Symposium on Steroid Therapy

Strategies for Minimizing Corticosteroid Toxicity: A

Review
Roosy Aulakh and Surjit Singh

Division of Pediatric Allergy and Immunology,Department of Pediatrics, Advanced Pediatric Centre, Post Gradu-
ate Institute of Medical Education and Research, Chandigarh, India

ABSTRACT
Glucocorticoids (GCs) are used commonly for the treatment of various pediatric inflammatory and autoimmune diseases.
Although potent and generally effective, they are not without risks for producing serious adverse effects, especially when
used in high doses for prolonged periods of time. For proper use of systemic glucocortcoids, a basic knowledge of the
pharmacology, clinical usage guidelines, and adverse reactions of these agents is imperative. This review article emphasis
on the commonly observed side-effects encountered with GC use in children and their underlying basic pathophysiological
mechanisms. The appropriate anticipation of these side-effects with timely implementation of the suggested evidence-
based guidelines has the potential significantly to prevent, minimize and treat common and disabling complications of
glucocortcoid therapy. [Indian J Pediatr 2008; 75 (10) : 1067-1073] E-mail : surjitsinghpgi@rediffmail.com

Key words : Glucocorticoid; Toxicity

Glucocorticoids are important regulators of diverse
physiological systems and are often used in the
treatment of a wide variety of pediatric inflammatory,
autoimmune, and neoplastic diseases. Hench, in 1949,
was the first to report on the beneficial effects of
adrenocorticotrophic hormone and cortisone in patients
with rheumatoid arthritis. It is estimated that as many
as 10% of children may require some form of
glucocorticoid at some point of their childhood.
Although the indications for glucocorticoids in these
various conditions are clear, the treating physician
must be aware of the potential side effects. Recent
advances in development of glucocorticoid or
glucocorticoid receptor ligands have improved
therapeutic effect/adverse reaction ratio.
For proper use of systemic glucocorticoids, a basic
knowledge of the pharmacology, clinical usage
guidelines, and adverse reactions of these agents is
imperative. The major purpose of this review is to
provide a practical approach to increasing efficacy and
minimizing side effects of glucocorticoid therapy.
Pathophysiology of glucocorticoid mediated side effects
The underlying molecular mechanisms for
Correspondence and Reprint requests : Dr. Surjit Singh,
Professor, Post Graduate Institute of Medical Education and
Research, Sector 12, Chandigarh-160012, India. Ph. : 0172-
2747585
[Received August 19, 2008; Accepted August 19, 2008]
glucocorticoid mediated side effects are complex and
only partly understood. Recent data suggest that certain
side effects are predominantly mediated via
transactivation (e.g., diabetes, glaucoma), whereas
others are predominantly mediated via transrepression
(e.g., suppression of the hypothalamic-pituitary-adrenal
axis). For conditions like osteoporosis the underlying
mechanisms are more complex.1
Selection of an appropriate glucocorticoid
The drug duration/dosage should take into account
the risk/benefit ratio. The adverse effects depend on
these parameters as well as on idiosyncratic factors. As
a rule of thumb, it can be stated that duration of steroid
therapy is of greater importance than the dose
administered. Side-effects are usually more severe after
systemic than topical application. Commonly
encountered side effects are enumerated in table 1.
General principles for minimizing glucocorticoid
toxicity
a) There should be definite indication to start GC
treatment.
b) Use short- and intermediate-acting GCs in preference
to longer acting ones.
c) Use minimum necessary dose and duration of
treatment.
d) Once-a-day morning administration should be
preferred over divided dose therapy.

Indian Journal of Pediatrics, Volume 75—October, 2008 1067

 R. Aulakh and S. Singh

TABLE 1. Side-effects of Short Term and Long Term Glucocortcoid Use

Short-term glucocorticosteroid therapy Long-term glucocorticosteroid therapy

Gastrointestinal intolerance Musculoskeletal Metabolic

Increased predisposition to infections Growth retardation Hyperglycemia
Delayed wound healing Osteoporosis Truncal obesity
Increased appetite Hyperglycemia Myopathy Hyperlipidemia
Fluid and sodium retention Avascular necrosis of bone Hypokalemia
Mood changes HPA axis Hypocalcemia
Weakness Suppression Cutaneous
Insomnia Withdrawal syndrome Hirsutism
Amenorrhea Adrenal crisis Atrophy
Acne Ophthalmologic Hyperpigmentation
Cataracts Acne
Glaucoma Nervous system
Gastrointestinal Mood and personality changes
Gastritis Psychosis
Peptic ulcer disease Pseudotumor cerebri
Pancreatitis
Intestinal perforation

