Abstracts & Literature Review 2

 

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Risk Factors, Prevention, and Treatment of Corticosteroid-induced Osteoporosis in Adults

 

Kathryn M. Ruf, BS; Nicole K. Johnson, PharmD: Timothy Clifford, PharmD, BCPS; Kelly M. Smith, PharmD, BCPS, FASHP
Orthopedics. Aug. 2008 Volume 31 • Number 8.

Editorial Reviewer:  Gary Carver, DC, FACO

Published: June, 2009
Journal of the Academy of Chiropractic Orthopedists
June 2009, Volume 6, Issue 2
Received: 14 May 2009
Accepted: 3 March 2009

The original article copyright belongs to the original publisher.  This review is available from: http://www.dcorthoacademy.com © 2009 Carver and the Academy of Chiropractic Orthopedists.  This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Editorial Summary:

  • This article addresses issues relating to corticosteroid-induced osteoporosis and how it relates to pathophysiology, risk of fracture, prevention, and treatment in adult patients.
  • An orthopedist can play a critical role in corticosteroid induced osteoporosis management by identifying at-risk patients and selecting appropriate prophylactic measures.
  • Corticosteroids are the cornerstone of therapy for many common chronic conditions including asthma, inflammatory bowel disease, and autoimmune disorders. Hyperglycemia hypothalamic pituitary axis suppression and electrolyte disturbances are well-recognized adverse effects associated with corticosteroid use. Osteoporosis can be a devastating manifestation of corticosteroid therapy that is frequently not adequately prevented.
  • Corticosteroids induce necrotic changes especially in trabecular rich bone.
  • A T-score threshold of <-2.5, which is appropriate to diagnose postmenopausal osteoporosis, is not appropriate to evaluate fracture risk in a patient undergoing corticosteroid therapy. In these patients, the risk of fracture increases when the T-score is <-1.5.”‘ Goals of therapy are aimed to either prevent bone loss for patients who have T-scores >-2.5, or to treat osteoporosis by restoring bone mass and preventing further loss for patients with T-scores <-2.5.”‘
  • When evaluating the influence of total daily corticosteroid dose on the risk of fracture, low-dose regimens must be distinguished from those that are considered high-dose. Low-dose regimens can be define as total daily doses of <1O mg of prednisone or equivalent, while high-dose regimens are those in which the daily dose exceeds 10 mg. Both high- and low-dose corticosteroid regimens increase the risk of vertebral and hip fractures, but high-dose regimens can be associated with higher risks of fracture. When compared to patients not receiving corticosteroids, patients using low-dose regimens have a 2.73-fold increased risk of vertebral fracture and 1.73- fold increased risk of hip fracture. An increased risk of fracture is evident in patients receiving daily doses of <5 mg. Similarly, patients undergoing high-dose corticosteroid regimens have a 3.15-fold increased risk of vertebral fracture and 2.04- fold increased risk of hip fracture compared to patients not using corticosteroids. Although the relationship between total daily dose and fracture risk is clear, identifying a similar relationship with duration of corticosteroid use is difficult.
  • Inhaled corticosteroids for treatment of conditions such as asthma and chronic obstructive pulmonary disease currently appear to be of a minimal concern as it relates to bone metabolism, however further exploration appears warranted.

Preventative measures may include attention to calcium, vitamin D supplementation, bisphosphonates, calcitonin, parathyroid hormone and cessation of smoking, reduction of alcohol consumption and employing weight bearing activities.

 

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