Treatment Of Steroid-induced Osteoporosis Research Articles

The 2023 Guidelines for the management and treatment of glucocorticoid-induced osteoporosis

IntroductionAlthough synthetic glucocorticoids (GCs) are commonly used to treat autoimmune and other diseases, GC induced osteoporosis (GIOP) which accounts for 25% of the adverse reactions, causes fractures in 30–50% of patients, and markedly decreases their quality of life. In 2014, the Japanese Society for Bone and Mineral Research (JSBMR) published the revised guidelines for the management and treatment of steroid-induced osteoporosis, providing the treatment criteria based on scores of risk factors, including previous fractures, age, GC doses, and bone mineral density, for patients aged ≥18 years who are receiving GC therapy or scheduled to receive GC therapy for ≥3 months.Materials and methodsThe Committee on the revision of the guidelines for the management and treatment of GIOP of the JSBMR prepared 17 clinical questions (CQs) according to the GRADE approach and revised the guidelines for the management and treatment of GIOP through systematic reviews and consensus conferences using the Delphi method.ResultsBisphosphonates (oral and injectable formulations), anti-RANKL antibody teriparatide, eldecalcitol, or selective estrogen receptor modulators are recommended for patients who has received or scheduled for GC therapy with risk factor scores of ≥3. It is recommended that osteoporosis medication is started concomitantly with the GC therapy for the prevention of fragility fractures in elderly patients.ConclusionThe 2023 guidelines for the management and treatment of GIOP was developed through systematic reviews and consensus conferences using the Delphi method.

Protective role of 3-oxypyridine derivatives in rats’ steroid-induced osteoporosis associated with reduced oxidative stress and recovery of nitric oxide formation

From the point of view of the mechanisms for the implementation of pathogenetic links in the development of steroid-induced osteoporosis considered in the paper, the increased risk of the oxidative stress in osteoblasts, as well as the development of the vessels endothelial dysfunction of the microcirculatory bloodstream in the bone tissue, are of particular interest. They lead to the impaired bone tissue trophism and progression of osteoporosis.The aim of the study was research of the osteoprotective effects of a 3-hydroxypyridine derivatives composition on the model of steroid-induced osteoporosis.Materials and methods. To model osteoporosis pathology, the animals (male Wistar rats) were injected with methylprednisolone (MP) at the dose of 5 mg/kg (intraperitoneally) every 5th day for 5 weeks. Аs a non-selective blocker of NO synthase, L-NAME was used at the dose of 25 mg/kg (intraperitoneally). Derivatives of 3-hydroxypyridine (hereinafter referred to as composition No. 1) were administrated at the dose of 50 mg/kg (per os) In all experimental groups, the level of microcirculation and the bone mineral density, as well as the analysis of histomorphological and biochemical samples, were assessed.Results. The study results showed that composition No. 1 (50 mg/kg) has an osteoprotective activity, effectively prevents a decrease in the level of the regional bone tissue microcirculation and in the development of an endothelial dysfunction. That makes it possible to increase the bone mineral density and to slow down the thinning of bone trabeculae. In addition, composition No. 1 (50 mg/kg) reduces the production of reactive oxygen species and increases the NO bioavailability.Conclusion. The data obtained indicate that the studied composition of 3-hydroxypyridine derivatives is considered a promising compound for the prevention and treatment of steroid-induced osteoporosis.

Prevention and treatment of steroid-induced osteoporosis – recommendations vs clinical practice

Prevention and treatment of steroid-induced osteoporosis – recommendations vs clinical practice

Effect of DHEA supplementation on serum IGF-1, osteocalcin, and bone mineral density in postmenopausal, glucocorticoid-treated women

DHEA therapy increases bone formation in postmenopausal women. We have found only a few reports of dehydroepiandrosterone replacement therapy in women receiving long-term glucocorticoid medication. The purpose of this study was to establish whether DHEA replacement therapy may be useful in the treatment of steroid-induced osteoporosis in postmenopausal women. Nineteen women, aged 50-78 years, treated at least for three years with average daily doses of more than 7.5 mg prednisone, with T-score L2/L4<-1.5 and bisphosphonates intolerance, were enrolled to the study. For the first year of the study the patients were given calcium, vitamin D3 and thiazide diuretics. For another year the patients received orally micronized DHEA 25-50 mg daily. Before the study, after twelve months of Calcium/D3 therapy, then after six weeks and six months of DHEA therapy, serum concentrations of DHEAS, androstenedione, testosterone, estradiol, FSH, IGF-1 and osteocalcin were assessed. Bone mineral density (BMD) in lumbar spine and femoral neck was measured before the treatment, after a year on Calcium/D3 and after six and twelve months of DHEA replacement therapy. In all treated women, DHEA significantly increased serum DHEAS, androstenedione and testosterone concentrations. A significant elevation of serum IGF-1 and osteocalcin concentrations was found as early as after six weeks of DHEA treatment. A significant increase of bone mineral density in the lumbar spine and femoral neck was observed after six and twelve months of DHEA treatment. Our results suggest a beneficial role of DHEA replacement therapy in the treatment of steroid-induced osteoporosis.

