Table 2 Examples of intervention thresholds (equivalent to the age-
Table 3 Clinical scenarios for women in the UK (BMI 024 kg/m2)
specific fracture probability in women with prior fragility fracture) as
showing the 10-year probability of a major fracture by age for a high
set by FRAX-based 10-year probability (in percent) of a major osteo-
dose of glucocorticoids (GC) (>7.5 mg/day) using the adjustment
porotic fracture in postmenopausal women with a previous fracture (no
factor [], an average dose of glucocorticoids (2.5–7.5 mg/day) in a
glucocorticoid treatment or other clinical risk factors, a body mass
woman with rheumatoid arthritis (RA), and an average dose of gluco-
index of 24 kg/m2 and without BMD) [
corticoids with a prior fracture (Fx)
dosage, duration and route of administration), fracture his-
The numbers in parentheses represent the approximate T-scores atwhich the probability would lie at or above the NOGG intervention
tory (type and trauma), alcohol intake, smoking, height loss,
threshold (FRAX version 3.4 for the UK)
family history of osteoporosis and hip fracture. The history
a Recommended BMD test
should include an assessment of dietary calcium intake,
b Recommended treatment
obtained either informally or using a food frequency ques-tionnaire. Height and weight should be measured. Routinebiochemical testing should be performed to exclude causes
considered in patients with back pain, documented loss of
of secondary osteoporosis other than glucocorticoid use
height or kyphosis, or low BMD.
including assessment of vitamin D status and renal function(Table ). Measurement of BMD by DXA at the spine andhip is generally recommended. Lateral imaging DXA with
Management of glucocorticoid-induced osteoporosis
vertebral fracture assessment (VFA) is of value in detecting
existing vertebral fractures ], but if this is not available,lateral X-rays of the thoracic and lumbar spine should be
General measures in the management of GIO
Certain general measures can be advocated in individualstaking glucocorticoids, although the evidence base for theireffects on fracture risk is weak (Table ). The dose ofglucocorticoids should be regularly reviewed and kept toa minimum. Alternative routes of administration (e.g.
topical, inhaled) or formulations (e.g. budesonide) may beconsidered, and in some situations, use of alternative immu-nosuppressive agents may enable reduction in the dose ofglucocorticoids. Adequate levels of dietary calcium intake,good nutrition and maintenance of a normal body weightshould be encouraged. Tobacco use and alcohol abuse shouldbe avoided, and appropriate levels of physical exercise shouldbe encouraged. Falls risk assessment and, where appropriate,advice to reduce the risk of falls should be performed in thoseat increased risk of falling.
Fig. 2 Assessment guidelines of the UK National Osteoporosis Guide-line Group based on the 10-year probability of a major fracture (in
percent). The dotted line denotes the intervention threshold. Whereassessment is made in the absence of BMD, a BMD test is recommen-
Although a number of interventions have been evaluated in
ded for individuals where the probability assessment lies in the mid-region. Adapted from ]
the management of GIO, the strength of evidence for their
Table 4 Investigations to ex-clude causes of secondary
Full blood count and ESR
Exclude anaemia; high ESR may suggest monoclonal
Creatinine, urea, eGFR
Exclude chronic kidney disease
Calcium, phosphate, alkaline phosphatase,
Exclude primary hyperparathyroidism, malignancy,
osteomalacia, Paget's disease
Liver function tests
Exclude chronic liver disease, alcohol abuse
Oestrogen, testosterone, LH, FSH
Exclude hypogonadisma
IgA anti-tissue transglutaminase antibody or IgA
Exclude coeliac disease
endomysial antibody
Immunoglobulins, Bence Jones Protein, serum
Exclude monoclonal gammopathy
free light chains
Exclude vitamin D deficiency
aNot required in women who are
Exclude hyperthyroidism
known to be postmenopausal
efficacy is weaker than that for postmenopausal osteoporo-
In the case of alfacalcidol , and calcitriol
sis, since fracture reduction has not been a primary end point
similar evidence exists for spine BMD, but data
of any study. This reflects the acceptance by regulatory
for effects on hip BMD are inconsistent. Evidence for ver-
authorities of bridging studies, using BMD, for agents pro-
tebral fracture reduction, albeit not as a primary end point,
posed for GIO that have been shown to reduce fractures in
was reported in placebo-controlled or comparator studies for
postmenopausal osteoporosis Fracture data in GIO
alendronate [etidronate [risedronate ] and ter-
studies are therefore only available as secondary end points
iparatide , ]. The lower grading for alendronate reflects
or as safety data. Studies in GIO are limited further by their
the omission, in the extension study, of patients who had
short duration and heterogeneity of trial populations with
fractured during the first year of the study. No data are
respect to age, sex, underlying disease, co-morbidities, con-
available for non-vertebral fractures or hip fractures.
