Medicines Q&As
Q&A 114.3
Are adults taking corticosteroids for adrenal insufficiency
at risk of osteoporosis?
Prepared by UK Medicines Information (UKMi) pharmacists for NHS healthcare professionals
Before using this Q&A, read the disclaimer at www.ukmi.nhs.uk/activities/medicinesQAs/default.asp
Date prepared: January 2013
Summary
 Evidence from observational studies indicates that some adults taking corticosteroids for adrenal
insufficiency (AI) have decreased bone mineral density (BMD). The risk of bone density loss may be
influenced by cumulative or daily corticosteroid dose, co-existent hormone imbalances and underlying AI.
 Accurate replacement of physiological levels of cortisol is impossible with currently available
corticosteroids. There is also no objective method of monitoring the accuracy of replacement in order to
avoid over- or under-treatment.
 The traditionally recommended dose of hydrocortisone of 20 to 30mg daily may be too high for many
patients. New techniques for measuring natural cortisol production indicate that the rate is much lower
than previously estimated and most adults with AI can be treated successfully with 15 to 20mg daily (or
10 to 12mg/m2/day).
 Adults with AI who have been receiving daily hydrocortisone doses higher than 25mg (or equivalent)
should be considered to have a clinical risk factor for fracture, and their ten year major fracture risk
should be assessed and managed as recommended in national osteoporosis guidelines. In all patients
with AI, calcium and vitamin D intake should be optimised and weight bearing exercise and a well
balanced diet encouraged; they should be advised to stop smoking and limit their alcohol intake.
Background
Long term oral corticosteroids significantly increase the risk of spine and hip fracture, even at daily doses
less than 7.5mg prednisolone or equivalent [1,2]. The risk of vertebral fracture remains significant even
when doses are less than 2.5mg daily (equivalent to 10mg hydrocortisone), and is greater than would be
expected from loss of bone mineral density (BMD) alone. UK guidelines for managing glucocorticoidinduced osteoporosis, issued in 2002, recommend that all patients who take oral corticosteroids should be
given lifestyle advice to minimise bone loss and calcium plus vitamin D supplements if dietary intake is low
[1,3]. A 2008 guideline for the diagnosis and management of osteoporosis states that postmenopausal
women (with no previous fragility fracture), and men aged 50 years and over, who are currently receiving
oral corticosteroids, should have their ten year major fracture risk assessed using the FRAX ® tool [4].
However the implications for patients with adrenal insufficiency (AI) taking corticosteroids for the purpose
of replacement, rather than disease suppression, are not discussed in any of these guidelines.
This Medicines Q&A reviews the evidence that corticosteroid replacement therapy (CRT) for adults with AI
increases the risk of osteoporosis, and discusses how to manage this risk.
Answer
Some adults taking corticosteroids for AI may be at an increased risk of osteoporosis. Observational
studies show that patients with AI have significantly reduced BMD (measured using DXA scans), and the
risk of bone loss is possibly influenced by cumulative or daily corticosteroid dose and co-existent hormone
imbalances [5-13]. Other studies have reported bone density is not reduced, although these involved
some patients on lower doses of CRT than in the studies reporting reduced BMD [17-20]. However, most
studies are small and use surrogate measures of osteoporosis, rather than fracture incidence. The
majority are retrospective so cumulative exposure to corticosteroids was estimated rather than accurately
calculated. Different hydrocortisone dose equivalence calculations have been used for patients with
congenital adrenal hyperplasia (CAH) than for those with other forms of AI. Finally, observational studies
Q&A 114.3 Are adults taking corticosteroids for adrenal insufficiency at risk of osteoporosis?
From the NHS Evidence website www.evidence.nhs.uk
only assess prevalence and controlled trials are needed to determine whether corticosteroids reduce BMD
or cause fractures in patients with AI.
In a cross-sectional study, mean z-scores at the femoral neck were significantly reduced in 292 patients
with Addison’s disease (187 from Norway [mean age 53 years] taking a mean hydrocortisone [HC] dose
[or equivalent] of 32mg, and 105 from the UK and New Zealand [mean age 46 years] taking a mean dose
of 27mg) [5]. The reduction in mean z-score was significantly associated with weight-adjusted HC dose in
Norwegian patients, but not in those from the UK or New Zealand. Mean lumbar spine (LS) z-scores were
reduced, but the decrease was only statistically significant in the UK/New Zealand cohort; mean total hip
z-score was decreased only in Norwegian patients. Fifteen patients were taking a bisphosphonate and 40
were taking hormone replacement therapy. Spinal x-rays were obtained in 84 Norwegian patients aged 50
years or more; fourteen (16.8%) patients had one or more fractures. This prevalence was not increased
compared with a reference population, but an effect on fracture could not be ruled out because the study
lacked sufficient power.
