Long-term glucocorticoid (GC) therapy is frequently indicated to treat autoimmune and chronic inflammatory diseases in daily clinical practice. Two of the most devastating untoward effects are bone loss and fractures. Doses as low as 2.5 mg of prednisone for more than 3 months can impair bone integrity. Population at risk is defined based on the dose and duration of GC therapy and should be stratified according to FRAX (Fracture Risk Assessment Tool), major osteoporotic fracture, prior fractures, and bone mineral density values (BMD). General measures include to prescribe the lowest dose of GC to control the underlying disease for the shortest possible time, maintain adequate vitamin D levels and calcium intake, maintain mobility, and prescribe a bone acting agent in patients at high risk of fracture. These agents include oral and intravenous bisphosphonates, denosumab, and teriparatide.
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http://dx.doi.org/10.1007/s40520-021-01823-0 | DOI Listing |
Sci Rep
January 2025
Department of Spine and Spinal Cord Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, No. 7 Weiwu Road, Jinshui District, Zhengzhou, 450003, Henan, China.
The use of pulsed electromagnetic field (PEMF) has demonstrated effectiveness in the management of femoral head osteonecrosis as well as nonunion fractures; however, the effects of PEMF on preventing glucocorticoid-induced osteoporosis (GIOP) have not been extensively studied. The aim of this investigation was to explore the effectiveness of PEMF stimulation in averting GIOP in rats and uncover the potential fundamental mechanisms involved. A total of seventy-two adult male Wistar rats composed the experimental group and were subsequently assigned to three groups for treatment.
View Article and Find Full Text PDFArch Dis Child
December 2024
Newcastle University Translational and Clinical Research Institute, Newcastle upon Tyne, UK.
Objective: To determine the incidence and describe the presentation and management of unexpected symptomatic glucocorticoid-induced adrenal suppression (AS) in children and young people aged 0-15 years.
Setting And Design: Surveillance study of symptomatic glucocorticoid (GC)-induced AS with supportive biochemical evidence or presenting as an adrenal crisis, reported via the British Paediatric Surveillance Unit (BPSU) from September 2020 to September 2022.
Results: Over a 25-month period, 190 reports of symptomatic GC-induced AS/adrenal crisis were made, of which 22 were confirmed cases: 18 AS and 4 adrenal crises.
Front Endocrinol (Lausanne)
January 2025
Department of Pharmacy, New Taipei City Hospital, New Taipei City, Taiwan.
Background: The increasing prevalence of glucocorticoid-induced osteoporosis (GIOP) due to long-term glucocorticoid therapy underscores the need for effective treatment options. Denosumab and bisphosphonates, both key in managing GIOP, require further comparative evaluation to determine their relative efficacy and safety profiles.
Methods: We conducted a systematic review and meta-analysis, adhering to PRISMA guidelines.
J Clin Endocrinol Metab
December 2024
Research Unit OPEN, Department of Clinical Research, University of Southern Denmark, Odense 5230, Denmark.
Context: Glucocorticoids (GCs) are widely used for their anti-inflammatory and immunosuppressive properties. Their effect on bone health is predominantly negative by decreasing bone formation and increasing risk of fractures.
Objective: This work aimed to quantify the short- and long-term changes in total hip bone mineral density (THBMD) after initiating systemic GC treatment in previously GC treatment-naive adults without bone protective agents.
Br J Hosp Med (Lond)
November 2024
MRC Lifecourse Epidemiology Centre, University Hospitals Southampton, Southampton, UK.
This review presents a current perspective on the association between rheumatoid arthritis (RA) and osteoporosis. Many factors contribute to the increased risk of osteoporosis and fracture in RA patients. These factors include advanced age, duration of disease, long-term glucocorticoid use, and poor inflammation control inflammation in RA.
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