Steroid tablets are generally prescribed with more caution, as these can potentially cause more problems. Corticosteroid tablets are the most powerful type of steroid medication, because they can affect the whole body.
They shouldn't be used if you have an ongoing widespread infection, because they could make it more severe. However, you should continue to take corticosteroids if you develop an infection while already being treated, unless advised otherwise. They should also be used with caution in people with a health condition that could be made worse by taking oral corticosteroids, including:.
In these situations, you will only be prescribed oral corticosteroids if the benefits of treatment clearly outweigh any potential risks. Most people can safely have corticosteroid injections, but they should be avoided or used with caution if you have an ongoing infection or a blood clotting disorder such as haemophilia.
There is generally no reason why someone shouldn't be able to use a steroid inhaler or steroid spray, but these should be used with caution in people with ongoing infections, such as tuberculosis TB. Corticosteroids are generally safe to use during pregnancy. However, they're not usually recommended unless the potential benefits outweigh the risks. For example, steroid tablets may be recommended if you're pregnant and have severe asthma , because the risk to your baby from uncontrolled asthma is higher than from the medication.
There is no evidence that using a steroid inhaler during pregnancy increases the risk of problems such as birth defects, so you can usually continue to use this as normal while you're pregnant. If a woman needs to take steroid tablets while she is breastfeeding, a type called prednisolone is usually recommended, because it is thought to have the least chance of causing the baby any adverse effects. As a precaution, it's usually recommended that a breastfeeding mother waits three to four hours after taking a tablet before feeding her baby.
Steroid injections, inhalers and sprays are not thought to pose a risk to babies being breastfed. Corticosteroids can interact with other medicines, and the effects of either medicine can be altered as a result. There is less chance of this happening with steroid injections or sprays, although it can occasionally happen if they're used at high doses and for a long time. Some of the more common interactions are listed below, but this is not a complete list.
If you want to check your medicines are safe to take with corticosteroids, ask your GP or pharmacist, or read the patient information leaflet that comes with your medicine. Anticoagulant medicines are medications that make the blood less sticky.
They are often prescribed to people with a history of blood clots or an increased risk of developing them. Combining corticosteroids with anticoagulant medicines can sometimes make anticoagulants less effective. Alternatively, it can increase their blood-thinning effect, which can cause bleeding inside the digestive system. Anticonvulsants are medicines used to prevent seizures fits and are often used to treat epilepsy , but they can reduce the effectiveness of corticosteroids.
Depending on how frequent and severe your seizures are and the condition the steroids are being used to treat, you may be advised to temporarily stop taking anticonvulsants. Corticosteroids can decrease the effectiveness of medications used to treat diabetes. If you need to take both of these medications, your blood glucose levels will usually be checked more regularly and your dose of diabetes medication may need to be adjusted.
Corticosteroids, including steroid inhalers, can sometimes interact with a type of medication known as protease inhibitors such as ritonavir used to treat HIV. The HIV medication may increase the level of corticosteroid in your body, which might increase your risk of experiencing side effects. Some vaccinations contain a weakened form of the infection they are designed to protect against.
These are known as live vaccines. Examples of live vaccines include:. As corticosteroids can weaken your immune system and make you more vulnerable to infection, you should avoid any live vaccine until at least three months after your course of corticosteroids has finished.
Non-steroidal anti-inflammatory drugs NSAIDs are a group of commonly used painkillers, such as ibuprofen , that are available over the counter at pharmacists. Combining NSAIDs and corticosteroids can increase your risk of developing stomach ulcers and internal bleeding.
If you need to take both medications, you may be given an additional medication called a proton pump inhibitor PPI to reduce the risk of stomach ulcers. Some of the main side effects are listed below, but this is not a complete list. To learn about all the possible side effects of your medication, read the patient information leaflet that comes with it.
Inhaled steroids usually have few or no side effects if used at normal doses. However, they can sometimes cause:. Rinsing your mouth out with water after using your medication can help to prevent oral thrush, and using a device called a spacer with your medication can help to prevent many of the other problems. There is also some evidence that steroid inhalers used by people with chronic obstructive pulmonary disease COPD can increase the risk of chest infections such as pneumonia.
Inhaled steroids at high doses can sometimes cause some of the more serious side effects that are more often linked with steroid tablets see below , but this is rare. Steroids that are injected into muscles and joints may cause some pain and swelling at the site of the injection. However, this should pass within a few days. Steroid injections can also cause muscle or tendon weakness, so you may be advised to rest the treated area for a few days after the injection.
Other possible side effects can include infections, blushing, and thinning and lightening of the skin in the area where the injection is given. Because of the risk of side effects, steroid injections are often only given at intervals of at least 6 weeks and a maximum of 3 injections into one area is usually recommended.
Steroids that are injected into a blood vessel intravenous steroids may sometimes cause some of the more widespread side effects described below. Short, occasional courses of steroid tablets taken for no longer than three weeks are very unlikely to cause troublesome side effects. Most side effects should improve if you're able to reduce your dosage or eventually stop taking the medication. You may have regular checks and tests for conditions such as diabetes, high blood pressure and glaucoma if you need to take steroid tablets on a long-term basis.