Eight smaller cross-sectional studies have also shown reduced BMD [6-13]. They involved a total of 173
pre- or postmenopausal women and 80 men with AI, aged 16 to 83 years, who had been taking CRT for
between six months and 44 years.
 Five studies recruited patients with Addison’s disease (primary AI) or secondary AI and showed
significantly reduced LS or femoral neck BMD in men and women [6], or only in certain subgroups
such as postmenopausal women [7-9] or men [10]. The current mean HC dose exceeded 28.5mg
(or equivalent) in three studies [6,7,10]. LS BMD was negatively correlated with current [6,8,10]
and/or cumulative corticosteroid dose [8]. Some studies reported that reduced BMD was only
seen in patients taking mean daily doses of HC (or equivalent) higher than 13.6mg/m2 [8,10].
 Three studies involved 71 patients with CAH and showed that mean LS [11] or mean total spine
[12] BMD was significantly lower than in controls, and mean femoral neck and LS z-scores were
significantly decreased [13]. The current mean daily HC dose varied between 19.1 and 19.2mg/m2
(or equivalent) (data unavailable for one study [12]). Higher current [13] and long-term cumulative
[12,13] doses significantly correlated with negative effects on BMD. Adrenal androgen levels were
significantly higher in premenopausal than in postmenopausal women, and were positively
correlated with BMD [11]. The aim of treating CAH with corticosteroids is not only to replace
deficient cortisol but to suppress excessive secretion of adrenocorticotropic hormone (ACTH),
thereby preventing over- production of adrenal androgens [12,14-16]. Doses are therefore
intentionally supra-physiological and the excess risk of bone loss possibly not unexpected. Loss of
bone density appears to occur despite the protective effects of increased body mass index and
hyperandrogenaemia commonly seen in patients with CAH [11,16,17], but does not manifest until
adulthood [11,16].
In contrast, four studies have shown no significant reduction in bone density in patients with primary or
secondary AI (122 women and 69 men), with no correlation between BMD and dose or duration of CRT
(where necessary adjusted for outliers) [17-20]. In two of these studies, patients were taking lower doses
than in the studies reporting reduced BMD (mean HC equivalent doses of 25mg [18] and 22mg in primary
AI [19], and 27mg (15.5mg/m2) in patients with CAH [19]). In another study [20], the result may have been
influenced by correction of calcium and vitamin D deficiency which had been previously identified in the
patient cohort [7].
Three prospective studies examined the effect of CRT on osteocalcin serum levels [6,21,22]. Osteocalcin
is a surrogate marker for bone formation and acute and chronic use of corticosteroids produces a dosedependent decrease in levels [1]. In a double-blind, cross-over study, nine patients with secondary AI
were randomised to 15mg, 20mg or 30mg daily doses of HC for two weeks and osteocalcin levels
measured weekly [21]. In the second study the mean daily dose of HC was reduced from 29.5mg to
20.8mg in 19 patients with primary or secondary AI and osteocalcin serum levels measured 3.5 months
later [6]. Both studies reported that mean/median osteocalcin levels were significantly lower with the 30mg
dose compared to the 20mg dose (mean difference 17 to 19%) although in one study they were noted to
remain within the normal range [21]. The authors of the studies concluded that mildly excessive doses
probably have adverse effects on bone formation. In the third study no significant difference in osteocalcin
levels was seen with different corticosteroid doses when nine patients with AI sequentially received openlabel HC 15mg daily, HC 20mg daily and dexamethasone 100microgram/15kg body weight daily for four
weeks in a random order [22]. The authors concluded that low CRT doses have little immediate impact on
bone turnover biomarkers.
Q&A 114.3 Are adults taking corticosteroids for adrenal insufficiency at risk of osteoporosis?
From the NHS Evidence website www.evidence.nhs.uk
Although the data described above suggest that higher cumulative CRT doses may increase the risk for
reduced BMD, a Swedish retrospective population-based cohort study found that the risk of hip fracture in
3,219 adults (60% women, median age 61 years), newly diagnosed with Addison’s disease and with no
history of prior fracture, decreased once they were receiving stable CRT [23]. Compared to 31,557 ageand sex-matched controls, patients with AI had a higher risk of hip fracture (hazard ratio 1.8 [95%
confidence interval 1.6 to 2.1]; p<0.001), and the risk was highest in the year before and after diagnosis.
