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Importance of guidelines on glucocorticoid-induced osteoporosisComment on the American college of rheumatology recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis.

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Importance of guidelines on glucocorticoid-induced
osteoporosis: comment on the American College of
Rheumatology Recommendations for the Prevention
and Treatment of Glucocorticoid-InducedOsteoporosis
To the Editor:
I was pleased to see that the American College of
Rheumatology (ACR) is taking the lead in the development
of guidelines for the prevention of glucocorticoid-induced
osteoporosis (1). This is an important area for guidelines
development because of the variety of physicians prescribing
glucocorticoids-from generalists to medical subspecialists
and other subspecialists-who may not be experienced in the
treatment of osteoporosis. Recent research suggests that many
patients who are receiving long-term glucocorticoid therapy
and who are at high risk for osteoporosis are not receiving
treatment to prevent bone loss ( 2 ) .
My colleagues and I recently completed a survey of
physicians (generalist and specialists), assessing their understanding of the risks of bone loss related to glucocorticoid use
and of the efficacy of medications to prevent bone loss (3). We
found that physicians were generally aware that glucocorticoid
use presents a significant risk for bone loss in postmenopausal
women who are estrogen deficient, but most physicians do not
consider high-dose steroid treatment a significant risk for
osteoporosis in premenopausal women or men, and so are not
prescribing preventive medications for this group of patients.
Also, many physicians do not realize that long-term use of
low-dose steroids is also a significant risk for bone loss, and are
not routinely prescribing preventive therapy in this setting,
even in postmenopausal women.
Because glucocorticoids are used to treat a wide variety of illnesses, a broad educational effort will be needed to
reach a wide spectrum of physicians. The ACR guidelines
should help to disseminate the current knowledge: defining
who is at risk, a stepwise approach to treatment, and how to
use bone densitometry to identify risk and monitor therapy.
Use of these guidelines will create a new standard of care for
patients receiving long-term glucocorticoid treatment, helping
physicians to realize that osteoporosis, like hypertension and
glucose intolerance, is a treatable side effect of steroid use.
Rheumatologists are likely to play a prominent role in this
effort, because of their experience with steroid use and their
expertise in the treatment of musculoskeletal diseases.
As noted by the ACR Task Force, new developments
will lead to the refinement of the guidelines over time.
Research at pharmaceutical companies will answer important questions about the effectiveness of new agents in the
prevention and treatment of glucocorticoid-induced osteoporosis. However, there are many other questions that should
be addressed by future research in order to continue to
develop and refine the most cost-effective approach to osteoporosis prevention for long-term users of glucocorticoids.
These include:
The differences in the effectiveness of available
agents in the setting of prevention (when glucocorticoid
treatment is initiated) versus the treatment of established osteoporosis.
The differences in the effectiveness of agents at
different sites: femur and spine.
The role of combination therapies in the treatment of severe osteoporosis.
The role of sequential treatments, with more
expensive agents reserved for periods of high bone loss.
The role of other risk factors (including genetic
factors) that increase susceptibility to loss of bone
mineral density (BMD) during glucocorticoid treatment.
The goal of preventive treatments: Should treatment be aimed at decreasing current fracture risk or
lifetime fracture risk? Should the goal of treatment be
based on BMD T score, Z score, both scores, or some
other standard?
The criteria for assessing the effectiveness of a
treatment in the setting of glucocorticoid initiation
versus long-term use: Loss of BMD of 5% over 6-12
months is acceptable in patients who have recently
begun high-dose glucocorticoid treatment given that
bone loss in the spine without preventive treatment can
be between 10% and 20% per year. However, loss of
BMD in long-term glucocorticoid users is generally
per year, so effective treatments should stabilize or
increase BMD.
The role of thiazide diuretics in the setting of
prevention of glucocorticoid-induced osteoporosis: Does
thiazide give any additional benefit if patients are already receiving high-dose calcium and vitamin D supplementation?
The role of estrogen treatment in premenopausal women: Are menstrual irregularities the best way
to identify estrogen-deficient women, or is there a more
sensitive way to detect hormonal abnormalities in
glucocorticoid-treated premenopausal women?
The duration of preventive measures: Should
osteoporosis treatment continue after glucocorticoids
are discontinued, in the “recovery period”? Which
agents optimize recovery?
Guidelines for long-term monitoring of BMD:
How frequently should physicians monitor BMD during
long-term glucocorticoid treatment? What is the most
cost-effective approach?
Further refinement of these guidelines will be possible
as these clinical questions are answered.
Lenore M. Buckley, MD, MPH
Medical College of Virginia
Virginia Commonwealth University
Richmond, VA
1. American College of Rheumatology Task Force on Osteoporosis
Guidelines: Recommendations for the prevention and treatment of
glucocorticoid-induced osteoporosis. Arthritis Rheum 39:17911801, 1996
2. Peat ID, Healy S , Reid DM, Ralston SH: Steroid induced osteoporosis: an opportunity for prevention? Ann Rheum Dis 54:66-68,
3. Buckley LM, Quarrles J, Marquez M, Downs R: Variations in
physician perception of the risks of osteoporosis in corticosteroid
users by physician specialty (abstract). Arthritis Rheum 39 (suppl
9):S124, 1996
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