d) Use targeted therapy like inhaled corticosteroids
in asthma.
e) Rinse mouth after use of inhalational steroids.
f) Use steroid sparing agents (immunosuppressants)
wherever applicable.
g) During treatment monitor for body weight, height,
blood pressure, serum lipids, blood and/or urine
glucose and ocular pressure and development of
cataract.
h) Careful withdrawl after long term steroid
administration.
i) Beware of drug interactions eg reduced levels of
GC occurs with concomitant use of Rifampicin.
Specific therapies to prevent systemic toxicity:
(a) Bone
i) Pathophysiology: One organ system that has the
potential to be profoundly affected by glucocorticoids is
the skeleton and glucocorticoids-induced osteoporosis
(GIO) is the most common form of secondary
osteoporosis. 2 Glucocorticoid impair the replication,
differentiation and function of osteoblasts and induce
the apoptosis of mature osteoblasts and osteocytes.
These effects lead to a suppression of bone formation, a
central feature in the pathogenesis of GIO.
Glucocorticoids also favor osteoclastogenesis and as a
consequence increase bone resorption3 (Table 2).
(ii) Clinical relevance: Since glucocorticoidss have their
strongest effect on cancellous bone, fractures are more
common in vertebral bodies and ribs. In our experience,
however, rib fractures are rarely encountered in
children on long term glucocorticoid therapy. Because
demineralization of bone is not detectable on conven-
tional radiographs until at least 30% of the bone mineral
density is lost, osteoporosis is best diagnosed by
documenting decreased bone mineral density, using a
bone densitometer. Despite the fact that glucocorticoids
can cause bone loss and fractures, many patients
receiving or initiating long-term glucocorticoids
therapy are not evaluated for their skeletal health.
Furthermore, patients are usually not counseled
regarding specific preventive or therapeutic agents
when indicated.
(iii) Strategies to prevent development of glucocor-
ticoid induced osteoporosis (GIO): A number of
approaches for the prevention of GIO have been
studied in adults but knowledge about similar
interventions in children are still limited. Supplemen-
tation with calcium and vitamin D, or an activated form
of vitamin D may be offered to all children receiving
glucocorticoids since several open studies suggest that
some children with rheumatic disease receiving
glucocorticoids may also benefit from calcium and
vitamin D.4-6
(iv) Strategies for treatment of established
osteoporosis: Treatment of osteoporosis consists of
attempting to decrease the glucocorticoid dose and/or
frequency, increasing calcium intake, providing

TABLE 2. Effects of Glucocorticoids on Bone Cells Leading to Glucocorticoids-induced Osteoporosis and Fractures.
Bone cells Effects of glucocorticoids Outcome

Osteoblasts ↓ function, ↑apoptosis, ↓ differentiation ↓ bone formation

Osteoclasts ↓ genesis, ↓ apoptosis ↓ boneresorption
Osteocytes ↓ function, ↑ apoptosis ↓ bone quality

