Steroids Side Effects Osteoporosis

Content:
  • Adverse effects of corticosteroids on bone metabolism: a review.
  • Steroid-induced osteoporosis
  • Preventing Steroid-induced Osteoporosis | Patient
  • Osteoporosis and long-term prednisone: What is the risk? - Mayo Clinic
  • Adverse effects of corticosteroids on bone metabolism: a review. - PubMed - NCBI
  • Steroids Side Effects in Hindi

    Adverse effects of corticosteroids on bone metabolism: a review.

    steroids side effects osteoporosis Glucocorticoid GC exposure is the most common etiology of drug-induced secondary osteoporosis. Twenty percent of all cases of osteoporosis have been attributed to GC exposure. GCs are known steroids side effects osteoporosis inhibit bone remodeling and to increase fracture risk. GC exposure alters the fragile balance between osteoclast and osteoblast activity in bone osteopoorsis. GC stimulates osteoclast-mediated bone resorption and reduces osteoblast-mediated bone formation, which results in increased overall net bone resorption. Specifically, the 2 main effects of GCs on bone steroids side effects osteoporosis are 1 inducing apoptosis in osteoblasts and osteocytes, thereby decreasing bone formation, and 2 prolonging the lifespan of osteoclasts and increasing bone resorption. The risk of fracture decreases 3 months after cessation of GC therapy; thus, a 3-month period may be ideal between GC illegal anabolic steroids side effects in patients at high risk for the development of osteoporosis.

    Steroid-induced osteoporosis

    steroids side effects osteoporosis

    Corticosteroids cause osteoporosis and fractures in a high percentage of patients. There is a dose-dependent effect, which is difficult to define because of varying durations at each dose. The beneficial effects of steroids on the underlying disease may partially offset the detrimental effects on bone.

    Because the effects are so variable and can be clinically severe, patients embarking on long-term steroid treatment should have bone density monitored, and measures taken to try to preserve bone.

    The figure shows effects of steroids on bone. The yellow boxes are effects on osteoblasts or osteocytes; the blue boxes are effects on osteoclasts, and the white boxes are other effects which will secondarily cause bone loss. The trabecular bone is affected more rapidly than the cortical bone. Some patients suffer multiple vertebral compression fractures within a year of initiating steroid therapy. Diagnostic work-up Bone density should be measured in patients who are expected to remain on corticosteroids.

    The same lab tests that are used for "ordinary" osteoporosis are indicated for steroid-induced osteoporosis. In males it is very important to remember to check the testosterone level. Females should be asked about amenorrhea which is probably a better indication of estrogen deficiency than estrogen levels. Measurement of LH or FSH will not be helpful in this situation, since the hypogonadism is usually hypogonadotropic, and thus low estrogen will not be associated with high FSH the way it is in a postmenopausal woman.

    A hour urine calcium is indicated, because often these patients have hypercalciuria. I usually check a urine N-telopeptide, too, to get an idea of how much of the hyercalciuria is due to bone resorption. Low urine calcium is also seen, especially if patients have any other reason for malabsorption. Vigorous treatment with calcium and vitamin D is too frequently undertaken without checking the urine calcium, and this could worsen hypercalciuria. In patients with markedly low bone density, prevalent fractures, or high doses of steroids I usually also check a PTH and hydroxyvitamin D level.

    In less severe cases I will just check these if the serum calcium or alkaline phosphatase is abnormal. Xrays of the spine are especially important in patients taking long-term corticosteroids, because sometimes the fractures are not clinically obvious, and if they are present the patient will need maximal therapy. Therapy The physiology of corticosteroid-induced osteoporosis is different than postmenopausal osteoporosis, so treatment cannot be expected to have the same results.

    For example, anti-resorptive therapy does not result in the same degree of increase in bone mass as in postmenopausal osteoporosis. Greater amounts are unlikely to be beneficial, and it probably is better to get the calcium from dietary sources instead of tablets. The use of vitamin D in corticosteroid-treated osteoporosis is debated, and there is still not enough data to make strong recommendations. The most recent studies do not show a difference in bone density with active vitamin D metabolites or high doses of ergocalciferol.