current medications and the variable timing of intervention
Since no treatment studies were designed to demonstrate
in relation to initiation of glucocorticoid therapy. In addi-
fracture reduction and, with the exception of four studies
tion, the number of men and premenopausal women in these
, ], there are no head-to-head comparisons of
studies has generally been low, so the evidence for treatment
interventions, inferences about the relative efficacy of dif-
of these other groups is weak.
ferent treatments cannot be made. In the comparator studies,superiority of BMD change was shown for zoledronic acidover risedronate [Teriparatide was significantly more
Pharmacological interventions in glucocorticoid-induced osteoporosis•
effective than alendronate in increasing BMD and in reduc-
Bone-protective treatment should be started at the onset of gluco-
corticoid therapy in patients at increased risk of fracture.
ing vertebral fracture, although the latter was not a primary
• Alendronate, etidronate, risedronate, zoledronic acid and teriparatide
end point , ]. The weaker evidence for alfacalcidol and
are the front-line therapeutic options for the majority of patients.
calcitriol with respect to changes in hip BMD helps to
• If glucocorticoid therapy is stopped, withdrawal of bone-protective
establish bisphosphonates and teriparatide as the front-line
therapy may be considered, but if glucocorticoids are continued long
options for the majority of patients. In clinical practice, the
term, bone protection should be maintained.
• Adequate calcium intake should be achieved through dietary intake if
possible, with the use of supplements if necessary.
Table 5 General measures in the management of GIO
• An adequate vitamin D status should be maintained, using
supplements if required.
Table summarizes the grading of recommendation for
Reduce dose of glucocorticoid when possible
pharmacological interventions approved for management of
Consider glucocorticoid-sparing therapy
GIO. For the bisphosphonates, alendronate –], etidronate
Consider alternative route of glucocorticoid
], risedronate –] and zoledronic acid and for
the osteoanabolic, teriparatide, there is good evidence from
Advise good nutrition especially with calcium and
placebo-controlled or comparator studies of beneficial effects
Regular weight-bearing exercise
on spine and hip BMD , The wording of the indication
Avoid tobacco use and alcohol abuse
for GIO varies between countries, but in EU countries, no
Assess falls risk and give advice if appropriate
distinction is made between prevention and treatment.
Fig. 3 Postmenopausal womenand men aged ≥50 years
choice of treatment in individual patients will be mainly
withdrawal of bone protection may be considered with
influenced by cost and tolerability.
reassessment of fracture risk, preferably including a mea-
Because rapid bone loss and increased fracture risk occur
surement of BMD. In those who continue to take glucocor-
soon after the initiation of glucocorticoid treatment, bone-
ticoids long term, treatment should be continued. In patients
protective therapy should be started at the onset of gluco-
treated with teriparatide, anti-resorptive therapy should be
corticoid therapy in individuals at increased risk of fracture.
considered following the permitted treatment duration of
If glucocorticoid therapy is subsequently stopped,
24 months [].