1068 Indian Journal of Pediatrics, Volume 75—October, 2008

 Strategies for Minimizing Corticosteroid Toxicity : A Review
supplemental vitamin D and increasing physical
activity (especially weight-bearing activities such as
walking). Avoidance of activities such as heavy lifting,
high-impact aerobics, and contact sports is
recommended because these activities can result in
compression fractures of the vertebral bodies (bending,
lifting, and contact sports) and fractures of the long
bones (contact sports). If hypercalciuria is present,
hydrochlorothiazide can be used alone or in
combination with a potassium-sparing diuretic. One
may consider the administration of other agents like
calcitonin, bisphosphonates, calcitriol, sodium fluoride
or treatment with sex steroids (where delayed puberty is
a consideration) in consultation with a bone specialist
and endocrinologist. Use of bisphosphonate therapy
has been shown to reduce fractures and improve bone
density in children with osteogenesis imperfecta, and
may prove to be of benefit in glucocorticoid mediated
osteoporosis.
(b) Muscles
(i) Pathophysiology: The catabolic effects of
glucocorticoids on skeletal muscle are mediated via
several cellular mechanisms. Glucocorticoids inhibit
the glucose uptake in skeletal muscles. This may
contribute to the breakdown of muscle proteins.
Glucocorticoids directly affect the muscle protein
content by both stimulation of protein degradation and
inhibition of protein synthesis.1
ii) Clinical relevance: Catabolic effects of glucocorticoid
on muscles lead to steroid myopathy, both acute and
chronic. In acute myopathy, after short term treatment
with high doses of steroids, generalized muscle atrophy
and rhabdomyolysis occur, including the respiratory
muscles. Glucocorticoid-related chronic myopathy is a
painless, symmetrical, proximal muscle weakness,
usually of the quadriceps and other pelvic girdle muscles.
Although possibly more common with fluorinated
glucocorticoids (e.g., dexamethasone) the condition can
occur with any agent. Diagnosis of myopathy may be
difficult as muscle enzymes, muscle biopsy, and
electromyographic studies will usually be normal. The
finding of elevated urinary creatine may be helpful in the
diagnosis. However, in our clinical experience, steroid
induced myopathy is not a commonly observed
glucocorticoids induced side-effect in children.
(iii) Strategies to prevent steroid induced myopathy: A
sedentary lifestyle may increase risk of glucocorticoid
induced myopathy. Hence, regular physical activity is
useful in preventing the development of glucocorticoid
induced myopathy in children receiving glucocorticoid
therapy.
iv) Strategies for treatment of established myopathy:
Gradual reduction of the glucocorticoid dose and/or
use of steroid sparing agents along with physical
therapy is useful in managing this complication,
Indian Journal of Pediatrics, Volume 75—October, 2008
although muscle function may not return to normal for
many months or up to 1 year. However, steroid
myopathy is often reversible with exercise. It is
important to rule out other treatable causes (e.g.
hypokalemia) in such cases.
(c) Ocular complications
i) Pathophysiology: The mechanisms that are involved
in cataract development are still unclear and include
increased glucose levels due to an increased
gluconeogenesis rate, inhibition of Na + /K + -ATPase
and glucose-6-phosphate-dehydrogenase; inhibition of
RNA synthesis; and covalent binding of steroids to lens
proteins.
Glucocorticoid-induced morphological and functional
changes in the trabecular meshwork (TM) are considered
to be main mechanisms leading to increased intraocular
pressure during glucocorticoid treatment. Glaucoma is
seen mainly with topical, high dose inhaled or oral
steroids and much less commonly with systemic steroids.
(ii) Clinical relevance: Steroid induced ocular
complications include posterior subcapsular cataract
and glaucoma, as well as more rare complications, such
as nonspecific keratitis, retinal emboli and maculopathy
and especially after topical treatment, infection. 7
Although there may be some individual susceptibility,
children are at greatest risk because they can develop
cataracts with lower doses and shorter treatment
durations than adults. It may be noted that cataract
development is not related to total dose of steroid,
duration of therapy or mean daily dose of steroids. It may
be seen as early as within 6 months of the treatment, and
even in children on alternate day therapy. Glucocorticoid
induced glaucoma is usually observed within a few
weeks after initiation of steroid therapy. However, with
systemic steroids, it may supervene after several years of
use. 8 Occasionally, it may also be seen years after
cessation of steroid therapy due to alteration in trabecular
network resulting in obstruction to outflow of aqueous
humour. Since the IOP-has a circadian rhythm which
parallels cortisol circadian rhythm by a lag of 3 hr, the
IOP should be measured preferably after 3 hours of
steroid administration. The monitoring should
continue even after the steroids are stopped.9
iii) Strategies to prevent development of steroid
induced ocular complications: Ophthalmologic
examinations are recommended every 6 months for
