Drugs Causing Bone Loss

Vestergaard, Peter

doi:10.1007/164_2019_340

Cited by 26 publications

(14 citation statements)

References 171 publications

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“…Among numerous drugs used for HPI-related diseases many are well known to contribute to OP/OFs. In regard to OP, these include corticosteroids, antidepressants (especially, selective serotonin- and serotonin-norepinephrine reuptake inhibitors), glitazones, opioids, benzodiazepines, antipsychotics, antiparkinsonian drugs, antiepileptics, PPIs, H2RA, thyroxine, furosemide, aromatase inhibitors, gonadotropin releasing hormone (GnRH) agonists, whereas hormone replacement therapy with estrogen, thiazides, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), spironolactone, beta-blockers, statins, antihistamines, metformin, sulphonylureas, glucagon-like peptide-1 receptor agonists (liraglutide) and nitrates have shown an osteoprotective effect [ 316 , 521 , 522 , 523 , 524 , 525 , 526 , 527 , 528 , 529 , 530 , 531 , 532 , 533 , 534 , 535 , 536 , 537 , 538 , 539 , 540 , 541 , 542 , 543 , 544 , 545 , 546 , 547 , 548 , 549 , 550 , 551 , 552 , 553 , 554 ].…”

Section: Hpi-associated Chronic Extra-gastroduodenal Diseases Medmentioning

confidence: 99%

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

Fisher

Smith

2020

JCM

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Osteoporosis (OP) and osteoporotic fractures (OFs) are common multifactorial and heterogenic disorders of increasing incidence. Helicobacter pylori (H.p.) colonizes the stomach approximately in half of the world’s population, causes gastroduodenal diseases and is prevalent in numerous extra-digestive diseases known to be associated with OP/OF. The studies regarding relationship between H.p. infection (HPI) and OP/OFs are inconsistent. The current review summarizes the relevant literature on the potential role of HPI in OP, falls and OFs and highlights the reasons for controversies in the publications. In the first section, after a brief overview of HPI biological features, we analyze the studies evaluating the association of HPI and bone status. The second part includes data on the prevalence of OP/OFs in HPI-induced gastroduodenal diseases (peptic ulcer, chronic/atrophic gastritis and cancer) and the effects of acid-suppressive drugs. In the next section, we discuss the possible contribution of HPI-associated extra-digestive diseases and medications to OP/OF, focusing on conditions affecting both bone homeostasis and predisposing to falls. In the last section, we describe clinical implications of accumulated data on HPI as a co-factor of OP/OF and present a feasible five-step algorithm for OP/OF risk assessment and management in regard to HPI, emphasizing the importance of an integrative (but differentiated) holistic approach. Increased awareness about the consequences of HPI linked to OP/OF can aid early detection and management. Further research on the HPI–OP/OF relationship is needed to close current knowledge gaps and improve clinical management of both OP/OF and HPI-related disorders.

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Section: Hpi-associated Chronic Extra-gastroduodenal Diseases Medmentioning

confidence: 99%

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

Fisher

Smith

2020

JCM

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“…Alternative immunosuppressants also have side effects, and it is often easier, more evidence-based and cheaper to apply GIOP prevention or treatment rather than switching to biologicals solely because of osteoporosis risk. Cyclosporine and tacrolimus are also associated with bone loss, while azathioprine and mycophenolic acid are not ( 20 ). Methotrexate is only very rarely associated with osteopathy, mainly at excessive doses or due to drug interactions ( 77 ).…”

Section: Resultsmentioning

confidence: 99%

“…Methotrexate is only very rarely associated with osteopathy, mainly at excessive doses or due to drug interactions ( 77 ). While the mammalian target of rapamycin (mTOR) pathway plays an important role in bone metabolism, the clinical effects of mTOR inhibitors on osteoporosis or fracture risk remain poorly understood ( 20 ).…”

Section: Resultsmentioning

confidence: 99%

“…Glucocorticoids promote osteoclastogenesis and the survival of osteoclasts, stimulate adipogenesis, inhibit osteoblastogenesis and induce apoptosis of osteoblasts and osteocytes ( 13 ) in part via suppression of Wnt agonists ( 18 ) and upregulation of Wnt signaling inhibitors such as sclerostin and Dkk1 ( 19 ). Not only does this lead to reduced bone mass, they may also affect the unmineralized bone matrix, which may partly explain their BMD-independent effects ( 20 , 21 ). Recent preclinical studies additionally show that glucocorticoid excess also disrupts the intestinal microbiota ( 18 ) endogenous biological rhythm of glucocorticoids, which may contribute to the detrimental effects on bone ( 22 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Prevention and Treatment of Glucocorticoid-Induced Osteoporosis in Adults: Consensus Recommendations From the Belgian Bone Club

et al. 2022

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Glucocorticoids are effective immunomodulatory drugs used for many inflammatory disorders as well as in transplant recipients. However, both iatrogenic and endogenous glucocorticoid excess are also associated with several side effects including an increased risk of osteoporosis and fractures. Glucocorticoid-induced osteoporosis (GIOP) is a common secondary cause of osteoporosis in adults. Despite availability of clear evidence and international guidelines for the prevention of GIOP, a large treatment gap remains. In this narrative review, the Belgian Bone Club (BBC) updates its 2006 consensus recommendations for the prevention and treatment of GIOP in adults. The pathophysiology of GIOP is multifactorial. The BBC strongly advises non-pharmacological measures including physical exercise, smoking cessation and avoidance of alcohol abuse in all adults at risk for osteoporosis. Glucocorticoids are associated with impaired intestinal calcium absorption; the BBC therefore strongly recommend sufficient calcium intake and avoidance of vitamin D deficiency. We recommend assessment of fracture risk, taking age, sex, menopausal status, prior fractures, glucocorticoid dose, other clinical risk factors and bone mineral density into account. Placebo-controlled randomized controlled trials have demonstrated the efficacy of alendronate, risedronate, zoledronate, denosumab and teriparatide in GIOP. We suggest monitoring by dual-energy X-ray absorptiometry (DXA) and vertebral fracture identification one year after glucocorticoid initiation. The trabecular bone score might be considered during DXA monitoring. Extended femur scans might be considered at the time of DXA imaging in glucocorticoid users on long-term (≥ 3 years) antiresorptive therapy. Bone turnover markers may be considered for monitoring treatment with anti-resorptive or osteoanabolic drugs in GIOP. Although the pathophysiology of solid organ and hematopoietic stem cell transplantation-induced osteoporosis extends beyond GIOP alone, the BBC recommends similar evaluation, prevention, treatment and follow-up principles in these patients. Efforts to close the treatment gap in GIOP and implement available effective fracture prevention strategies into clinical practice in primary, secondary and tertiary care are urgently needed.

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“…Unlike skin and other soft organs, bone has the innate ability to regenerate without scarring by means of complex biological cascades (2,3). However, bone maintenance and/or healing can be impaired as a result of age (4,5), lifestyle (6)(7)(8), pathological conditions (9)(10)(11), medical treatment (12)(13)(14), and injury (15)(16)(17). To help bone regeneration, strengthen skeletal integrity, stabilize an implanted bone prosthesis, or relieve joint pain, surgical strategies that are often coupled to bone grafting have been developed.…”

Section: Introductionmentioning

confidence: 99%