Fig. 4 Premenopausal womenand men aged ≤50 years
Table 6 Grading of evidence for pharmacological interventions used
and active vitamin D metabolites were included and com-
in the management of GIO
pared with calcium alone or placebo [, ]. Both anal-
yses showed a beneficial effect of combination therapy on
BMD. In contrast, other outcomes including fracture inci-dence were not significantly affected. There is no evidence
that active vitamin D metabolites are more effective than
native vitamin D (cholecalciferol, vitamin D3) in preventing
bone loss or fractures in glucocorticoid-treated patients
]. However, the risk of developing hypercalcaemia
and hypercalciuria is higher with active metabolites.
Based on the available evidence, current UK guidelines
recommend an adequate calcium and vitamin D intake to allindividuals on glucocorticoids for three or more months
nae not adequately evaluateda
Similarly, the updated recommendations from the American
College of Rheumatology recommend a total daily calcium
Data inconsistent
intake of 1,200 to 1,500 mg with 800 to 1,000 IU (20–
Not a primary end point
25 μg) vitamin D for all patients starting glucocorticoidtherapy Although some recent studies have suggested
Calcium and vitamin D
an association between use of calcium and vitamin D sup-plementation and risk of cardiovascular disease, this
Because glucocorticoid therapy is associated with reduced
remains controversial , ]. Where possible, dietary
intestinal and renal calcium absorption and increased uri-
means should be used to achieve an adequate intake of
nary calcium excretion, increasing calcium intake seems a
calcium and the use of supplements reserved for individuals
logical approach []. However, in most studies in which
with low intakes.
calcium alone served as the control therapy, bone loss wasnot prevented by calcium supplementation. For instance,despite a daily dose of 500 mg [800 mg [] or even
Cost-effectiveness of the treatment of GIO
1,000 mg ] of calcium, lumbar spine BMD continued todecline in patients on at least 7.5 mg/day of prednisone (by
Although the cost-effectiveness of treatments for osteoporo-
2.8, 4.6 and 4.3 % over 12 months, respectively). These
sis has been assessed in a number of studies [few
findings suggest that calcium alone may not be sufficient
have specifically addressed GIO , –]. However, if
to prevent glucocorticoid-induced bone loss
the assumption is made that drugs provide similar efficacy
Calcium supplementation should be combined with vita-
and safety in GIO as observed for postmenopausal osteopo-
min D as patients on glucocorticoids commonly have vita-
rosis [], cost-effectiveness estimates for PMO can be
min D insufficiency ]. Combined calcium and vitamin
transferred to GIO at equivalent fracture risk.
D supplementation—either native vitamin D [or acti-
A pan-European study from 2004 estimated the cost-
vated vitamin D metabolites ]—was more effective in
effectiveness of branded alendronate in nine countries in
preserving BMD than either calcium alone or no therapy. In a
non-glucocorticoid-treated postmenopausal women [
2-year randomized trial in patients with rheumatoid arthritis
In this study, alendronate was shown to be cost saving
receiving a mean daily dose of 5.6 mg prednisone, patients on
compared to no treatment in women with osteoporosis (with
1,000 mg calcium and 500 IU (12.5 μg) vitamin D3 daily had
and without previous vertebral fracture) from the Nordic
significant gains in BMD (0.7 and 0.9% per year at the spine
countries (Norway, Sweden and Denmark). The cost-
and hip, respectively), while those on placebo lost BMD (at a
effectiveness of alendronate compared to no treatment was
yearly rate of 2.0 and 0.9%, respectively) ]. Similarly, in a
also within acceptable ranges in Belgium, France, Germany,
1-year randomized trial, patients receiving high doses of glu-
Italy, Spain and the UK. However, with the decreased price
cocorticoids (prednisone ≥30 mg per day) gained lumbar spine
of generic alendronate, analyses based on a branded drug
BMD 0.39% over 1 year when randomized to calcium 405 mg
price have become obsolete and would require an update.