patients on long-term systemic glucocorticoid therapy.
Progression of the cataract may still occur despite
decreasing the glucocorticoid dose, but discontinuing it
may occasionally deter further cataract formation or
reverse lens opacification.8
(iv) Strategies for treatment of established ocular
complications: The cataracts often are small but can
affect visual acuity significantly, requiring surgical
1069
 R. Aulakh and S. Singh
intervention. Stopping treatment will halt the progress
of cataract but will usually not reverse the changes
already present.
(d) Gastrointestinal complications
(i) Pathophysiology: Experimentally, glucocorticoid have
been shown to increase gastric acid secretion, to reduce
gastric mucus, to cause gastrin and parietal cell hyperplasia,
and to delay the healing of ulcers in animal studies. These
events are considered to be responsible for the
gastrointestinal side effects of glucocorticoid.
ii) Clinical relevance-Adverse effects on the gastro-
intestinal system caused by glucocorticoid include
gastritis, peptic ulcers, upper gastrointestinal bleeding,
and, especially after inhalative usage, oral candidiasis.
There does seem to be an increased incidence in patients
treated concomitantly with nonsteroidal anti-
inflammatory drugs or aspirin, such as those patients
with rheumatoid arthritis Acute pancreatitis is another
major complication, especially in children.
iii) Strategies to prevent development of steroid
induced gastrointestinal complications: The risk of
peptic ulcer disease can be minimized by
administration of the oral glucocorticoid with food and
the use of antacid medications, including H2 receptor
antagonists or proton pump inhibitors.
(iv) Strategies for treatment of established gastro-
intestinal complications: Any suggestion of peptic ulcer
disease should be promptly investigated with
gastroduodenoscopy and appropriate treatment started
in consultation with gastroenterologist.
(e) Neurological complications
(i) Pathophysiology: The mechanistic spectrum of
glucocorticoid-mediated CNS effects ranges from
disruption of cellular metabolism, to an increase in the
vulnerability of hippocampal neurons and an
augmented extracellular glutamate accumulation.10-12
(ii) Clinical relevance: Existing psychiatric problems
can be aggravated by glucocorticoid treatment.
However, mood swings, euphoria, depression, and
suicide attempts may all also occur in previously stable
persons. ‘‘Steroid psychoses’’ (i.e., mania,
hallucinations, and delusions) have been reported.
However, in our clinical experience, steroid psychosis is
not a commonly observed steroid induced side-effect in
children.
(iii) Strategies to prevent development of steroid
induced neurological complications-A clear dose-
response relationship was found, with psychotic
symptoms increasing dramatically with increase in
glucocorticoid dose. Hence, glucocorticoid should be
used at minimum effective dose.
1070
(iv) Strategies for treatment of established steroid
induced neurological complications- Pseudotumor
most often, develops after rapid tapering or
discontinuation of the glucocorticoid, so that a return to
previous doses with more gradual tapering is
recommended. When psychiatric disturbances occur,
the reduction or discontinuation of glucocorticoid
should be taken into account. Treatment of psychiatric
symptoms is needed when psychiatric disorder is
severe or the patient is suicidal or agitated. In such
cases the use of neuroleptics, antidepressants and other
drugs may be required. The outcome is generally good
and the majority of patients make a good recovery.
(f) HPA axis suppression
(i) Pathophysiology: Corticosteroid administration
results in a negative feedback effect via glucocorticoid
receptors in the anterior hypothalamus, which, in turn,
suppresses the production of corticotrophin-releasing
hormone (CRH) and adrenocorticotrophic hormone
(ACTH). The prolonged suppression of adrenocor-
ticotropin levels leads to atrophy of the adrenal cortex
and secondary adrenal insufficiency. The
glucocorticoid related adrenal insufficiency becomes
only clinically relevant if exogenous glucocorticoid
therapy is withdrawn too rapidly.
ii) Clinical relevance: Four aspects of glucocorticoid
withdrawal deserve special attention. First, the illness
treated by steroids may relapse. Second, the HPA may
remain suppressed for a long time. Third,
psychological dependence to these hormones often
develops. Fourth, a nonspecific withdrawal syndrome
may develop even while patients are receiving
physiological replacement doses of glucocorticoid. The
severity of the withdrawal syndrome depends on the
phase and degree of dependence and includes many
symptoms as anorexia, nausea, emesis, weight loss,
fatigue, myalgias, arthralgias, headache, abdominal
pain, lethargy, postural hypotension, fever, and skin
desquamation. The concern, of course, is whether and
how rapidly the adrenal will be able to secrete cortisol
on demand once prolonged steroid treatment has been
stopped. Fatalities have been reported as long as 12 to
18 months off treatment because the gland could not
do so under stress.
The impact of exogenous steroid use on the HPA axis
depends on
Amount of steroid used: In general, larger than
