Steroids cause osteoporosis

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ls of the Rheumatic Diseases 2002;61:1-2

© 2002 by ls of the Rheumatic Diseases

Steroids cause osteoporosis

Excellent treatment options exist. So why don't we all prevent or treat

it?

Paget

Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021

When doctors institute steroids for any illness and for any length of

time, they take on a lifelong responsibility to that patient to both

taper the drug as quickly as is possible and safe and prevent or treat

the many well recognised steroid related side effects.1 This is

particularly true when steroid treatment lasts for more than one month

and certainly for many months or years. Rheumatologists have a

particular accountability because of the 1% of the population who are

receiving long term steroids, most have rheumatological disorders.2,3

Further, rheumatologists should have the best understanding of when the

treatment course will be prolonged, the profound and negative

physiological impact of steroids on bone, and the need to deal with this

important issue in both men and women.4,5

A recent topic search for steroid-induced osteoporosis (SIO) yielded 79

000 articles since 1966 and 13 000 since l998, most of which focused on

the pathogenesis, clinical manifestations, and treatment of SIO. Despite

the saturation publication on this topic for years, doctors do not seem

to take heed: the majority of bone loss is rapid; most of the 50% of

patients with atraumatic fractures develop them in the first year; SIO

is the third most common cause of osteoporosis; vertebral and hip

fractures are associated with profound short and long term morbidity and

mortality; and, most importantly, SIO is both avoidable and

treatable.6,7 It is not a matter of whether clinically significant and

quality of life altering bone loss will occur, but when. Similarly, it

should not be a matter of whether treatment should be started, but how

soon, and which therapeutic options should be instituted.

These facts make the results of the paper by Gudbjornsson et al in this

journal all the more disturbing (see 32).8 Over a two year period, they

carefully studied a well defined population of 26 664 patients in

northeast Iceland to determine their corticosteroid use and clinical

information about their medical disorders and possible steroid related

side effects. Owing to the centralisation of drug distribution and

medical care and the use of questionnaires, one can assume excellent

capture of drug data and clinical data. If anything, their data probably

underreport the breadth of steroid related bone disorders. One hundred

and ninety one patients, or 0.7% of the population, were receiving

chronic steroid treatment, defined conservatively as a time period of

over three months of treatment. Although over a third of patients were

receiving either calcium or vitamin D supplements, only 9% were taking

bisphosphonates and 21% hormone replacement therapy. The take-home

lesson from their excellent population and prevalence study in a well

defined part of Iceland spells out a seemingly worldwide finding: a

surprisingly large proportion of doctors who treat life or organ

threatening inflammatory disorders do not appear automatically to

connect the institution of steroids with the need for preventive, bone

protecting treatment and monitoring for SIO.9

All doctors who write an initial prescription for a thiazide diuretic

for hypertension would reflexively monitor and replace potassium and,

similarly, those starting a chemotherapeutic agent for cancer would

check a white blood cell count. We are now trying to decrease the use of

antibiotics to avoid worsening bacterial resistance. Yet, the majority

of steroid treated patients who should be given calcium, vitamin D3, and

anti-resorptive agents, such as bisphosphonates, oestrogen replacement

therapy, and calcitonin, are not. What can account for such a medical

conundrum?

Mixed messages about the safety of oestrogen replacement therapy, the

slowness of incorporation of medical advances into practice, and the

newness of data about the effectiveness of bisphosphonates in preventing

or reversing SIO all have a role.10,11 Also, despite a near educational

blitz on this topic by pharmaceutical companies and doctors, it appears

that doctors and patients are slow to learn in this setting of a bone

disorder that may remain silent for many years after steroid

institution. Clearly, also, many doctors who institute steroids believe

that the course will be short. Then, when the regimen turns into a

chronic phase, they either forget the drug's bone toxicity or are

preoccupied by the disease that they are treating or the other more

clinically apparent and disturbing steroid related side effects, such as

infections, diabetes, or psychological and sleep problems.