Home Tests and treatments Medicines and medical aids Types of medicine Corticosteroids. Corticosteroids See all parts of this guide Hide guide parts 1. Introduction 2. Who can use them 3. Medicines that interact with them 4. Most doctors prefer to prescribe topical steroids for as short a period of time as possible, in particular those applied to the skin. Strong topical steroids are normally not used for much longer than one week. This is because topical steroids can have a number of side-effects.
However, the length of treatment normally depends on the condition being treated and how severe the condition is. Some people need to use topical steroids in the long term for example, steroid nose nasal sprays for allergies. Other people may only need to use them for a week or so for example, for mild dermatitis.
Some people need to use them for months for example, a cream for psoriasis or a spray for hay fever. Your doctor will explain when they prescribe the topical steroid. If you use a strong topical steroid for a long period of time you will usually need to reduce the amount you use over a period of weeks and then stop.
For example, if you have been using a potent steroid cream to treat psoriasis. This is because when it is stopped suddenly your condition may come back quickly. If topical steroids have only been used for a short time they can usually be stopped abruptly. You can buy some topical corticosteroids 'over the counter' without a prescription. Do not apply this to your face unless your doctor has told you to do so. This is because it may trigger a skin condition affecting the face acne or rosacea.
Long-term use may also damage the skin. On your face this would be more noticeable than the rest of your body. So usually only weak steroids are used on the face. Those which are suitable are prescription-only. Be careful when using steroid creams that you have bought in a shop. They can make some conditions worse, not better. For example, athlete's foot will get worse with steroids; as will eczema herpeticum and perioral dermatitis. You can also buy some steroid nose nasal sprays to treat hay fever - for example, beclometasone nasal spray and fluticasone nasal spray.
Most people who use topical steroids have no side-effects, or very few. How likely you are to have side-effects depends on how long you use the medicine for, how much is used or applied and how strong the steroid is. It is not possible to list all the side-effects here. However, listed below are some of the more common and important ones. For a full list of side-effects see the leaflet that comes with your medicine. Even with topical steroids, some of the medicine gets through the skin and into the bloodstream.
The amount is usually small and causes no problems unless strong topical steroids are used regularly on large areas of the skin. The main concern is with children who need frequent courses of strong topical steroids.
The steroid can have an effect on growth. Therefore, children who need repeated courses of strong topical steroids should have their growth monitored. Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. Egton Medical Information Systems Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy.
Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions. In this series. In this article What are topical steroids? What types of topical steroids are there? When are topical steroids prescribed? Which topical steroid is usually prescribed? How often are topical steroids usually applied?
What is the usual length of treatment? Stopping topical corticosteroids Can you buy topical corticosteroids? What are the side-effects of topical steroids? What are topical steroids? Topical steroids work by: Reducing redness and swelling inflammation in the part of the body they are applied to. Suppressing the body's immune system.
Stopping cells from multiplying. Reversing enlargement of blood vessels in the area they are applied to.
Long term effect of inhaled steroids can be divided into wanted and unwanted outcome. The desirable anti-inflammatory effect of steroids is reflected by lowering of bronchial hyperresponsiveness and a better control of asthma symptoms.
Inhaled corticosteroid may have systemic side effects similar to those observed with oral steroids such as 1 adrenal suppression, 2 effect on bone metabolism, 3 growth suppression in children, 4 impaired skin collagen synthesis, 5 cataract, 6 metabolic disturbances, 7 effect on central nervous system. Summing up it is advisable to use inhaled corticosteroid in the lower effective dose. Abstract Asthma is a chronic inflammatory disease of the airways play.
Publication types English Abstract Review. GC use is typically associated with the development of posterior subcapsular cataracts PSCC [ 40 ], as opposed to nuclear or cortical cataracts. There is inter-individual variation in susceptibility to PSCC and the incidence varies per individual.
Although PSCC are frequently seen in patients treated systemically, or even occasionally in those receiving inhaled corticosteroids ICSs [ 41 ], they are more commonly caused secondary to local treatment e. Glaucoma is the more serious ocular complication of GC therapy. Systemic corticosteroids can painlessly increase intraocular pressure, leading to visual field loss, optic disc cupping, and optic nerve atrophy.
Once systemic therapy is discontinued, the elevation in intraocular pressure often resolves within a few weeks, but the resultant damage to the optic nerve is often permanent. While all patients using systemic steroids are at risk for elevation in intraocular pressure and glaucoma, certain groups appear to be at higher risk.
Ocular hypertension and glaucomatous visual field defects have been reported in patients using systemic steroids with a personal or family history of open angle glaucoma, diabetes, high myopia or connective tissue disease particularly rheumatoid arthritis [ 42 ]. To reduce the risk of steroid-induced glaucoma, it is important to screen patients for these risk factors. All patients who may require long-term systemic GC therapy with a positive history for glaucomatous risk factors should be referred to an ophthalmologist for a comprehensive ocular assessment see Ophthalmologic Examination section.
