Therapy For Glucocorticoid-induced Osteoporosis Research Articles

Pulsed electromagnetic fields as a promising therapy for glucocorticoid-induced osteoporosis.

Glucocorticoid-induced osteoporosis (GIOP) is considered the third type of osteoporosis and is accompanied by high morbidity and mortality. Long-term usage of glucocorticoids (GCs) causes worsened bone quality and low bone mass via their effects on bone cells. Currently, there are various clinical pharmacological treatments to regulate bone mass and skeletal health. Pulsed electromagnetic fields (PEMFs) are applied to treat patients suffering from delayed fracture healing and non-unions. PEMFs may be considered a potential and side-effect-free therapy for GIOP. PEMFs inhibit osteoclastogenesis, stimulate osteoblastogenesis, and affect the activity of bone marrow mesenchymal stem cells (BMSCs), osteocytes and blood vessels, ultimately leading to the retention of bone mass and strength. However, the underlying signaling pathways via which PEMFs influence GIOP remain unclear. This review attempts to summarize the underlying cellular mechanisms of GIOP. Furthermore, recent advances showing that PEMFs affect bone cells are discussed. Finally, we discuss the possibility of using PEMFs as therapy for GIOP.

Autophagy as a target for glucocorticoid-induced osteoporosis therapy.

Autophagy takes part in regulating the eukaryotic cells function and the progression of numerous diseases, but its clinical utility has not been fully developed yet. Recently, mounting evidences highlight an important correlation between autophagy and bone homeostasis, mediated by osteoclasts, osteocytes, bone marrow mesenchymal stem cells, and osteoblasts, and autophagy plays a vital role in the pathogenesis of glucocorticoid-induced osteoporosis (GIOP). The combinations of autophagy activators/inhibitors with anti-GIOP first-line drugs or some new autophagy-based manipulators, such as regulation of B cell lymphoma 2 family proteins and caspase-dependent clearance of autophagy-related gene proteins, are likely to be the promising approaches for GIOP clinical treatments. In view of the important role of autophagy in the pathogenesis of GIOP, here we review the potential mechanisms about the impacts of autophagy in GIOP and its association with GIOP therapy.

MR spectroscopy for assessing the effects of oxytocin on marrow adipogenesis induced by glucocorticoid in rabbits.

Previous studies suggest that oxytocin (OT) negatively modulates adipogenesis while promoting osteogenesis invitro. Because of its effects on marrow stromal cells, OT might have potential utility in therapy for glucocorticoid-induced osteoporosis (GIO). To explore the effects of OT on marrow adipogenesis in a rabbit model of GIO. Thirty-six-month-old female New Zealand rabbits were randomly assigned to the control, GIO, and GIO + OT groups. Magnetic resonance (MR) spectroscopy and multi-detector computed tomography (MDCT) were performed to detect marrow fat content (MFC) and bone mineral density (BMD) at baseline, and 1, 2, and 3 months. After 3 months of treatment, marrow adipocytes were quantitatively evaluated by histopathology. In the GIO group, MFC substantially increased from 34.1% to 43.2% at month 1, and it was maintained until month 3 (by 59.2%, all P <0.01). MFC values in the GIO group were significantly different from the control and OT-treated groups over time. Early OT treatment reversed marrow adiposity to levels of the controls. BMD values were significantly lower in the GIO group at months 2 and 3 compared to the controls; however, partial recovery of vertebral BMD (87.1% of baseline) and femoral BMD (89.3% of baseline) in the OT-treated group were observed. The mean diameter and density of adipocyte and percentage of adipocyte area increased by 30.0%, 70.1%, and 88.9%, respectively (all P <0.05) in the GIO group, but remained unchanged in the OT-treated group. Early OT treatment was sufficient to eliminate glucocorticoid-induced marrow adiposity.

An Internet-based Controlled Trial Aimed to Improve Osteoporosis Prevention among Chronic Glucocorticoid Users

To address the low prevention and treatment rates for those at risk of glucocorticoid-induced osteoporosis (GIOP), we evaluated the influence of a direct-to-patient, Internet-based educational video intervention using "storytelling" on rates of antiosteoporosis medication use among chronic glucocorticoid users who were members of an online pharmacy refill service. We identified members who refilled ≥ 5 mg/day of prednisone (or equivalent) for 90 contiguous days and had no GIOP therapy for ≥ 12 months. Using patient stories, we developed an online video addressing risk factors and treatment options, and delivered it to members refilling a glucocorticoid prescription. The intervention consisted of two 45-day "Video ON" periods, during which the video automatically appeared at the time of refill, and two 45-day "Video OFF" periods, during which there was no video. Members could also "self-initiate" watching the video by going to the video link. We used an interrupted time series design to evaluate the effectiveness of this intervention on GIOP prescription therapies over 6 months. Among 3017 members (64.8%) exposed to the intervention, 59% had measurable video viewing time, of which 3% "self-initiated" the video. The GIOP prescription rate in the "Video ON" group was 2.9% versus 2.7% for the "Video OFF" group. There was a nonsignificant trend toward greater GIOP prescription in members who self-initiated the video versus automated viewing (5.7% vs 2.9%, p = 0.1). Among adults at high risk of GIOP, prescription rates were not significantly affected by an online educational video presented at the time of glucocorticoid refill. ClinicalTrials.gov Identifier: NCT01378689.

