho, MD, FACE1; Steven M. Petak, MD, JD, FACP, FCLM, MACE, CCD2; Neil Binkley, MD3; Dima L. Diab, MD, FACE, FACP, CCD4; Leslie S. Eldeiry, MD5; Azeez Farooki, MD6; Steven T. Harris, MD, FACP, FASBMR7; Daniel L. Hurley, MD, FACE8; Jennifer Kelly, DO, FACE9; E. Michael Lewiecki, MD, FACE, FACP, CCD10; Rachel Pessah-Pollack, MD, FACE11; Michael McClung, MD, FACP, FACE12; Sunil J. Wimalawansa, MD, PhD, MBA, FCCP, FACP, FRCP, DSc, FACE13; Nelson B. Watts, MD, FACP, CCD, FASBMR, MACE14 The American Association of Clinical Endocrinologists’ Medical Guidelines for Practice are systematically developed statements to assist health-care professionals in medical decision-making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflect the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines must be made considering local resources and individual patient circumstances.
    [Show full text]
  • AACE/ACE Guidelines AMERICAN ASSOCIATION of CLINICAL
    AACE/ACE Guidelines AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY CLINICAL PRACTICE GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS — 2016 Pauline M. Camacho, MD, FACE; Steven M. Petak, MD, MACE, FACP, FCLM, JD; Neil Binkley, MD; Bart L. Clarke, MD, FACP, FACE; Steven T. Harris, MD, FACP Daniel L. Hurley, MD, FACE; Michael Kleerekoper, MBBS, MACE; E. Michael Lewiecki, MD, FACP, FACE; Paul D. Miller, MD; Harmeet S. Narula, MD, FACP, FACE; Rachel Pessah-Pollack, MD, FACE; Vin Tangpricha, MD, PhD, FACE; Sunil J. Wimalawansa, MD, PhD, MBA, FCCP, FACP, FRCP, DSc, FACE; Nelson B. Watts, MD, FACP, MACE The American Association of Clinical Endocrinologists/American College of Endocrinology Medical Guidelines for Practice are systematically developed statements to assist healthcare professionals in medical decision-making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances. From 1Professor
    [Show full text]