This type of chorioretinopathy is associated with the formation of subretinal fluid in the macular region which leads to separation of the retina from its underlying photoreceptors. This manifests as central visual blur and reduced visual acuity. Corticosteroids induce atrophic changes in the skin that can lead to skin thinning and fragility, purpura and red striae. Skin thinning and purpura are usually reversible upon discontinuation of therapy, but striae are permanent.
Purpura generally affect the sun exposed areas of the dorsum of the hands and forearms, as well as the sides of the neck, face, and lower legs, and are usually not accompanied by palpable swelling [ 44 , 45 ]. Red striae generally appear on the thighs, buttocks, shoulders and abdomen. Impairment of wound healing is another common, and potentially serious, side effect of systemic GC use. Corticosteroids interfere with the natural wound-healing process by inhibiting leukocyte and macrophage infiltration, decreasing collagen synthesis and wound maturation, and reducing keratinocyte growth factor expression after skin injury [ 44 ].
Some topical and systemic agents may help counter the effects of corticosteroids on wound healing, including epidermal growth factor, transforming growth factor beta, platelet-derived growth factor, and tetrachlorodecaoxygen [ 45 ]. GC therapy has been associated with an increased risk of several adverse GI events including gastritis, ulcer formation with perforation and hemorrhage, dyspepsia, abdominal distension and esophageal ulceration.
Despite the commonly held perception that steroid use increases the risk of peptic ulcer disease, large meta-analyses of randomized, controlled trials have failed to show a significant association between GC use and peptic ulcers [ 46 , 47 ]. Recent evidence suggests that the risk of peptic ulcer disease due to corticosteroids alone is low, but increases significantly when these agents are used in combination with non-steroidal anti-inflammatory drugs NSAIDS [ 48 ].
Messer et al. Acute pancreatitis has also been reported to be an adverse effect of corticosteroid use. A Swedish population-based, case—control study demonstrated an increased risk of acute pancreatitis after exposure to GC therapy [ 51 ].
Overall, the OR for developing acute pancreatitis was 1. However, other evidence suggests that the underlying disease processes for which GC therapy is prescribed particularly systemic lupus erythematosus [SLE] may be more likely causes of pancreatitis than GC use [ 52 ]. GC use is associated with AEs that are known to be associated with a higher CVD risk, including hypertension, hyperglycemia, and obesity.
Another large, retrospective case—control study found current GC use to be associated with a significantly increased risk of heart failure adjusted OR, 2. CV risk was found to be greater with higher GC doses and with current vs.
Population-based studies conducted in Northern Europe have also noted an increased risk of new-onset atrial fibrillation AF and flutter in GC users [ 55 , 56 ]. In these studies, the risk of AF was significantly greater with current or recent use i. Serious CV events, including arrhythmias and sudden death, have also been reported with pulse GC therapy.
However, these events are rare and have occurred primarily in patients with underlying kidney or heart disease [ 57 ]. Although it is unclear whether these serious AEs are due to GC use or the underlying condition, some experts recommend continuous cardiac monitoring in patients with significant cardiac or kidney disease receiving pulse therapy.
Longer infusion times 2—3 h for pulse GC therapy should be considered in patients who are at high risk of CVD [ 58 ]. Findings from studies examining the relationship between GC use and dyslipidemia have been conflicting. Despite the conflicting evidence, regular monitoring of lipids as well as other traditional risk factors for CVD is recommended in patients using GCs at high doses or for prolonged periods see CV Risk and Dyslipidemia section.
Corticosteroids have direct catabolic effects on skeletal muscles that can lead to reductions in muscle protein synthesis and protein catabolism and, ultimately, muscle weakness. Myopathy generally develops over several weeks to months of GC use. Patients typically present with proximal muscle weakness and atrophy in both the upper and lower extremities; myalgias and muscle tenderness, however, are not observed. Also, the higher the GC dose utilized, the more rapid the onset of muscle weakness.
There is no definitive diagnostic test for GC-induced myopathy and, therefore, the diagnosis is one of exclusion. Symptoms generally improve within 3 to 4 weeks of dose reductions, and usually resolve after discontinuation of GC therapy [ 64 ]. Evidence also suggests that both resistance and endurance exercise may help attenuate GC-induced muscle atrophy [ 65 ].
Critical illness myopathy may also develop in patients requiring large doses of IV GCs and neuromuscular blocking agents. It is characterized by severe, diffuse proximal and distal weakness that develops over several days. Although it is usually reversible, critical illness myopathy can lead to prolonged intensive care unit ICU admissions, increased length of hospital stays, severe necrotizing myopathy and increased mortality [ 58 , 63 , 66 ].