    In those cases with low urine calcium or clinical malabsorption or renal insufficiency the more potent vitamin D should be used such as calcitriol at 0. Gonadal steroids estrogen in women and testosterone in men should be replaced as appropriate unless there are contraindications. Anti-resorptive therapy can prevent some of the bone loss. Clinical trials using bisphosphonates have shown benefits after one to two years; long-term studies are still needed. These therapies should not be used in patients with low serum calcium, and adequate dietary intake should be assured before they are started.

    Also avoid them in patients with reflux esophagitis, patients who are bedridden and can't be upright after taking the medication, and patients with renal insufficiency, and premenopausal women who may wish to become pregnant in the future. The bone resorption may be high when steroids are initiated, but with longer use the osteoclasts are inhibited by the steroids so it does not make as much sense to continue anti-resorptive therapy.

    More recent studies comparing teriparatide to bisphosphonates have shown that there is significantly lower fracture rates in the patients treated with teriparatide. One of the studies lasted for 3 years and the P1NP was better than baseline throughout the study. Should bisphosphonates be used for long-term treatment of glucocorticoid-induced osteoporosis? Glucocorticoids and the osteoclast. Effects of teriparatide versus alendronate for treating glucocorticoid-induced osteoporosis: Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis.

    The New England journal of medicine. Corticosteroid-induced bone loss in men. The Journal of clinical endocrinology and metabolism. Glucocorticoids suppress bone formation via the osteoclast. The Journal of clinical investigation.

    Sclerostin-antibody treatment of glucocorticoid-induced osteoporosis maintained bone mass and strength. Uncertainties in the prevention and treatment of glucocorticoid-induced osteoporosis. Journal of bone and mineral research: Glucocorticoids and osteocyte autophagy. Bone density threshold and other predictors of vertebral fracture in patients receiving oral glucocorticoid therapy.

    Oral corticosteroids and fracture risk: Rizzoli R, Biver E. Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone. Comparative effects of teriparatide and risedronate in glucocorticoid-induced osteoporosis in men: Calcitonin for the treatment and prevention of corticosteroid-induced osteoporosis.

    Cochrane Database Syst Rev. Bare-Bones Fact - Children are not small adults. The Epidemiology of Corticosteroid-Induced Osteoporosis: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy. The cumulative incidence of and risk factors for latent beaking in patients with autoimmune diseases taking long-term glucocorticoids and bisphosphonates. Prevention of glucocorticoid induced-apoptosis of osteoblasts and osteocytes by protecting against endoplasmic reticulum ER stress in vitro and in vivo in female mice.

    Lems WF, Saag K. Bisphosphonates and glucocorticoid-induced osteoporosis: Restoration of the coupling process and normalization of bone mass following successful treatment of endogenous Cushing's syndrome: A meta-analysis of prior corticosteroid use and fracture risk. American College of Rheumatology recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis.

    Advances in experimental medicine and biology. Bisphosphonates for the prevention and treatment of osteoporosis in patients with rheumatic diseases: Bone formation markers in patients with glucocorticoid-induced osteoporosis treated with teriparatide or alendronate.

    Glucocorticoid-induced osteoporosis and osteonecrosis. Endocrinol Metab Clin North Am. Fracture risk associated with different types of oral corticosteroids and effect of termination of corticosteroids on the risk of fractures.

    Use of oral corticosteroids and risk of fractures. Oral glucocorticoid use is associated with an increased risk of fracture. Meta-analysis of tumor necrosis factor inhibitors and glucocorticoids on bone density in rheumatoid arthritis and ankylosing spondylitis trials.

    Efficacy of alphacalcidol and calcitriol in primary and corticosteroid-induced osteoporosis: Health technology assessment Winchester, England. Glucocorticoids in early rheumatoid arthritis: The role of Wnt signaling and sclerostin in the pathogenesis of glucocorticoid-induced osteoporosis. Dai Y, Hu S. Recent insights into the role of autophagy in the pathogenesis of rheumatoid arthritis.

    Prevention of glucocorticoid induced bone changes with beta-ecdysone. Glucocorticoids in patients with rheumatic diseases: The effect of tocilizumab on bone mineral density, serum levels of Dickkopf-1 and bone remodeling markers in patients with rheumatoid arthritis.

    Preventing Steroid-induced Osteoporosis | Patient

    steroids side effects osteoporosis

    Osteoporosis and long-term prednisone: What is the risk? - Mayo Clinic

    steroids side effects osteoporosis

    Adverse effects of corticosteroids on bone metabolism: a review. - PubMed - NCBI

    steroids side effects osteoporosis