Ostéoporose cortisonique

Bone-related steroid involvement is one of the most frequent complications of steroid treatment. Epidemiological data demonstrate that osteoporosis starts early during the treatment, predominantly involves trabecular bone and is correlated to dosage and treatment duration. Mechanisms and consequences of steroid bone involvement are related to osseous and extra-osseous mechanisms. In clinical practice, steroid-induced osteoporosis remains underdiagnosed and undertreated both in preventive and curative approaches. Recently, new molecules as teriparatide and zoledronic acid got indication for the treatment of steroid-induced osteoporosis. To guide treatment strategies, several recommendations are available: French, not updated recommendations since 2003 (Afssaps, 2003), European elaborated by the EULAR in 2007 and those of the ACR updated in 2010.

What Is New in the Treatment of Steroid-Induced Osteoporosis?

Glucocorticoid-induced osteoporosis (GIOP) is a serious complication resulting from long-term steroid treatment. In addition to several nonpharmacologic therapies recommended by the American College of Rheumatology, various pharmacologic therapies, such as calcium, vitamin D, hormone-replacement therapy, calcitonin, and bisphosphonates, can be used to prevent and/or treat GIOP. Bisphosphonates, which are potent inhibitors of bone resorption, are considered the most effective and first-line agents for increasing bone mineral density and decreasing the risk of fracture. Human parathyroid hormone has emerged as a promising agent for the treatment of severe GIOP when used alone or in combination with a bisphosphonate.

What Is New in the Treatment of Steroid-Induced Osteoporosis?

Glucocorticoid-induced osteoporosis (GIOP) is a serious complication resulting from long-term steroid treatment. In addition to several nonpharmacologic therapies recommended by the American College of Rheumatology, various pharmacologic therapies, such as calcium, vitamin D, hormone-replacement therapy, calcitonin, and bisphosphonates, can be used to prevent and/or treat GIOP. Bisphosphonates, which are potent inhibitors of bone resorption, are considered the most effective and first-line agents for increasing bone mineral density and decreasing the risk of fracture. Human parathyroid hormone has emerged as a promising agent for the treatment of severe GIOP when used alone or in combination with a bisphosphonate.

Glucocorticoid-Induced Osteoporosis Evaluation, Prevention, and Treatment

Systemically administered glucocorticoids are widely used in rheumatology and have many serious side effects. Approximately 30-50% of patients chronically taking glucocorticoids develop osteoporosis. Studies looking at specific rheumatologic diseases, such as rheumatoid arthritis, suggest that subpopulations of rheumatology patients are particularly at risk for development of osteoporosis.Over the last few years, several studies have validated the role of routine administration of calcium and low dose vitamin D. Early limited studies suggest that hormonal replacement of testosterone and estrogen in selected patients may be of value, and newer therapies such as bisphosphonates and calcitonin have revolutionized the prevention and treatment of steroid-induced osteoporosis. These newer therapies, combined with the increased availability and accuracy of tests that measure bone mineral density, such as dual energy x-ray absorptiometry (DXA), make it important to use such tests and to individualize needed interventions for all patients requiring long-term systemic gluocorticoids.

Possible prevention and treatment of steroid-induced osteoporosis

Patients with steroid-induced, juvenile and senile osteoporosis were studied using balance techniques. The changes in calciun and phosphorus balance associated with glucocorticoid therapy were corrected with vitamin D and bendrofluazide given in combination. No hypercalcaemia occurred in osteoporotic patients who continued to receive glucocorticoids. Calcium and phosphorus balance was also improved in the osteoporotic subjects not receiving steroids, but these patients became hypercalcaemic during treatment. It is suggested that vitamin D, bendrofluazide and steroids antagonize the actions of one another on the renal tubule, gut and bone and in this way prevent the increased calciuria which occurs with glucocorticoid therapy. Since the increased calciuria and negative calcium balance induced by glucocorticoids is considered to be the result of excessive bone resorption, an adequate dose of bendrofluazide and vitamin D in combination might prevent the development of, or even reverse, steroid-induced osteoporosis.