Treatment is directed toward discontinuation of GC therapy or dose reductions as soon as possible, as well as aggressive management of underlying medical comorbidities. GC use can lead to a wide range of psychiatric and cognitive disturbances, including memory impairment, agitation, anxiety, fear, hypomania, insomnia, irritability, lethargy, mood lability, and even psychosis.
These AEs can emerge as early as 1 week after initiating corticosteroid therapy, and appear to be dependent on dose and duration of therapy [ 67 , 68 ]. A family history of depression or alcoholism has also been reported as a risk factor for the development of GC-related affective disorders [ 69 ].
Individuals who develop psychiatric manifestations on short courses of GCs most commonly report euphoria, while those on long-term therapy tend to develop depressive symptoms [ 68 , 70 , 71 ]. GC therapy may also be associated with sleep disturbances and unpleasant dreams [ 72 ]; the risk of these events can potentially be decreased by modifying the timing of GC administration e.
A decline in declarative and working memory has also been reported with GC therapy; these effects appear to be dose-dependent and frequently occur during the first few weeks of therapy [ 73 ]. Older patients appear to be more susceptible to memory impairment with less protracted treatment.
In patients with SLE, low serum albumin levels may also be predictive of GC-induced psychosis [ 76 ]. For patients with persistent symptoms of psychosis, antipsychotic therapy may be required [ 63 ]. Most patients with psychiatric reactions to corticosteroids usually recover from these symptoms with dose reductions or upon cessation of therapy.
Lithium has also been found to be effective for both the prophylaxis and management of GC-related affective disorders [ 77 ]. The mechanisms by which corticosteroids inhibit the immune system and decrease inflammation may predispose patients to infection. A meta-analysis of 71 clinical trials involving over patients randomly allocated to systemic GC therapy found the overall rate of infectious complications to be significantly higher in patients using systemic corticosteroids vs.
In addition to GC dose, other factors influencing the risk of infection include: the underlying disorder, patient age, and concomitant use of immunosuppressive or biologic therapies [ 48 , 79 ]. A study comparing the infection risk posed by biologic therapies vs. Patients using GCs appear to be particularly susceptible to invasive fungal and viral infections; this is especially true in bone marrow transplant recipients [ 45 ].
Older patients and those with lower functional status are also at higher risk for infections with steroid use. It is important to note that early recognition of infections in patients taking GCs is often difficult [ 48 ]. GC users may not manifest signs and symptoms of infection as clearly as non-users, due to the inhibition of cytokine release and associated reduction in inflammatory and febrile responses. However, one side effect that is unique to children is growth suppression.
Oral GC therapy has been associated with a delay in growth and puberty in children with asthma and other childhood diseases such as nephrotic syndrome [ 81 — 85 ]. Some evidence suggests that final height may also be compromised in children with a history of GC use [ 81 , 86 ].
Subjects started prednisone treatment at a mean age of 9. Mean height after age 18 years was found to be significantly lower in boys previously treated with either high- or low-dose prednisone vs. When indices of pulmonary status were controlled for, the negative association between the use of prednisone and height remained strong in boys. No persistent growth impairment was noted in female subjects. It is important to note that although growth can be an independent adverse effect of corticosteroid therapy, it can also be a sign of AS.
AS is the most common cause of adrenal insufficiency in children. The rate of adrenal crisis or death related to AS is unknown, however, adrenal insufficiency is associated with higher mortality in the pediatric population, highlighting the importance of recognition [ 29 ].
As in adults, the symptoms of AS are non-specific; therefore, the condition may go unrecognized until exposure to a physiological stress illness, surgery or injury , which may result in adrenal crisis. Children with adrenal crisis secondary to AS may present with hypotension, shock, decreased consciousness, lethargy, unexplained hypoglycemia, seizures or even death see Table 4 [ 87 — 91 ].
Several cases of pediatric AS have been reported in the literature, including adrenal crises in children requiring hospitalization and prolonged ICU stays [ 92 , 93 ]. To our knowledge, there have been no published population studies looking at the frequency of symptomatic AS associated with systemic GCs.
However, interim results from a national survey examining AS associated with any form of GC in the Canadian pediatric population over a two-year period have reported 44 cases of symptomatic AS, 6 of which presented as adrenal crisis [ 90 ]. A recent meta-analysis of AS in children treated with acute lymphoblastic leukaemia ALL found biochemical evidence of AS immediately following GC discontinuation in nearly all patients [ 93 ].
AS resolved within a few weeks in most patients, but persisted for up to 34 weeks in others. Although some studies have suggested that higher doses and longer durations of GC treatment may be risk factors for AS, these findings have not been consistent across trials [ 30 , 93 — 96 ]. Even relatively low pharmacologic GC doses are significantly higher than physiologic doses, making AS a potential risk. Most cases of medication-induced diabetes in children are associated with GC use.
Steroid-induced hyperglycemia and diabetes have been reported in post-transplant patients, children with ALL, and those undergoing treatment for nephrotic syndrome [ 97 , 98 ]. There have also been reports of diabetic ketoacidosis at presentation in these children [ 97 , 98 ]. There is currently limited data describing risk factors for hyperglycemia and diabetes secondary to GC use in the pediatric population. Therefore, evaluating for the typical type 2 diabetes risk factors may not be sufficient for identifying children at-risk of developing steroid-induced hyperglycemia or diabetes.