plus alfacalcidol 1 μg daily. In contrast, patients randomized to
In a study from the UK by Kanis et al. [generic
calcium alone lost BMD at a rate of 5.7% ].
alendronate was shown to be cost effective in the prevention
Two meta-analyses have confirmed the beneficial effect
and treatment of fractures in postmenopausal women with a
of combined calcium and vitamin D in the prevention of
10-year fracture probability for a major fracture that
glucocorticoid-induced osteoporosis. In these analyses, both
exceeded 7.5%. Thus, the treatment scenarios envisaged
trials with calcium and native vitamin D and with calcium
by NOGG can be considered as cost effective (Table
Other drugs that are approved for GIO (risedronate, teripara-
glucocorticoid-treated patients who are at increased risk of
tide and zoledronic acid) are associated with higher cost-
effectiveness ratios compared to no treatment mainly due totheir higher price. A recent study by Borgström et al. [],
Osteonecrosis of the jaw
again conducted in a UK setting, showed that risedronatewas cost effective above a 10-year probability of 13% for a
An increased risk of osteonecrosis of the jaw (ONJ) has
major osteoporotic fracture. However, the cost-effectiveness
been reported in patients treated with bisphosphonates, par-
of different interventions will vary between countries due to
ticularly in those exposed to high doses of bisphosphonates
differences in drug costs, fracture risk, costs of treating
for treatment of skeletal malignancy. In patients treated with
fractures, utility estimates and willingness to pay.
the lower doses used for osteoporosis, however, the inci-dence of ONJ is very low (between 1/10,000 and 1/100,000person exposure years) Although glucocorticoid
Safety of treatments in GIO
therapy has been reported in some cases of bisphosphonate-associated ONJ, there is no evidence that ONJ is more
Treatment studies in GIO have generally been smaller and
common in bisphosphonate-treated patients taking gluco-
of shorter duration than those in postmenopausal osteopo-
corticoids than in those treated with bisphosphonates alone
rosis so that information on adverse effects, particularly
those occurring with long-term treatment, is relatively
In patients receiving treatment for GIO who are at in-
sparse. Adverse events might be expected to occur more
creased risk of fracture, therefore, the benefit/risk balance of
frequently in glucocorticoid-treated individuals because of
bisphosphonate therapy is strongly positive. However,
co-morbidities and co-medications. However, there is no
because of the well-established role of dental disease
positive evidence to indicate that the safety profile of
and trauma in the pathogenesis of ONJ, where possible,
bisphosphonates and other drugs used in GIO differs signif-
invasive dental procedures should be avoided in patients
icantly from that observed in women treated for postmeno-
taking bisphosphonates, and pre-existing severe dental
disease should be treated prior to initiation of bisphosph-onate therapy. In addition, patients should be instructedto maintain good oral health.
Atypical femoral fractures
Recently, concerns have arisen about a possible association
Bisphosphonates and pregnancy
between bisphosphonate use and atypical subtrochantericand femoral shaft fractures (AFFs) [, These frac-
The use of bisphosphonates in women of childbearing age
tures are rare, comprising approximately 1% of all hip and
raises potential concerns about fetal safety because of the
femoral fractures ], but carry a high morbidity. Al-
long half-life of bisphosphonates in bone and their ability to
though epidemiological studies have reported conflicting
cross the maternal placenta. In animal models, high doses of
results on whether bisphosphonate therapy is associated
bisphosphonates cause fetal underdevelopment and skeletal
with increased risk of AFFs, several recent studies indicate
retardation [However, data in humans are available
an association between duration of bisphosphonate use and
only from sporadic clinical cases, and no systematic studies
the incidence of AFFs [Glucocorticoids have
have been conducted. A review of the scientific literature
been proposed as a risk factor for the development of AFFs
evaluated a total of 58 women treated with bisphosphonates
in a number of studies –], although in a recent
just before or during pregnancy and found no evidence of
case control study in which atypical fractures were con-
abnormalities in the offspring []. Two cohort studies
firmed radiologically, the use of glucocorticoids was not
analysing pregnancy outcomes in women treated with
associated with increased risk of AFFs in patients who were
bisphosphonates up to the third month of pregnancy
taking bisphosphonates [].
