The lowest possible dose of corticosteroid should be used to control the condition
under treatment. When reduction in dosage is possible, the reduction should
be gradual. Since complications of treatment with glucocorticoids are dependent
on the size of the dose and the duration of treatment, a risk/benefit decision
must be made in each individual case as to dose and duration of treatment and
as to whether daily or intermittent therapy should be used.
Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid
therapy, most often for chronic conditions. Discontinuation of corticosteroids
may result in clinical improvement.
As sodium retention with resultant edema and potassium loss may occur in patients receiving corticosteroids, these agents should be used with caution in patients with congestive heart failure, hypertension, or renal insufficiency.
Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, rather than betamethasone, are the appropriate choices as replacement therapy in adrenocortical deficiency states.
Steroids should be used with caution in active or latent peptic ulcers, diverticulitis,
fresh intestinal anastomoses, and nonspecific ulcerative colitis, since they
may increase the risk of a perforation.
Signs of peritoneal irritation following gastrointestinal perforation in patients
receiving corticosteroids may be minimal or absent.
There is an enhanced effect of corticosteroids in patients with cirrhosis.
Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation (i.e., decreasing absorption and increasing excretion) and inhibition of osteoblast function. This, together with a decrease in the protein matrix of the bone secondary to an increase in protein catabolism, and reduced sex hormone production, may lead to inhibition of bone growth in pediatric patients and the development of osteoporosis at any age. Special consideration should be given to patients at increased risk of osteoporosis (i.e., postmenopausal women) before initiating corticosteroid therapy.
Although controlled clinical trials have shown corticosteroids to be effective
in speeding the resolution of acute exacerbations of multiple sclerosis, they
do not show that they affect the ultimate outcome or natural history of the
disease. The studies do show that relatively high doses of corticosteroids are
necessary to demonstrate a significant effect. (See DOSAGE
An acute myopathy has been observed with the use of high doses of corticosteroids,
most often occurring in patients with disorders of neuromuscular transmission
(e.g., myasthenia gravis), or in patients receiving concomitant therapy with
neuromuscular blocking drugs (e.g., pancuronium). This acute myopathy is generalized,
may involve ocular and respiratory muscles, and may result in quadriparesis.
Elevation of creatinine kinase may occur. Clinical improvement or recovery after
stopping corticosteroids may require weeks to years.
Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Intraocular pressure may become elevated in some individuals. If steroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored.
Carcinogenesis, Mutagenesis, Impairment of Fertilit
No adequate studies have been conducted in animals to determine whether corticosteroids
have a potential for carcinogenesis or mutagenesis.
Steroids may increase or decrease motility and number of spermatozoa in some
Pregnancy: Teratogenic Effects: Pregnancy Category C.
Corticosteroids have been shown to be teratogenic in many species when given in doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an increased incidence of cleft palate in the offspring. There are no adequate and well-controlled studies in pregnant women. Corticosteroids should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Infants born to mothers who have received corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.
Systemically administered corticosteroids appear in human milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other untoward effects. Caution should be exercised when corticosteroids are administered to a nursing woman.
The efficacy and safety of corticosteroids in the pediatric population are
based on the well-established course of effect of corticosteroids which is similar
in pediatric and adult populations. Published studies provide evidence of efficacy
and safety in pediatric patients for the treatment of nephrotic syndrome ( > 2
years of age), and aggressive lymphomas and leukemias ( > 1 month of age).
Other indications for pediatric use of corticosteroids, e.g., severe asthma
and wheezing, are based on adequate and well-controlled trials conducted in
adults, on the premises that the course of the diseases and their pathophysiology
are considered to be substantially similar in both populations.
The adverse effects of corticosteroids in pediatric patients are similar to
those in adults (see ADVERSE REACTIONS). Like adults, pediatric patients
should be carefully observed with frequent measurements of blood pressure, weight,
height, intraocular pressure, and clinical evaluation for the presence of infection,
psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.
Pediatric patients who are treated with corticosteroids by any route, including
systemically administered corticosteroids, may experience a decrease in their
growth velocity. This negative impact of corticosteroids on growth has been
observed at low systemic doses and in the absence of laboratory evidence of
HPA axis suppression (i.e., cosyntropin stimulation and basal cortisol plasma
levels). Growth velocity may therefore be a more sensitive indicator of systemic
corticosteroid exposure in pediatric patients than some commonly used tests
of HPA axis function. The linear growth of pediatric patients treated with corticosteroids
should be monitored, and the potential growth effects of prolonged treatment
should be weighed against clinical benefits obtained and the availability of
treatment alternatives. In order to minimize the potential growth effects of
corticosteroids, pediatric patients should be titrated to the lowest
No overall differences in safety or effectiveness were observed between elderly subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out.