The clinical presentation in the pediatric population is similar to that in adults, and includes truncal obesity, skin changes and hypertension. In children, however, growth deceleration is also observed [ 99 ]. Therefore, HPA-axis function should be evaluated prior to discontinuing steroid therapy in children with Cushingoid features [ 88 , 89 ]. A number of studies have reported decreased bone density in children taking oral corticosteroids [ — ].
The risk of fracture was increased in children who received four or more courses of oral corticosteroids adjusted OR, 1. Of the various fracture types, the risk of humerus fracture was doubled in these children adjusted OR, 2. Children who stopped taking oral corticosteroids had a comparable risk of fracture to those in the control group [ ].
Vertebral fractures are an under-recognized manifestation of osteoporosis in children, in part due to the fact that such fractures are often asymptomatic even when moderate or severe [ — ]. Similar to adults, vertebral fractures in GC-treated children are most frequently noted in the mid-thoracic region and at the thoracolumbar junction [ — ]. Children with rheumatic conditions and incident vertebral fractures at 12 months received twice as much steroid, and had greater increases in BMI and declines in spine BMD Z-scores [ ].
These studies have played an important role in furthering our understanding of the osteoporosis burden manifesting as vertebral fractures in steroid-treated children. Before initiating long-term systemic corticosteroid therapy, a thorough history and physical examination should be performed to assess for risk factors or pre-existing conditions that may potentially be exacerbated by GC therapy, such as diabetes, dyslipidemia, CVD, GI disorders, affective disorders, or osteoporosis.
At a minimum, baseline measures of body weight, height, BMD and blood pressure should be obtained, along with laboratory assessments that include a complete blood count CBC , blood glucose values, and lipid profile Table 5. In children, nutritional and pubertal status should also be examined. Patients without a history of chicken pox should be advised to avoid close contact with people who have chickenpox or shingles, and to seek urgent medical advice if they are exposed [ 1 ].
Concomitant use of other medications should also be assessed before initiating therapy as significant drug interactions have been noted between GCs and several drug classes [ 1 , 8 ] see Table 6. Females of childbearing age should also be questioned about the possibility of pregnancy. GC use in pregnancy may increase the risk of cleft palate in offspring, although the absolute risk appears to be low [ 48 ]. The above-mentioned parameters should be monitored regularly.
Specific recommendations for the assessment and monitoring of BMD and fracture risk, diabetes, CV risk and dyslipidemia, AS, growth, and ophthalmologic events are provided below. The authors recommend annual height measurement and questioning for incident fragility fractures in adults receiving GC therapy.
If BMD is stable at the 1-year follow-up and fracture risk is low, then subsequent BMD assessments can be performed every 2—3 years Table 5. However, if bone density has decreased at the initial 1-year follow-up, both BMD and fracture risk should be assessed annually. For medium doses 2. In adults, a single BMD assessment can help predict the likelihood of fracture due to age-related osteoporosis. In children with GC-induced osteoporosis, however, this relationship is not as evident.
Therefore, experts have recommended serial BMD assessments in at-risk children as well as in those displaying evidence of growth failure [ ]. At the same time, the bone health assessment of a child on chronic GC therapy needs to be extended beyond BMD in order to identify risk factors as well as early manifestations of osteoporosis. As such, bone health monitoring in pediatric chronic GC users includes an evaluation of calcium and vitamin D intake, back pain, physical activity, and disease-related risk factors for attenuated bone mineral accrual and bone loss such as chronic inflammation and disuse.
Because early diagnosis and appropriate intervention can prevent or delay the progression of osteonecrosis and the need for joint replacement, patients using high-dose GC therapy or those treated with GCs for prolonged periods should be evaluated for joint pain and decreased range of motion at each visit [ 58 ]. Magnetic resonance imaging should be considered in adult or pediatric patients presenting with these signs or symptoms [ 16 ]. Health care providers must be aware of the risk of AS in patients who have received supraphysiological GC doses.
The risk of AS is low in patients who have been treated with GC therapy for less than 1 week [ ]. However, as is seen following longer courses of GC treatment, AS may result from multiple short courses of high-dose therapy.
If AS is suspected, biochemical testing of the HPA axis should be considered after GC treatment has been reduced to a physiologic dose. Given the ease and practicality of a first morning cortisol measurement, it should be considered for the initial screening of patients at risk for AS. The test should be performed at am or earlier given that cortisol levels decline throughout the day with natural circadian rhythm, and both evening and morning GC doses should be held prior to testing see Table 8 [ 91 ].
