Drug-Induced Bone Loss

Abstract

Bone loss leading to osteoporosis is common after the menopause and in the elderly but uncommon in normal young adults without predisposing factors. The risk factors usually associated with osteoporosis include a family history of osteoporosis or fractures, aging, prior diseases, sedentary lifestyle, low calcium intake, hypogonadism, vitamin D deficiency, smoking, and excessive alcohol consumption. However, the issue of drugs has to be considered in 'normal' individuals who present with osteoporosis or bone loss without predisposing genetic or other environmental factors. The list of drugs is extensive and includes, amongst others, glucocorticoids, thyroid hormone (excess), alcohol, medroxyprogesterone acetate, luteinizing hormone-releasing hormone agonists, anti-seizure medications, cyclosporine A, aluminium, lithium, and exchange resins. This paper reviews the pathophysiology and mechanisms of drug-induced bone loss, which includes osteoporosis and osteomalacia, and treatment concepts. Undoubtedly, physician awareness, appropriate investigation, careful prescribing, monitoring, and proper therapy for this eminently preventable side effect can preserve bone in the patients receiving bone-losing drugs.

Influence of Rituximab on markers of bone remodeling in patients with rheumatoid arthritis: a prospective open-label pilot study

“…Furthermore, the first report on improvement in bone turnover after application of the IL-6 receptor inhibitor tocilizumab has been published (21). On the other hand, methotrexate or cyclosporine may have in part unfavorable effects on bone density and quality indicating divergent effects on juxtaarticulare and systemic bone (22,23).…”

Cyclosporin A Enhances Callus Formation in Rabbit Tibia Fractures

“…In contrast, others have reported that CsA treatment in rats causes a high turnover osteoporosis due to increased bone resorption [3,[12][13][14] This is in agreement with the finding of early bone loss in patients receiving CsA and glucocorticoids after heart transplantation [15]. However, the combination therapy used in transplantation patients makes it difficult to detect specific effects of the different drugs [3,5]. CsA treatment has been found to correlate to a slight osteoclast stimulation, osteblast suppression and decreased bone mineral density in renal transplant patients [1].…”

“…In addition, Orcel et al found that CsA stimulated bone formation in rat bone and inhibited bone resorption without affecting PTH or vitamin D [12]. In contrast, others have reported that CsA treatment in rats causes a high turnover osteoporosis due to increased bone resorption [3,[12][13][14] This is in agreement with the finding of early bone loss in patients receiving CsA and glucocorticoids after heart transplantation [15]. However, the combination therapy used in transplantation patients makes it difficult to detect specific effects of the different drugs [3,5].…”

“…However, a frequent complication to this treatment is the development of osteopenia as well as fractures [1][2][3][4][5]. Little is known about the mechanisms behind these effects.…”

Osteoporose após transplante de órgãos sólidos

“…Os glicocorticóides têm grandes efeitos na homeostasia mineral. Os esteróides podem estimular a secreção de paratormônio (PTH) diretamente (5) (8). No rim há diminuição da reabsorção tubular de cálcio e fosfato.…”