physiologic doses of steroid are required to suppress the
axis. Because normal cortisol production rates are
approximatel, 10 mg/ day (6.8 ± 1.9 mg/m2 per day),
most therapeutic regimens exceed physiologic
production.
Duration of therapy: Although definitive evidence is
lacking, the general consensus is that the axis is
Indian Journal of Pediatrics, Volume 75—October, 2008
 Strategies for Minimizing Corticosteroid Toxicity : A Review
suppressed significantly when treatment lasts more
than 2 weeks.
Time of day of steroid administration: Because cortisol
production peaks early in the morning, night time
dosing suppresses the axis maximally.
Half-life of steroid used: Those preparations that have
the longest half-life (e.g., dexamethasone) are associated
with the greatest degree of axis suppression.13
(iii) Strategies to prevent steroid induced HPA axis
suppression: Acute adrenal insufficiency is a feared
complication but probably rare. It is usually seen during
stress situations and can be observed long after steroid
withdrawal. There is no good predictive marker to
anticipate acute adrenal insufficiency and clinical
evaluation of the patient remains a key element in its
diagnosis. If adrenal insufficiency is suspected, HPA
suppression can be assessed with dynamic tests.
During stress situation, steroid administration is then
recommended depending on the severity of the stress.
Long-term steroids should be tapered gradually to
allow the adrenal glands to resume cortisol production.
The first step is reduction from pharmacological to
physiological doses. This depends on the disease
activity and the level of control with steroids. The next
step is to taper from physiological dose to complete
withdrawal and this depends on the degree of HPA
suppression.14
In short term treatments (< 10 days), irrespective of
dosage or type of corticoid, cessation of corticotherapy
should be abrupt, shortening total length of therapy and
diminishing side effects.
In intermediate term treatments (10-30 days),
glucocorticoid should be withdrawn over a period of 2
weeks, with dose reduction every 4 days.
In long term treatments, some principles for dose
reduction should be observed prior to medication
withdrawal: (a) switch to short or intermediate-acting
glucocortcoids; (b) reduce number of doses, aiming at
once-a-day dosing in the morning; (c) gradual
glucocortcoid dose reduction (e.g., for doses of
prednisolone above 20 mg, the reduction should be no
more than 25% every 4 days; for doses between 10-20
mg, the reduction should be no more than 2.5 mg every
7 days and for doses < 10 mg the reduction should be
no more than 2.5 mg every 15 days).
iv) Strategies for management of established HPA
axis suppression: In the end of the protocol for dose
reduction, HPA axis testing can be performed with
morning dosage of serum cortisol. Levels greater than
10 mcg/dL indicate adequate recovery of the axis and
allow glucocorticoid withdrawal. Levels less than 5
mcg/dL indicate suppressed axis and need of dose
reduction, with an additional waiting period of 2-4
Indian Journal of Pediatrics, Volume 75—October, 2008
weeks before cessation. Cortisol concentration kept
between 5 and 10 mcg/dL might require adrenocor-
ticothrophic hormone stimulation test (Synacthen) to
ensure adrenal recovery and adequate endogenous
cortisol production in the face of stressful situations.15
(g) Immune suppression
i) Pathophysiology: The inhibition of the inflammatory
and specific immune systems represents a central target
of pharmacological glucocorticoid treatment but can
also result in suppression of body’s immune
mechanisms against infections.
ii) Clinical relevance : Adverse effects of glucocorticoids
therapy on immune system include an increased risk for
all kinds of infection. Moreover, due to the
immunosuppression, a masking of infection symptoms
may occur, preventing early clinical recognition. Any live
virus vaccine should not be given to children being
treated with glucocorticoids. HIV positive children
receiving glucocorticoids may be considered for
Pneumocystis jeroveci prophylaxis.
iii) Strategies to prevent development of steroid
induced immune suppression: Alternate-morning
therapy and doses of less than 10 mg/day of
prednisone equivalent may significantly reduce the
chance of opportunistic infection. A history of
tuberculosis contact should be obtained prior to
beginning therapy, with a baseline chest radiograph
and Mantoux test. Infection prevention can be improved
by general measures like frequent hand washing,
avoiding exposure to infectious cases and use of
appropriate vaccines.
iv) Strategies for treatment of established immune
suppression: One must anticipate that any infection in
children on glucocorticoids can be dangerous and must
remain on the alert to detect it early. There should be no
abrupt stoppage of steroid treatment, for this will almost
certainly lead to acute adrenocortical insufficiency. The
only safe course of action in this circumstance is to
lower the dose of steroid to a level which should no
longer suppress the host’s defences and yet which is
adequate to prevent the development of acute
glucocorticoids withdrawl. This level is approximately
one and one-half to two times a physiologic