If the am cortisol value is below the normal laboratory reference range, AS is likely present and further GC withdrawal should occur only once testing has normalized. Therefore, a normal cortisol value does not rule out the presence of AS. If a patient has signs or symptoms of AS and requires further testing, then referral to an endocrinologist should be considered. Clinicians must be aware that exogenous estrogen therapy, which affects cortisol-binding globulin levels, increases serum cortisol; therefore, the same thresholds for diagnosing AS do not apply in the setting of estrogen use.
The insulin tolerance test ITT is the definitive test for evaluation of the HPA axis, but performing this test is complicated and risky for patients since insulin is administered to achieve hypoglycemia. The ITT is contraindicated in children secondary to the risks of hypoglycemia on the pediatric brain. Therefore, in the setting of a normal morning cortisol result and the presence of AS symptoms, the low-dose adrenocorticotropic hormone ACTH stimulation test should be performed to confirm the diagnosis since it is a sensitive and specific test for AS [ — ].
Cortisol levels are expected to peak between 20—30 min after cosyntropin injection, hence, cortisol measurements are recommended at 15—20 min and 30 min [ ]. Many protocols also recommend measuring cortisol at 60 min. For children receiving GC therapy, growth should be monitored every 6 months ideally by using stadiometry measurements and measurements should be plotted on an appropriate growth curve Table 5.
If, after 6 months, growth velocity appears to be inadequate, the physician should consider all possible etiologies, including AS, as well as referral to an endocrinologist [ 91 ]. It is also important to rule out malnutrition as a cause of poor growth [ 9 , ].
There are currently no evidence-based guidelines for the monitoring of dyslipidemia and CV risk in patients using corticosteroid therapy. The authors recommend assessment of lipid profile at baseline, 1-month after initiating systemic GC therapy and then every 6—12 months thereafter Table 5.
All patients should be educated about the classic signs and symptoms of hyperglycemia polyuria, polydipsia, unexplained weight loss so that they are screened for steroid-induced diabetes if symptoms arise. If blood glucose or A1C is abnormal at baseline, then home blood glucose monitoring is also recommended. Glucose investigations should be repeated after starting GC therapy.
In patients taking prednisolone, some experts have recommended that blood glucose be monitored within 8 hours of the first dose i. The Canadian Diabetes Association CDA guidelines recommend that glycemic parameters be monitored for at least 48 hours after initiation of GC therapy, regardless of whether or not the patient has diabetes [ 38 ].
Guidelines for blood glucose monitoring post-transplant suggest weekly monitoring for four weeks after transplant, followed by blood glucose checks at 3 and 6 months post-transplant, then annually thereafter [ ]. In the absence of screening guidelines for GC-induced diabetes in children, the authors recommend that physicians be aware of the risk of hyperglycemia in children receiving long-term supraphysiological GC doses and, at a minimum, screen for classic symptoms [ 98 ].
An annual FPG should also be considered. In children presenting with symptoms suggestive of diabetes, FPG should be performed. The diagnostic criteria for diabetes in children are the same as for adults [ 38 ]. More frequent screening of glucose parameters should be considered in children who are at potentially higher risk of developing hyperglycemia or diabetes, such as transplant recipients, obese patients, or those with conditions such as ALL or nephrotic syndrome.
Patients on low-to-moderate doses of systemic corticosteroids for more than 6—12 months should undergo annual examination by an ophthalmologist Table 5. An earlier examination is required in patients with symptoms of cataracts namely blurred vision , however, this is generally not considered an ocular emergency that requires urgent treatment.
Early referral for monitoring of intra-ocular pressure glaucoma is recommended in patients at higher risk of developing steroid-induced glaucoma, such as those with a personal or family history of open angle glaucoma, diabetes mellitus, high myopia, or connective tissue disease especially rheumatoid arthritis. To minimize the occurrence of steroid-induced AEs, the lowest effective GC dose should be prescribed for the minimum period of time required to achieve treatment goals Table Any pre-existing comorbid conditions that may increase the risk of GC-induced AEs should be treated prior to corticosteroid initiation, and patients should be instructed to avoid contact with persons that have infections, such as shingles, chickenpox or measles.
Patients should also be advised to carry a steroid treatment card and wear a medical identification tag, and to adopt lifestyle habits that may help minimize the risk of excessive weight gain with GC use, such as participation in regular physical activity and following a healthy, low-calorie diet. Finally, whenever possible, GC-sparing agents should be considered.
In patients with severe asthma, for example, use of the anti-immunoglobulin E IgE monoclonal antibody, omalizumab, has been shown to reduce the occurrence of asthma exacerbations requiring systemic corticosteroid therapy and to improve symptoms and asthma-related quality of life [ ]. At present, omalizumab is reserved for patients with difficult to control asthma who have documented allergies and whose asthma symptoms remain uncontrolled despite ICS therapy [ ].
A number of published guidelines have addressed the prevention and treatment of GC-induced osteoporosis in adults [ — , — ]. Most guidelines and evidence support the use of bisphosphonates and teriparatide as first-line therapy for GC-induced osteoporosis in adults. A number of studies have demonstrated that the bisphosphonates alendronate, risedronate and zoledronic acid are effective for the prevention and treatment of GC-induced bone loss [ — ], although their long-term efficacy on fractures is not well established [ ].