reported no obvious excess of adverse fetal outcomes, al-
A causal association between bisphosphonate use and
though one case of Apert's syndrome (an autosomal domi-
AFFs and the possible role of glucocorticoids in the patho-
nant condition associated with a fibroblast growth factor 2
genesis of these fractures remain to be firmly established.
mutation causing acrocephalosyndactyly) occurred in a
Nevertheless, imaging should be considered in patients tak-
woman exposed to bisphosphonates [,
ing bisphosphonates who develop unexplained thigh or
Although overall these data are reassuring, bisphospho-
groin pain. In view of the rare occurrence of AFFs and the
nates should be avoided in premenopausal women, most of
proven efficacy of bisphosphonates, the overall benefit/risk
whom have a low absolute risk of fracture, unless there are
balance of bisphosphonate therapy is strongly positive in
strong indications for treatment (see ).
In postmenopausal osteoporosis, there is growing evi-
dence that biochemical markers have potential value in
The goal of bone-protective therapy in glucocorticoid-
monitoring the response to treatment [their use in
treated individuals is to reduce the risk of fractures. Minimal
monitoring treatment in glucocorticoid-treated patients is
follow-up includes verification that the patient is taking the
less well established but is an important area for future
medication, that the dosing procedure for the drug is appro-
research. Absence of an increase in serum PINP after
priate and that the patient is taking sufficient calcium and
3 months of teriparatide may identify patients in whom
vitamin D. During follow-up, a careful assessment of new
adherence is sub-optimal []. It should be noted that the
fractures should be included; rib and vertebral fractures are
underlying disease may itself affect bone turnover markers
particularly common in GIO. Annual height measurements
(BTMs), and the relationship between changes in BTMs and
should be included in the monitoring visit, and spine radio-
fracture risk has not been evaluated in GIO.
graphs or vertebral fracture assessment (VFA) by DXAshould be obtained if there has been significant height loss(more than 2 cm) or if there are other symptoms or signs that
Management of GIO in younger men
raise suspicion of fracture (note that vertebral fractures are
and premenopausal women
often asymptomatic in GIO) (Table However, the inci-dence of fragility fractures on treatment is low, and absence
Younger men (≤50 years)
of fracture during treatment does not necessarily mean treat-ment is effective. Therefore, surrogate indices of treatment
There are very few data on the use of glucocorticoids in
efficacy are recommended.
younger men. In the reported randomized double-blind trials,
In glucocorticoid-treated patients not receiving bone-
the majority of men were over the age of 50 years, with none
protective therapy, BMD measurements using DXA are
of the trials reporting on subsets of younger men. As such, any
recommended at baseline and at appropriate intervals there-
recommendations that can be made are based on expert opin-
after depending on the baseline level, the dose of GC, the
ion. In men, therapy with a bisphosphonate is of benefit when
disease for which it is given and the age and gender of
compared to placebo in maintaining bone mass. No conclu-
the patient. In patients receiving bone-protective therapy,
sions may be drawn regarding reduction in fracture risks.
monitoring with BMD is recommended, the frequency ofwhich will depend on the same factors. The BMD mea-
Premenopausal women
surement precision error (the least significant change ateach skeletal site established for the laboratory) must be
In general, premenopausal women on glucocorticoids are
considered when interpreting serial assessments in order
less susceptible to fracture than postmenopausal women.
