Drug-Induced Metabolic Bone Disorders

Lawson, Jack

doi:10.1055/s-2002-36727

Cited by 20 publications

(5 citation statements)

References 61 publications

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“…Many patients have pre-existing nutritionally inadequate diets [EL 4 [44, 98, (6) 133]), and deficiencies are commoner in the older and more overweight EL2A (EL 2b [183,184]) and may be exacerbated by drugs commonly used to treat obesity comorbidities (EL 4 [180,280]). Such deficiencies are more likely to be exacerbated rather than improved by bariatric surgery, especially malabsorptive procedures (EL 4 [27,91,130,194,268]).…”

Section: Long-term After-carementioning

confidence: 99%

Obesity surgery: Evidence-based guidelines of the European Association for Endoscopic Surgery (EAES)

Sauerland

Angrisani

Belachew³

et al. 2004

Surg Endosc

454

280

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After the patient's multidisciplinary evaluation, obesity surgery should be considered in adults with a documented BMI greater than or equal to 35 and related comorbidity, or a BMI of at least 40. In addition to standard laboratory testing, chest radiography, electrocardiography, spirometry, and abdominal ultrasonography, the preoperative evaluation of obesity surgery patients also includes upper gastrointestinal endoscopy or radiologic evaluation with a barium meal. Psychiatric consultation and polysomnography can safely be restricted to patients with clinical symptoms on preoperative screening. Adjustable gastric banding (GB), vertical banded gastroplasty (VBG), Roux-en-Y gastric bypass (RYGB) and biliopancreatic diversion (BPD) are all effective in the treatment of morbid obesity, but differ in degree of weight loss and range of complications. The choice of procedure therefore should be tailored to the individual situation. There is evidence that a laparoscopic approach is advantageous for LAGB, VBG, and GB (and probably also for BPD). Antibiotic and antithromboembolic prophylaxis should be used routinely. Patients should be seen 3 to 8 times during the first postoperative year, 1 to 4 times during the second year and once or twice a year thereafter. Outcome assessment after surgery should include weight loss and maintainance, nutritional status, comorbidities and quality-of-life.

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Section: Long-term After-carementioning

confidence: 99%

Obesity surgery: Evidence-based guidelines of the European Association for Endoscopic Surgery (EAES)

Sauerland

Angrisani

Belachew³

et al. 2004

Surg Endosc

454

280

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“…Second, for treatment of osteoporosis, the compounds that would “normalize” rather than totally block osteoclast activity are desired [2], [3]. Moreover, bone related side effects of numerous medications, including corticosteroids, immunosuppressants and anticonvulsants [4] provide ongoing need to assess potential effects of new therapies on bone cells, including osteoclasts. To assist in drug development and testing, different types of in vitro osteoclast formation and activity assays are commonly used for screening pharmacological compounds [5], [6].…”

Section: Introductionmentioning

confidence: 99%

Complex Dynamics of Osteoclast Formation and Death in Long-Term Cultures

et al. 2008

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BackgroundOsteoclasts, cells responsible for bone resorption, contribute to the development of degenerative, metabolic and neoplastic bone diseases, which are often characterized by persistent changes in bone microenvironment. We aimed to investigate the dynamics of osteoclast formation and death in cultures that considerably exceeded the length of standard protocol and to design a mathematical model describing osteoclastogenesis.Methodology/Principal FindingsRAW 264.7 monocytic cells fuse to form multinucleated osteoclasts upon treatment with pro-resorptive cytokine RANKL. We have found that in long-term experiments (15–26 days), the dynamics of changes in osteoclast numbers was remarkably complex and qualitatively variable in different experiments. Whereas 19 of 46 experiments exhibited single peak of osteoclast formation, in 27 experiments we observed development of successive waves of osteoclast formation and death. Periodic changes in osteoclast numbers were confirmed in long-term cultures of mouse bone marrow cells treated with M-CSF and RANKL. Because the dynamics of changes in osteoclast numbers was found to be largely independent of monocytes, a two-species model of ordinary differential equations describing the changes in osteoclasts and monocytes was ineffective in recapitulating the oscillations in osteoclast numbers. Following experimental observation that medium collected from mature osteoclasts inhibited osteoclastogenesis in fresh cultures, we introduced a third variable, factor f, to describe osteoclast-derived inhibitor. This model allowed us to simulate the oscillatory changes in osteoclasts, which were coupled to oscillatory changes in the factor f, whereas monocytes changed exponentially. Importantly, to achieve the experimentally observed oscillations with increasing amplitude, we also had to assume that osteoclast presence stimulates osteoclast formation.Conclusions/SignificanceThis study identifies the critical role for osteoclast autocrine regulation in controlling long-term dynamic of osteoclast formation and death and describes the complementary roles for negative and positive feedback mediators in determining the sharp dynamics of activation and inactivation of osteoclasts.

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“…Retinoids.-Retinoids accelerate bone maturation, with more rapid enchondral bone formation and subperiosteal appositional growth of the cortex, increased bone remodeling, and premature epiphyseal fusion. The predominant radiographic feature is skeletal hyperostosis, which is manifested by vertebral osteophytes, ossification of ligaments, and osseous bridges between vertebral bodies (60). The findings may resemble those of diffuse idiopathic skeletal hyperostosis, also known as DISH.…”

Section: Hyperostosis and Osteosclerosismentioning

confidence: 99%

Imaging Features of Therapeutic Drug–induced Musculoskeletal Abnormalities

Sidhu¹,

Venkatanarasimha²,

Bhatnagar³

et al. 2012

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Increasing use of a wide variety of therapeutic drugs with known musculoskeletal side-effect profiles necessitates a rigorous understanding and approach when evaluating imaging features suggestive of drug-induced musculoskeletal abnormalities. The etiology of such abnormalities is diverse, and the clinical and imaging manifestations may be nonspecific. The recognition of adverse effects depends, first, on the physician's vigilant review of clinical information for relevant drug history and indicative signs, and second, on the radiologist's ability to detect musculoskeletal changes consistent with known potential effects of specific drugs. Musculoskeletal abnormalities induced by therapeutic drugs may be broadly categorized as embryopathic, juvenile, or postmaturation. Embryopathic skeletal abnormalities result from the teratogenic effects of drugs administered to pregnant women (eg, thalidomide, anticonvulsants). Other therapeutic agents characteristically lead to abnormalities during postnatal skeletal maturation (eg, high-dose vitamins or prostaglandin) either because they are used exclusively in children or because they have idiosyncratic effects on immature musculoskeletal structures. Many drugs (eg, statins) may have musculoskeletal side effects that, although independent of the stage of skeletal maturation, are most often seen in adults or elderly people because they are commonly prescribed for people in these age groups. Drug-induced musculoskeletal abnormalities may be further characterized according to the predominant skeletal manifestations as osteomalacic, proliferative, or osteoporotic and according to the involvement of soft tissues as musculotendinous or chondral.

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Drug-Induced Metabolic Bone Disorders

Cited by 20 publications

References 61 publications

Obesity surgery: Evidence-based guidelines of the European Association for Endoscopic Surgery (EAES)

Obesity surgery: Evidence-based guidelines of the European Association for Endoscopic Surgery (EAES)

Complex Dynamics of Osteoclast Formation and Death in Long-Term Cultures

Imaging Features of Therapeutic Drug–induced Musculoskeletal Abnormalities

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