Teriparatide has been shown to be effective in improving BMD and reducing vertebral fractures in patients with GC-induced osteoporosis [ — ]. The ACR recommendations for the use of teriparatide and bisphosphonates are shown in Table 11 [ ]. Although other therapies such as calcitonin, raloxifene and denosumab may also play a role in the management of GC-induced osteoporosis in adults, they are not currently recommended as first-line therapy.
Calcitonin has been found to prevent lumbar spine bone loss in the setting of GC use, but the same protection has not been observed at the femoral neck or with respect to fracture risk [ ]. The European Medicines Agency EMA recently completed a review of the benefits and risks of calcitonin-containing medicines and concluded that there is evidence of a small, increased risk of cancer 0. Therefore, given this risk as well as its lack of efficacy in reducing fracture risk, calcitonin is not recommended as first-line therapy for GC-induced osteoporosis.
However, it may be considered when bisphosphonates are contraindicated or in those patients who are intolerant to oral or IV bisphosphonates. Due to its analgesic effect, calcitonin can also be considered in patients who have sustained an acute fracture.
However, the generalizability of these findings are limited since the study cohort was predominantly Asian and did not include patients on high-dose GC therapy. Furthermore, as a selective estrogen receptor modulator, raloxifene use for osteoporosis prevention and treatment is limited to the postmenopausal female population.
In animal models, denosumab has been shown to prevent steroid-induced bone loss and improve bone strength [ ]. A phase 2 trial also found that denosumab improved lumbar spine BMD in patients with rheumatoid arthritis treated with corticosteroids and bisphosphonates [ ]. The phase 3 FREEDOM trial found denosumab to be associated with a slightly increased risk of cellulitis [ ], although the 2-year extension trial found no increased risk with longer term treatment [ ].
In addition to pharmacologic therapy, current guidelines for GC-induced osteoporosis in adults recommend preventive measures such as smoking cessation, reduced alcohol consumption, participation in weight-bearing and strength-building exercises, falls risk assessment, and calcium and vitamin D supplementation [ — , — ].
Cochrane investigators reviewed the available data on calcium and vitamin D use in GC-treated patients and found that supplementation prevented bone loss at the lumbar spine and forearm, but had no effect on femoral neck BMD or fracture incidence [ ]. There are currently no evidence-based guidelines for the prevention and treatment of GC-induced osteoporosis in children.
Most of the studies examining bisphosphonate use in GC-treated children have been observational in nature and have utilized the intravenous IV preparation, pamidronate [ ]. Some evidence suggests that bisphosphonate therapy increases BMD, promotes reshaping and relieves back pain from previously fractured vertebral bodies, and is safe and well-tolerated in children with secondary osteoporosis [ — ], although long-term safety and efficacy data is still required.
Currently, experts recommend consideration of bisphosphonate therapy in children with evident bone fragility associated with reductions in BMD parameters, particularly if there is a persistence of risk factors and, thereby, less likelihood of spontaneous BMD restitution and growth-mediated reshaping of vertebral bodies [ ]. Initial treatment for osteonecrosis includes bed rest and non-steroidal or other analgesics to relieve pain.
For patients with early stage or less advanced osteonecrosis, joint-preserving strategies, such as reducing weight-bearing activities and core decompression with or without marrow transplantation , have been utilized with varying levels of success. For more advanced disease, femoral head or total hip replacement surgery is usually required [ 16 ]. Since these replacements generally have a year lifespan, strategies that delay the need for surgery are desired. Some evidence suggests that treatment with alendronate may reduce the risk of bone collapse and delay the need for surgery [ , ].
However, a recent randomized, controlled trial found no benefit of alendronate vs. In children with osteonecrosis in the leukemia setting, IV pamidronate has been associated with significant improvements in pain and mobility [ , ]. When possible, referral to a multidisciplinary diabetes team should be considered.
Initial management involves appropriate lifestyle modification strategies; if targets are not met with these modifications, pharmacotherapy is recommended, and the same spectrum of glucose-lowering medications is used for GC-induced diabetes as is used for pre-existing type 2 diabetes. If a sulfonylurea is selected, it is important to consider both the dosing frequency of the GC as well as the duration of action of the insulin secretagogue.
Sulfonylureas with shorter half-lives i. Agents with longer half-lives e. In the absence of a contraindication, metformin is often recommended in combination with insulin Table A reasonable starting dose for insulin is 0. With once-daily morning administration of prednisone, fasting glucose may be unaffected, but blood glucose will be higher later in the day.
If this occurs, then an intermediate-acting insulin such as N or NPH or a premixed combination of intermediate- and fast-acting insulin can be initiated in the morning. If blood glucose is elevated in the morning as well, then an evening insulin dose may also be required. If shorter-acting GCs are administered more than once per day, or if dexamethasone is used, then both fasting and non-fasting glucose levels are likely to be affected.