to determine whether the change is real []. How-
However, a small study suggested that glucocorticoid-treated
ever, it should be emphasised that improvement in BMD
premenopausal women fractured at higher BMD than their
during treatment with anti-resorptive drugs accounts for a
postmenopausal counterparts Vertebral fractures in pre-
predictable but small part of the observed reduction in
menopausal women treated with glucocorticoids may be as-
the risk of vertebral fracture in postmenopausal osteopo-
sociated with lower cortical bone mass than in those without a
rosis [and the relationship between BMD changes
fracture ]. Independently of BMD, elevated BTMs might
and fracture risk reduction in patients treated for
identify cases with prevalent vertebral fracture ]. Factors
glucocorticoid-induced osteoporosis is unknown. Poor
other than glucocorticoids that help to identify premenopausal
adherence to therapy, failure to respond to therapy or
women at increased fracture risk are prior fractures ,
previously unrecognised secondary causes of osteoporo-
low BMD [family history of osteoporosis [
sis should be searched for in patients with documented
low BMI or low weight , ], age ], age at
BMD loss [].
menarche ], major depression [] and alcohol
Table 7 Recommendations formonitoring during glucocorti-
Grading of evidence
Assessment of adherence to therapy, including calcium and vitamin D, at each visit
Measurement of BMD at appropriate intervals
Annual height measurement
Vertebral fracture assessment by X-ray or DXA if fracture is suspected
Measurement of serum PINP after 3 months of teriparatide therapy
intake [In those on glucocorticoids, sustained high doses
postmenopausal women treated with teriparatide and
may increase the risk of fracture ].
alendronate, respectively, with corresponding figures fornon-vertebral fracture of nine and six []. However,fracture was not a primary end point of this study, and
Management of glucocorticoid-induced osteoporosis in premenopausal
women and men aged 50 years or less
the small number of fractures in premenopausal women
• Premenopausal women and younger men have a lower risk of fracture
and younger men precludes any conclusions about the
than older individuals.
relative anti-fracture efficacy of alendronate and teripara-
• Data on the effects of pharmacological interventions in this
tide in these populations.
population are sparse, particularly with regard to fracture risk.
In studies limited to premenopausal women, alendronate
• Bone-protective therapy may be appropriate in some premenopausal
was more effective in maintaining BMD compared to either
women and younger men, particularly in individuals with a previous
calcitriol or alfacalcidol [Etidronate was also
history of fracture or receiving high doses of glucocorticoids.
found to be more effective at preventing bone loss than
Caution is advised in the use of bisphosphonates in women of
childbearing age.
alfacalcidol in premenopausal women treated with gluco-corticoids [In patients with systemic lupus eryth-
Men and premenopausal women on oral glucocorticoids
ematosus (SLE) treated with high-dose glucocorticoids, of
are less likely to undergo BMD testing and to receive bone-
whom 70% of women were premenopausal, risedronate was
protective therapy than postmenopausal women [], pos-
of benefit in preventing bone loss at the lumbar spine
sibly because indications for the prevention of bone loss and
In a study of glucocorticoid-treated patients with chronic
fractures are not as clearly defined as in postmenopausal
kidney disease in which women in the study were predom-
women. There are a few treatment studies that are confined
inantly premenopausal, risedronate was effective in prevent-
to premenopausal women; however, in general, the studies
ing bone loss at the lumbar spine when compared to active
that have been done include premenopausal women as a
vitamin D In another small study of predominantly
subset of the overall study, and there are very few fracture
premenopausal women with renal disease, the combination
data from which conclusions may be drawn. As a result, the
of risedronate and alfacalcidol appeared to be of greater
available evidence is based on BMD data.