Bisphosphonates and glucocorticoid-induced osteoporosis: Efficacy and tolerability

In this review, the efficacy concern relating to bisphosphonates therapy for glucocorticoid-induced osteoporosis is considered. Sole the randomised clinical trials that including more than 50 patients in each treatment arm were considered. This review also covered the safety of bisphosphonates in the setting of glucocorticoid-induced osteoporosis with specific focus on atrial fibrillation, osteonecrosis of the jaw, upper gastrointestinal adverse events and esophageal cancer risk, atypical fractures and renal safety. These last adverse events have been selected due to the rationale of a possible additive, pathophysiologic or synergetic, deleterious effect of bisphosphonates and glucocorticoid on these organs. The available evidence for glucocorticoid-induced osteoporosis treatment and management is much less important than for post-menopausal osteoporosis. However, based on randomised clinical trials with lumbar spine BMD as the primary endpoint after one year, bisphosphonates can be considered as efficacious. Alendronate, etidronate, risedronate and zoledronate prevented declines in spine BMD in adults receiving glucocorticoid. Treatment and prevention studies in glucocorticoid-induced osteoporosis have a short duration and have included smaller population than in post-menopausal osteoporosis. However in this setting, the safety profile of bisphosphonates in glucocorticoid-induced osteoporosis was good. Long-term use of bisphosphonates in patients treated with glucocorticoid might be cautiously monitored in order to prevent adverse effects.

A hospital-based study of prophylactic therapy in glucocorticoid-induced osteoporosis

To find out the proportion of patients who qualifies to receive prophylactic therapy for glucocorticoid-induced osteoporosis. Retrospective record review. Participants Current users of oral glucocorticoids referred for bone mineral density estimation to assess their fracture risk (n=134). Clinical history and bone mineral density of the spine and proximal femur. Based on the current U.K. guidelines published by the College of Physicians of London in 2002, 22 of 57 (probability of 0.39) patients under 20 years, 19 of 38 (probability of 0.5) between 20-49 years, 22 of 28 (probability of 0.79) between 50-64 years and 10 of 11 (probability of 0.9) above 64 years, qualified for the diagnosis of glucocorticoid-induced osteoporosis and prophylactic therapy was indicated for them. The prevalence of glucocorticoid-induced osteoporosis was not different between men and women in any age group. Due to the restricted availability of DXA scan facility, initiation of prophylactic therapy without baseline bone mineral density appears rational in current users of oral glucocorticoids older than 50 years as 80-90% of them would qualify for such therapy. However, only 40-50% of current glucocorticoids users younger than 50 years would require such therapy and simultaneous prescribing of prophylaxis appears unnecessary in 50-60% of them. Attempts should be made to estimate baseline bone mineral density in this group of patients.

皮膚科領域におけるステロイド内服剤の使用に伴うステロイド性骨粗鬆症に対する予防的治療の実態（第二報）

皮膚科領域におけるステロイド内服剤の使用に伴うステロイド性骨粗鬆症に対する予防的治療の実態（第二報）

Prevention, Diagnosis, and Treatment of Glucocorticoid Induced Osteoporosis by Rheumatologists in a Latin-American City

To examine current practices for the diagnosis and therapy for glucocorticoid-induced osteoporosis (GIOP) in patients under treatment with corticosteroids at outpatient clinics of rheumatologists in a Colombian Caribbean city. All patients noted to be using of glucocorticoids (GC) on an index consult from February to May 2004 were included in a descriptive cross sectional study. Criteria for inclusion of patients were to have had, at least, one previous visit to the service. We evaluated the study population for osteoporosis diagnosis, procedures, and treatment. Of the 121 patients included, 103 (85.1%) were female and 18 (14.9%) were male; 76 patients (62.8%) were under 50 years, and 45 (37.2%) were over 50 years. Main reasons for corticosteroid use were rheumatoid arthritis in 68 patients (56.2%) and systemic lupus erythematous (SLE) in 31 patients (25.6%). Diagnostic testing for osteoporosis was reported on 50.1% of patients. Peripheral dual energy x-ray absorptiometry was the most frequently used method (52.6%). Therapeutic agents for GIOP were used in 96 patients (79.3%), with Calcium plus Vitamin D (55.2%) the principal treatments prescribed. We found similar rates of diagnosis and treatment for GIOP to those reported in North America and Europe, although in this study treatment was mainly with calcium and vitamin D. There was a statistically significant relationship between being studied with any diagnostic method and being treated for GIOP. There may be undertreatment for GIOP in Latin America. Local interventions to improve care for patients in chronic use of steroids are needed.