The overall absolute risk of hip fracture in adults with AI was 784 per 100,000 person-years, an excess of
350 per 100,000 person-years over those without AI. However, at least five years after diagnosis the risk
of fracture was still significantly increased (1.3 [1.1 to 1.6]; p=0.008), with an excess risk of 156 per
100,000 person-years. Unfortunately, it was not possible to determine the effect of CRT dose on fracture
risk since this information was not collected. A UK retrospective cohort study investigated the prevalence
of co-morbidity in 48 patients with Addison’s disease (65% women, mean age 50 years) [24]. Nearly three
quarters of patients were taking a daily HC dose of 25mg or less. In 28 patients with DXA data, 17.9% had
spinal osteoporosis and 53.5% had spinal osteopenia. Reduced BMD was not correlated with HC dose.
It is widely acknowledged that accurate replacement of physiological pulsatile levels of cortisol is
impossible with currently available corticosteroids [25-30]. In patients receiving CRT there are periods
throughout the day when cortisol levels will inevitably be supra-physiological [29]. There is also no
objective method of monitoring the accuracy of replacement, which has to be determined by clinical
assessment of non-specific signs and symptoms whilst balancing the risks of under-treatment on patients’
morbidity and mortality [25,26,28-30]. Patients with secondary AI (and sometimes primary) [18] may have
additional deficiencies of growth hormone or sex hormones, or receive excessive doses of levothyroxine
which can also reduce BMD [6,30].
There is debate about the dose of HC for replacement in patients with AI, including whether weight/surface area-based dosing or dividing the daily dose into three or more doses achieves a more
physiological pattern of replacement [25,27-29]. Traditionally the recommended dose of HC has been 20
to 30mg daily, given in two divided doses, with half to two thirds taken in the morning [29,30]. This daily
dose is quoted in the British National Formulary [31] and is based upon estimates of cortisol secretion
rates of 12 to 15mg/m2/day calculated over half a century ago [22,25,30]. New techniques for measuring
cortisol production indicate that the actual rate could be as low as 5.7mg/m2/day [25,27,32]. Taking into
account wide inter-individual variation in first pass hepatic metabolism of HC, daily doses of 15 to 25mg
(or 10 to 12mg/m2) have been recommended [25,28,29,33]. For many years some patients have therefore
potentially been over-treated. Two studies reported that 75% of patients were receiving excessive doses
as assessed by serum and urinary cortisol measurements [6,33]. An international survey in 2003 of 850
patients with primary AI showed that the mean daily doses of HC prescribed were 13.9mg/m 2 and
14.3mg/m2 for men and women, respectively [34]. Added to this, patients with AI are routinely given
empirical advice to supplement their usual doses of corticosteroid during times of illness or physical
stress. However there is a lack of high quality evidence to support these ‘sick day’ and ‘well day’ rules and
it appears that supplemental doses are often too high and taken for excessive periods [25,35].
How should this potential risk be managed?
The lowest effective dose of HC (or equivalent) should be prescribed that allows the patient to feel well
without showing clinical signs of AI [25,27] (except in patients with CAH who need doses that suppress
excessive ACTH secretion). It has been recommended that most adults can be treated successfully with
15 to 20mg daily [22,25,27,30,36], whilst others suggest limiting the dose to no more than 25mg or using
weight-/surface area-based dosing [28,30]. The daily dose should be split into at least two doses, but
preferably three or more, and the last dose of the day should be taken in the afternoon to avoid overnight
supra-physiological levels [25,27,30,36]. There is no convincing evidence of significant differences
between replacement corticosteroids in their effect on BMD [7,13,20,27]. In patients still experiencing
symptoms of insufficiency with 20mg daily, cortisol day curves may be considered in preference to further
dose increases, to facilitate adjustment of dose or timing of administration [25] (but see below*).
Supplemental doses should be tailored to the patient and the severity of the stressful event [35]. Studies
measuring quality of life of patients on differing doses of corticosteroids have shown increasing dose to be
associated with no improvement in [22], or greater impairment of, subjective health status [37]. In a longterm follow-up study, 12 patients underwent repeat DXA scans approximately two years after their median
dose was reduced from 30mg to 20mg daily [38]. No change in median BMD was seen, although 50% of
patients had an increase in LS bone density.
Patients with CAH should have their adrenal androgen levels monitored to ensure accurate replacement
of corticosteroids and adequate suppression of androgens [11,15,17,33]. Corticosteroid dose adjustment
Q&A 114.3 Are adults taking corticosteroids for adrenal insufficiency at risk of osteoporosis?