benefit than either alone []. In studies limited to calcitriol
In large randomized controlled trials in which subsets of
compared to calcium and vitamin D [and vitamin D
premenopausal women and men were studied, therapy with
compared to placebo [], no significant benefit of
alendronate [risedronate [and etidronate [has
calcitriol over calcium and vitamin D or vitamin D over
been reported to prevent bone loss at the lumbar spine when
placebo was demonstrated. In a small study of inhaled
compared to placebo. In the comparative study of zoledronic
and intermittent oral glucocorticoids, which did contain
acid versus risedronate ], a subset analysis of men in the
premenopausal women, calcitriol did not offer any benefit
trial demonstrated significantly greater increases in lumbar
spine BMD at 1 year in men treated with zoledronic acid
In a small study of hypogonadal women with SLE, hor-
than in those treated with risedronate, both in the prevention
mone replacement therapy was more effective than calcitriol
and treatment subpopulations. Total hip BMD increased
in preventing bone loss In another small study of
significantly in men treated with zoledronic acid, although
alfacalcidol compared to placebo alfacalcidol was of
the treatment difference was not significantly greater than
benefit in maintaining bone mass.
that seen in risedronate-treated men []. In a post hoc
Despite the lack of evidence for fracture reduction in
analysis in premenopausal women included in this trial,
glucocorticoid-treated premenopausal women, bone-
significantly greater increases in total hip, but not lumbar
protective therapy may be appropriate in some cases, particu-
spine, BMD were seen at 12 months in women treated with
larly in patients treated with high doses of glucocorticoids and
zoledronic acid when compared with those treated with
in those with a previous history of fracture. Long-term use of
risedronate [].
bisphosphonates and the potential for side effects remain a
Teriparatide has been shown to result in larger increases
concern. Caution is advised to women of childbearing age as
in BMD than alendronate in premenopausal women and
bisphosphonates cross the placenta and may affect the skeletal
men with GIO []. Radiographic vertebral fractures were
health of the developing fetus (see ).
not seen in any premenopausal women or men treated withteriparatide and were present in four men, but no premeno-
We are grateful to Amanda Sherwood and Heidi-
pausal women, treated with alendronate. Non-vertebral frac-
Mai Warren from the European Calcified Tissue Society and Judy
tures occurred in two premenopausal women and one man
Stenmark from the International Osteoporosis Foundation, for admin-istrative support. This paper has been consulted by the IOF Committee
treated with teriparatide and two men, but no premenopausal
of National Societies and the following associations: EFFORT, AO
women, treated with alendronate. In comparison, radio-
Trauma, International Society of Orthopaedic Surgery and Traumatol-
graphic vertebral fractures were seen in one and six
ogy, Endocrine Society, International Society of Endocrinology,
AACE, ILAR, EULAR, ACR, International Menopause Society, Inter-
national Association of Gerontology and Geriatrics, European UnionGeriatric Medicine Society, American Geriatrics Society and ASBMR.
1. Compston JE (2010) Management of glucocorticoid-induced
Conflict of interest
Adachi J.D. is consultant/speaker for Amgen, Eli
osteoporosis. Nature Rev Rheumatol 6:82–88
Lilly, GSK, Merck, Novartis, Pfizer, Procter & Gamble, Roche, Sanofi
2. American College of Rheumatology ad hoc Committee on
Aventis and Warner Chilcott and received grants for clinical trials from
Glucocorticoid-induced Osteoporosis (2001) Recommendations
Amgen, Bristol-Myers Squibb, Eli Lilly, Merck, Novartis, Pfizer,
for the prevention and treatment of glucocorticoid-induced oste-
Procter & Gamble, Sanofi Aventis, Roche and Warner Chilcott.
oporosis: 2001 update. Arthritis Rheum 44:1496–1503
Agnusdei D. is a stock holder and employee of Eli Lilly and
3. Royal College of Physicians (2002) Glucocorticoid-induced
osteoporosis. Guidelines on prevention and treatment. Bone
Bilezikian J.P. receives consultancies and speaker fees for Amgen,
and Tooth Society of Great Britain, National Osteoporosis
Lilly, Merck and Novartis; consultancies for Radius Pharmaceuticals,
Society and Royal College of Physicians. Royal College of
NPS Pharmaceuticals and GSK; and research support from NPS
Physicians, London
4. Brown JP, Josse RG, Scientific Advisory Council of the Osteo-
Boonen S. receives research support and/or consulting fees from
porosis Society of Canada (2002) Clinical practice guidelines for
Amgen, Merck, Novartis, Sanofi Aventis and Warner Chilcott.
the diagnosis and management of osteoporosis in Canada. CMAJ
Cooper C. receives lecture fees and consultancy from ABBH,
Amgen, Eli Lilly, GSK/Roche, MSD, Novartis, Nycomed and Servier.