maintenance dose of cortisol or cortisone. Appropriate
cultures should be obtained, but until the results are
known a broad spectrum antibiotic should be given.
(h) Endocrine complications
(i) Pathophysiology: glucocorticoids excess causes both
decreased beta-cell insulin production and insulin
resistance. The mechanism of hypertriglyceridemia is likely
related to relative insulin insufficiency. The mechanism for
growth suppression is not known, but may involve
1071
 R. Aulakh and S. Singh
suppression of growth hormone production and/or direct
inhibitory effects on bone and connective tissue.
(ii) Clinical relevance- Endocrine complications of
glucocorticoids use include disturbance in glucose
metabolism, which may lead to induction or
aggravation of pre-existing diabetes; adrenal
insufficiency; growth suppression and hypogonadism.
The effects of glucocorticoids on hyperglycemia usually
remit within 48 hr of discontinuation of oral
administration.
iii) Strategies to prevent development of steroid
induced endocrine complications- Regular monitoring
of blood glucose levels and hemoglobin A 1C during
glucocorticoid therapy is important, and many patients
on oral antidiabetic agents will need to be switched to
insulin. Because glucocorticoid induces relative insulin
resistance, the insulin dose often has to be increased in
those patients who are already insulin-dependent. A
diet low in saturated fat and calories should be
instituted in all patients on long-term glucocorticoid to
prevent development of dyslipidemias. A direct
relationship exists between the dose of glucocorticoids
used and statural growth Hence, every effort should be
made to decrease the amount of oral glucocorticoid to
less than 10 to 15 mg on alternate days. Doses at or
below this value do not impede growth velocity
significantly. The use of knemometry, a sensitive
technique for measuring the growth of long bones in
children has increased the accuracy of growth rate
measurements. Many factors, such as disease process,
sex, daily vs alternate day therapy, ethnic variations or
whether the patient has been immobilized must be
considered when evaluating the effects on stature of a
particular glucocorticoid. Although alternate day
therapy may benefit some patients (particularly those
with juvenile chronic arthritis), not all patients respond
beneficially to this type of regimen. New generations of
glucocorticoid which may not be as detrimental to the
growing child may be considered.
iv) Strategies for treatment of established endocrine
complications: The treatment of glucocorticoid-induced
diabetes resemble essentially the treatment of Type 2
diabetes. If growth retardation is observed, one should
shift to minimum possible doses and add steroid
sparing agents wherever possible. The risk of short
stature can be reduced if the steroids are withdrawn
before the pubertal spurt. Growth hormone therapy in
glucocorticoid-dependent children with growth
suppression remains experimental.
(i) Cardiovascular complications
i) Pathophysiology: The mechanisms of glucocorticoid-
induced hypertension include increased systemic
vascular resistance, increased extracellular volume, and
increased cardiac contractility. There is increasing
1072
evidence for a role of oxidative stress and nitric oxide
deficiency in glucocorticoid induced hypertension.16
ii) Clinical relevance: Hypertension, dyslipidemia, and a
reduced fibrinolytic potential have been identified as the
main adverse effects of glucocorticoid on the
cardiovascular system. glucocorticoid induced
hypertension is an uncommon complication observed in
our clinical experience mainly because the therapeutic
preparations of glucocorticoid used have little or no
mineralocorticoid activity.
iii) Strategies to prevent steroid induced cardiovascular
complications: In patients receiving long-term
glucocorticoid therapy, sodium restriction is important.
Alternate day morning therapy may minimize development
of hypertension.
iv) Strategies for treatment of Glucocorticoid induced
hypertension: Though usually glucocorticoid mediated
hypertension is usually transient, it may at times
require use of appropriate antihypertensive agents.
(j) Others : The recent medical literature records such
steroid effects as avascular necrosis of bone, the development
of subcutaneous fatty tumors, panniculitis, unexplained
arthropathy of the hip, and fat embolism to mention a few.
Glucocorticoid are used commonly for the treatment of
various pediatric inflammatory and autoimmune
diseases. Although potent and generally effective, they
are not without risks for producing serious adverse
effects, especially when used in high doses for prolonged
periods of time. This review article emphasis on the
commonly observed side-effects encountered with
glucocorticoid use in children. A detailed knowledge of
these side-effects of corticosteroid agents will assist the
physician in making informed judgement on the
potential benefits/risk of treatment with these drugs. The
appropriate anticipation of these side-effects with timely
implementation of evidence-based guidelines has the
potential significantly to prevent, minimize and treat
common and disabling complications of glucocorticoid
therapy.
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