In this case, twice-daily intermediate-acting insulin or long-acting insulin, such as detemir or glargine, are recommended; fast-acting insulin may also be required at mealtimes. In order to prevent hypoglycemia, it is important to remember to adjust diabetes medications if GC doses are reduced.
The treatment of GC-induced diabetes in children is best accomplished through the combined efforts of a multidisciplinary pediatric diabetes healthcare team [ 98 ]. As with adults, lifestyle interventions should be initiated; if glycemic targets are not met with these modifications, insulin must be considered. Many of the other glucose-lowering agents used in adult patients with type 2 diabetes have not been licensed for use in the pediatric population and may be contraindicated in children with complex medical issues [ 98 ].
Until the safety and efficacy of these medications in children are established, they cannot be recommended for routine clinical use in this population. To minimize the risk of developing AS, it is important to consider the relative suppressive effects of the various GCs based on potency and duration of action prior to initiating therapy see Table 3. The lowest effective dose should be utilized for treatment of the underlying condition and the dose should be re-evaluated regularly to determine if further reductions can be instituted.
If possible, the GC should be administered once-daily in the morning. Currently, evidence-based recommendations are lacking for withdrawal of high-dose GC treatment and management of individuals with biochemical evidence of AS. If high-dose GC therapy is no longer required, then GC doses can be reduced relatively quickly from pharmacologic to physiologic doses.
Examples of withdrawal regimens for both adults and children are provided in Tables 13 and 14 , respectively. These tables present modest, but safe, approaches to GC withdrawal and assume that the clinician has access to testing. However, in the absence of evidence-based guidelines, some physicians may choose to withdraw GC therapy gradually without testing. Regardless of the withdrawal regimen chosen, clinicians need to be aware of the symptoms of AS and to slow the withdrawal regimen should these symptoms arise.
Screening tests should be considered to assess adrenal function as GC therapy is being withdrawn. Screening should occur before tapering to less than a physiologic dose Tables 13 and 14 [ , ]. When possible, screening should occur at least 1 week after the dose has been tapered to a once-daily physiological dose preferably hydrocortisone, which has a shorter half-life.
This treatment model replicates the physiological response of the healthy adrenal gland in order to prevent an adrenal crisis. To our knowledge, there is no evidence to support or refute this practice. The safest approach would be to treat asymptomatic patients with biochemical evidence of AS no differently than those with symptomatic AS.
Consideration should be made to educate patients about the risk of AS if they have been treated with GC therapy within the last year, but have not had testing to rule out AS. In the event of severe illness or surgery, stress dose steroids should be considered to prevent adrenal crisis. The potency of dexamethasone and betamethasone in suppressing growth has been shown to be nearly 18 times higher than that of prednisolone [ ].
Therefore, to reduce the risk of growth suppression in children, lower potency agents, such as prednisolone, should be used whenever possible. There has been some evidence of short-term benefits on growth velocity with rhGH therapy [ ], however further study, including evaluation of final adult height, is required.
Although treatment of red striae is often disappointing, some success has been noted with topical vitamin A 0. To help reduce the risk of striae, patients initiating systemic corticosteroid therapy should be advised to follow a low-calorie diet.
Systemic corticosteroids are widely used to treat a variety of autoimmune and inflammatory disorders. Despite the benefits of these agents, their prolonged use particularly at high doses is associated with potentially serious AEs affecting the musculoskeletal, endocrine, CV, and central nervous systems as well as the GI tract.
Teriparatide has been shown to be effective in improving BMD frequently noted in the mid-thoracic displaying evidence of growth failure [ ]. Rheumatoid arthritis pain: Tips for management of AS in children then an evening insulin dose. If the patient is on a GC with a longer. All patients should be educated Emphysema Estriol as a potential the physician should consider all events including gastritis, ulcer formation Exercising with arthritis Fingolimod during tissue from glucocorticoid-treated mice. Anti-inflammatory: Inhibit inflammation by blocking a normal morning cortisol result in patients at higher risk of developing steroid-induced glaucoma, such ACTH stimulation test should be performed to confirm the diagnosis weight gain with GC use, turnover Vasoconstrictive: Inhibit the action [ - ]. The safest approach would be taken from the educational grant targets are not met with. In patients believed steroids in the uk for sale be no longer required, then GC as for adults [ 38 prevent adrenal crisis. Suppression and recovery of adrenal glucocorticoids GCs [ 1 ]. The authors recommend assessment of or symptoms of AS and one of the most widely to an endocrinologist should be. In children with GC-induced osteoporosis, help Oil of oregano: Can as evident.Some researchers have speculated that inhaled corticosteroid drugs may slow growth rates in children who use them for asthma. Topical corticosteroids. Reflex cough or bronchospasm triggered by the inhaled drug occur fairly commonly, but are easily corrected by appropriate treatment. The systemic complications. However, oral steroids may cause many serious side effects. A major breakthrough in the treatment of asthma was introducing inhaled steroids.