5. Devogelaer JP, Goemaere S, Boonen S, Body JJ, Kaufman JM,
Diez Perez A. receives honoraria as consultant or speaker from Amgen,
Reginster JY, Rozenberg S, Boutsen Y (2006) Evidence-based
Eli Lilly and MSD as well as research funds from Alliance of Bone
guidelines for the prevention and treatment of glucocorticoid-
Health and Servier.
induced osteoporosis: a consensus document of the Belgian Bone
Eastell R. is a member of the Procter & Gamble National Advisory
Club. Osteoporos Int 17:8–19
Board, Medical Research Council, European Calcified Tissue Society,
6. Geusens PP, Lems WF, Verhaar HJ, Leusink G, Goemaere S,
Biobank MSK Advisory Board; a consultant for Amgen, AstraZeneca,
Zmierczack H, Compston JE (2006) Review and evaluation of the
GlaxoSmithKline, Medtronics, Nastech, Nestle, Fonterra Brands,
Dutch guidelines for osteoporosis. J Eval Clin Pract 12:539–548
Novartis, Ono Pharma, Osteologix, Pfizer, Eli Lilly, Sanofi Aventis,
7. Gourlay M, Franceschini N, Sheyn Y (2007) Prevention and
Tethys, Unilever, Unipath, Inverness Medical, Johnson & Johnson,
treatment strategies for glucocorticoid-induced osteoporosis. Clin
SPD and MSD and IDS; received grants from AstraZeneca, Unilever,
Rheumatol 26:144–153
Amgen, Department of Health, National Institute for Health Research,
8. Hoes JN, Jacobs JW, Boers M, Boumpas D, Buttgereit F, Caeyers
Sheffield Teaching Hospitals Trust, Queen Mary University of London,
N, Choy EH, Cutolo M, Da Silva JA, Esselens G, Guillevin L,
Procter & Gamble, Unipath Limited, Novartis, Medical Research Council
Hafstrom I, Kirwan JR, Rovensky J, Russell A, Saag KG, Svensson
UK, Arthritis Research UK, Nestle Foundation and Sanofi Aventis;
B, Westhovens R, Zeidler H, Bijlsma JW (2007) EULAR evidence-
received payment for lectures including service on speakers
based recommendations on the management of systemic glucocor-
bureaus from Takeda, Eli Lilly, Amgen, National Osteoporosis
ticoid therapy in rheumatic diseases. Ann Rheum Dis 66:1560–
Foundation, Procter & Gamble, GlaxoSmithKline Nutrition and
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with skeletal metabolism.
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Cómo referenciar este artículo / How to reference this article Gelabert Gual, Ll. (2014). Ideario y aportaciones metodológicas de Baltasar Bibiloni a la enseñanza musical en las Islas Baleares. Foro de Educación, 12(17), pp. 147-163. Ideario y aportaciones metodológicas de Baltasar Bibiloni a la enseñanza musical en
The American Journal of Pathology, Vol. 176, No. 4, April 2010 Copyright © American Society for Investigative Pathology Cardiovascular, Pulmonary and Renal Pathology Therapeutic Targeting of Classical and LectinPathways of Complement Protects fromIschemia-Reperfusion-Induced Renal Damage Giuseppe Castellano,* Rita Melchiorre,* of classical and lectin pathways of complement in a