From the NHS Evidence website www.evidence.nhs.uk
may be needed in women after the menopause [11]. Patients with other causes of primary AI and those
with secondary AI cannot be reliably monitored with biochemical tests such as ACTH levels or 24 hour
urinary cortisol excretion [28,29]. *Cortisol day curves are an option for determining the accuracy of
replacement with HC (but not other corticosteroids) although their value is debated and they are not
universally recommended [18,25,27,29,30].
There is disagreement over the need to assess fracture risk with DXA scans in patients with AI. Some
consider that DXA scans are not necessary for patients who receive daily HC doses less than 30mg (or
equivalent) [13,18,28,39]. Others recommend that scans should be considered for all patients with AI
[32,33], or possibly just for women [9], men [10], or those with other risk factors for bone loss such as
premature menopause, previous Cushing’s syndrome or those on large doses or with long disease
duration [14,30]. The Addison’s Disease Self Help Group recommends that BMD should be measured
every five to ten years, at the time of the menopause in women, and considered at diagnosis of AI [40].
The available evidence indicates that patients most at risk of decreased bone density are those taking HC
daily doses higher than 25mg; their use of corticosteroids should be considered a clinical risk factor for
fracture and their ten year risk of major fracture should be assessed and managed as recommended in
national guidelines [4]. In all patients with AI it seems reasonable to suggest that calcium and vitamin D
intake should be optimised and weight-bearing exercise and a well balanced diet encouraged [1,3].
Patients should be advised to stop smoking and limit their alcohol intake.
Limitations
This Medicines Q&A reviews evidence for CRT and risk of osteoporosis in adults with AI. It does not
address risk in children, other risks associated with over-replacement, such as cardiovascular disease or
glucose metabolism, or the effect of other hormone imbalances on risk of osteoporosis in patients with AI.
References
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Q&A 114.3 Are adults taking corticosteroids for adrenal insufficiency at risk of osteoporosis?
From the NHS Evidence website www.evidence.nhs.uk
14. Labarta JI, Bello E, Ruiz-Echarri M, et al. Childhood-onset congenital adrenal hyperplasia: long-term
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Q&A 114.3 Are adults taking corticosteroids for adrenal insufficiency at risk of osteoporosis?
From the NHS Evidence website www.evidence.nhs.uk
Quality Assurance
Prepared by
Joanne McEntee, North West Medicines Information Centre, 70 Pembroke Place, Liverpool, L69 3GF.
Contact
druginfo@liv.ac.uk
Date Prepared
January 2013.
Checked by
Justine Howard, Simone Henderson, and Christine Proudlove. North West Medicines Information Centre,
Pharmacy Practice Unit, 70 Pembroke Place, Liverpool, L69 3GF.
Date of check
January/February 2013.
Search strategy
 Embase 1980 to date ([exp OSTEOPOROSIS/ OR exp CORTICOSTEROID INDUCED
OSTEOPOROSIS/ OR exp FRACTURE/ OR exp BONE DENSITY/] AND exp ADRENAL
CORTEX INSUFFICIENCY); (exp *ADRENAL INSUFFICIENCY/ limit to [Publication Types
Review]), for information added since 2011/01/01.
 Medline 1950 to date ([exp OSTEOPOROSIS/ OR exp CORTICOSTEROID INDUCED
OSTEOPOROSIS/ OR exp FRACTURE/ OR exp FRACTURES, BONE/ OR exp BONE
DENSITY/]] AND [exp ADRENAL CORTEX INSUFFICIENCY/ OR exp ADRENAL
INSUFFICIENCY/]); (exp *ADRENAL INSUFFICIENCY/ limit to [English Language and Review
Articles]), for information added since 2011/01/01.
 Cochrane Library, accessed 4th January 2013 ([osteoporosis OR bone OR fracture] AND [adrenal
insufficiency OR Addison]).
 NeLM (osteoporosis).
 www.addisons.org.uk
 www.library.nhs.uk/guidelinesFinder/ ([adrenal OR osteoporosis])
 In-house database/ resources.
 Expert opinion (contacted January 2009):
- Professor Stafford Lightman, Professor of Medicine, Henry Wellcome Laboratories for
Integrative Neuroscience and Endocrinology, University of Bristol.
- Mrs Katy Mellor, Senior Pharmacist Diabetes and Endrocrinology, Salford Royal Hospitals
Foundation NHS Trust.
- Dr Terence O’Neill, Consultant Rheumatologist, Salford Royal Hospitals Foundation NHS
Trust.
- Professor John Wass, Professor of Endocrinology (Oxford University) and Consultant
Endocrinologist, Churchill Hospital and the Nuffield Orthopaedic Centre, Oxford.
Q&A 114.3 Are adults taking corticosteroids for adrenal insufficiency at risk of osteoporosis?
From the NHS Evidence website www.evidence.nhs.uk