Clearly, the answer is education and more rapid dissemination of

information through journals and the internet. Neither the definition

and measurement of bone loss with dual x ray absorptiometry nor the

prophylaxis and treatment of SIO is perfect. However, the data strongly

support their place in mainstream medicine in a manner similar to the

measurement, treatment, and monitoring of hypertension, atherosclerosis,

diabetes, asthma, and peptic ulcer disease. Reports like the one in this

journal go a long way towards resetting the well meaning doctor's mind

and putting SIO on their therapeutic radar screen. Hopefully, this group

will look at this topic again in another two years and see whether their

report, various excellent guidelines from national organisations, and

the clinical use of new and exciting drugs, such as the bisphosphonates

and the anabolic agent parathyroid hormone, will improve the focus and

doctor's acceptance of, and action on, this important topic.

REFERENCES

1.. Saag KG, Koehnke R, Caldwell JR, Brasington R, Burmeister LF,

Zimmerman B, et al. Low-dose, long-term corticosteroid therapy in

rheumatoid arthritis: an analysis of serious adverse events. Am J Med

1994;96:115-23.

2.. Walsh LJ, Wong CA, Pringle M, Tattersfield AE. Use of oral

corticosteroids in the community and the prevention of secondary

osteoporosis: a cross sectional study. BMJ 1996;313:344-6

3.. Soucy E, Bellamy N, Adachi JD, Pope JE, Flynn J, Sutton E, et al.

A Canadian survey on the management of corticosteroid-induced

osteoporosis by rheumatologists. J Rheumatol 2000;27:1506-12.

4.. Weinstein RS. The pathogenesis of glucocorticoid-induced

osteoporosis. Clin Exp Rheumatol 2000;18(suppl 21):S35-40.

5.. Goldring SR, Gravallese EM. Mechanisms of bone loss in

inflammatory arthritis: diagnosis and therapeutic implications.

Arthritis Res 2000;2:33-7

6.. American College of Rheumatology Ad Hoc Committee on

Glucocorticoid-induced Osteoporosis. Recommendations for the prevention

and treatment of glucocorticoid-induced osteoporosis: 2001 update.

Arthritis Rheum 2001;44:1496-503.

7.. Peat ID, Healy S, Reid DM, Ralston SH. Steroid-induced

osteoporosis: an opportunity for prevention. Ann Rheum Dis 1995;54:66-8.

8.. Gudbjornsson B, Juliusson UI, Gudjonsson FV. The prevalence of

long-term steroid therapy and the frequency of decision making to

prevent steroid-induced osteoporosis in daily clinical praxis. Ann Rheum

Dis 2002;61:32-6

9.. Hougardy DM, GM, Bleasel MD, Randall CT. Is enough

attention being given to the adverse effects of corticosteroid therapy?

J Clin Pharm Ther 2000;25:227-34.

10.. Saag KG, Emkey R, Schnitzer TJ, Brown JP, Hawkins F, Goemaere S,

et al. Alendronate for the prevention and treatment of

glucocorticoid-induced osteoporosis. N Engl J Med 1998;339:292-9.

11.. Reid DM, RA, Laan RFJM, Sacco-Gibson NA, Wenderoth DH,

Adami S, et al. Efficacy and safety of daily residronate in the

treatment of corticosteroid-induced osteoporosis in women and men: a

randomized trial. J Bone Miner Res 2000;15:1006-1013.

12.. Mazzantini M, Lane NE. Rheumatic diseases, glucocorticoid

treatment and bone mass: recent developments. Clin Exp Rheumatol

2000;18(suppl 21):S2-4

13.. Lane NE, S, Modin GW, Genant HK, Pierini E, Arnaud CD.

Parathyroid hormone treatment reverses glucocorticoid-induced

osteoporosis: results of a randomized controlled trial. J Clin Invest

1998;102:1627-33.

I'll tell you where to go!

Mayo Clinic in Rochester

http://www.mayoclinic.org/rochester

s Hopkins Medicine

http://www.hopkinsmedicine.org