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Usually it is beneficial to take a multivitamin every day, but speak with your doctor to see which one is right for you, since some vitamins can adversely affect certain conditions. For example, people with antiphospholipid antibodies, especially those taking anticoagulants such as warfarin Coumadin , should avoid vitamin K because it can increase the risk of blood clots.
Steroids can also contribute to a thinning of the bones known as osteoporosis, which may put you at an increased risk for bone fractures. Your doctor may prescribe a drug for osteoporosis or advise you to take a calcium or hormone supplement. Bisphosphonates such as Actonel, Fosamax, and Boniva are commonly prescribed, as are parathyroid hormone Forteo and other medications. To help keep your bones as strong as possible, try to increase your intake of calcium and vitamin D.
Calcium helps to keep bones strong and vitamin D helps your body make use of calcium. Foods high in calcium include milk and milk products, tofu, cheese, broccoli, chard, all greens, okra, kale, spinach, sourkraut, cabbage, soy beans, rutabaga, salmon, and dry beans.
In addition to increasing your risk of osteoporosis, steroid medications can weaken your muscles. Staying as active as possible will help you to maintain strong muscles and bones. Weight-bearing activities such as walking, dancing, and running will help your muscles stay strong and healthy. Many people report that these activities make them feel better mentally as well. However, you should never put yourself through more than reasonable discomfort when exercising.
People with lupus should never smoke due to their increased risk of cardiovascular disease. Steroid medications increase this risk by upping blood pressure, triglycerides, and cholesterol. Smoking, steroids, and lupus make a very bad combination.
Steroid medications can also increase the risk of infection; this risk increases if you are also taking immunosuppressive drugs. For this reason, it is important that you try to avoid colds and other infections. Washing your hands regularly is perhaps the best way to keep germs at bay. GCs are, by far, the most effective anti-inflammatory drugs for treating chronic inflammatory diseases, allergies, and autoimmune pathologies, such as RA, asthma, multiple sclerosis, and systemic lupus erythematosus 8 , 9.
Their mechanism of action has not yet been completely elucidated, owing to the different levels of tissue expression, several glucocorticoid receptor GR isoforms, and the complex gene regulation mediated by the activated monomeric or dimeric forms of GR. As drugs, GCs are generally considered immunomodulatory rather than simply immunosuppressive, because of their complex effects on the cells of the immune system. Nevertheless, some pro-inflammatory effects of GCs have been reported, such as the induction of the expression of NLRP3, a central component of the inflammasome 16 , Furthermore, an extensive body of evidence suggests that GCs have different effects on the immune system depending on the duration of their administration.
Prolonged exposure to GCs may cause immunosuppression, whereas acute exposure can activate the immune system In the case of chronic autoimmune or inflammatory diseases, long-term therapy with high-dose GCs elicits immunosuppressive and anti-inflammatory effects, which are necessary for symptomatic relief. Unfortunately, the consequent adverse effects are sometimes quite severe, requiring specific additional therapies or suspension of GC therapy.
In some pathologies, such as asthma, the side effects of GCs have been partially resolved by topical administration However, generally, adverse effects due to high doses cannot be fully avoided in systemic GC therapy. Attempts have been made to develop the so-called dissociated steroids, with the aim to favor the transrepression of activated monomeric GR over GR dimer transactivation, which is considered the cause of side effects. Studies in GR Dim mutant mice, which harbor a mutation that causes impaired homodimerization of the ligand-bound GR, have initially shown a reduced functionality of the transcriptional activity However, other recent studies have revealed that this mutant GR can still dimerize, although to a lower degree, making this model suboptimal for distinguishing differences between GR monomeric and homodimeric related effects Furthermore, some side effects, but also some therapeutic effects, depend on both transactivation and transrepression.
Thus, the concept of separating the beneficial anti-inflammatory effects from the adverse effects of GCs cannot be based on the simple separation of transrepression from transactivation activities The dynamics of gene regulation by GR and its binding to the DNA remains a complex mechanism that needs to be more deeply studied.
This is the reason why none of the selective glucocorticoid receptor agonist and modulators developed so far has still reached the market. Knowing the biology of the complex functions of these hormones will allow the development of pharmacological tools specifically targeting one of their sophisticated mechanisms 22 , Another important aspect to consider in long-term treatments with GCs is that patients could develop adrenal insufficiency e.
It takes some time for the HPA axis to function properly after suppression. Recent studies have demonstrated that it takes as long as 1 year for a suppressed adrenal to again secrete these hormones.
Conversely, if GC treatment lasts 1—2 weeks, it takes only 1 day to again secrete endogenous GCs Interestingly, the suppression occurs also locally, at the level of adrenal steroidogenic activity Furthermore, enzymes of the steroid biosynthesis are expressed not only by the adrenal cortex but also by other tissues, such as the lung, brain, spleen, skin and cells of the immune system.
Interestingly, dysregulation of local steroidal activity has been found to be involved in the pathogenesis of some autoimmune or inflammatory diseases, such as lupus erythematosus, multiple sclerosis, RA, and psoriasis When local hormone production is altered, many GC-responsive genes are aberrantly expressed and may contribute to the pathogenesis of the above-mentioned diseases.
Sometimes, GC treatments are not efficacious because of the development of resistance to GC effects. Resistance was described first in the s in in vitro cell systems and has been largely studied in asthma and RA For comprehensive reviews on this subject, see references 31 — Overcoming the problem of resistance by reactivating the sensitivity to GCs, when possible, is the only strategy for using GC treatment in pathologies that cannot be treated with alternative drugs.
GCs are released by the HPA axis under a specific rhythm, which is regulated by the circadian clock in anticipation of daily energy-demanding situations.
In rodents, GC release peaks slightly before nighttime, whereas in humans, this happens before daybreak, just in the proximity of their respective active phase Therefore, the time of administration of exogenous GCs in chronic autoimmune or inflammatory diseases is critical and should be carefully chosen because of the circadian clock.
Furthermore, the existence of cross-talk between the HPA axis and the immune system further complicates the scenario in which GCs must act. It has been suggested that late-night administration is more effective than early morning administration, since the immune system starts to be activated between and a.
This immune activation increases in some inflammatory conditions, such as RA, gout, or allergic asthma, and cannot be controlled by endogenous GCs, whose production is already inadequate due to chronic inflammation and consequent downregulation of the HPA axis. Therefore, administration of exogenous GCs during nighttime ameliorates morning symptoms in RA patients Considering the multiple aspects related to GCs as drugs, the need to optimize GC therapy is crucial, especially in the case of rare diseases where GCs are the only choice and often used in combination with other drugs Figure 1.
Figure 1 Complex regulation of glucocorticoid GC activity during pharmacological administration: GCs exert immunomodulatory activities, both by transactivating anti-inflammatory proteins such as glucocorticoid-induced leucine zipper GILZ and transrepressing pro-inflammatory genes, such as those encoding for pro-inflammatory cytokines, and therefore exerting powerful anti-inflammatory and immunosuppressive effects. They can also favor inflammation, e. Importantly, long-term GC treatment causes undesired adverse drug reactions ADR , which can often result in severe pathologies such as diabetes, osteoporosis, and metabolic disorders.
The hypothalamic—pituitary—adrenal HPA axis is inevitably suppressed after long-term treatment, thus indicating the use of dose-escalating regimens to avoid life-threatening consequences. The occurrence of resistance to GC efficacy can further complicate the management of autoimmune and inflammatory diseases, especially for diseases whose treatments other than GCs are not available. Rare diseases are usually defined as those conditions that affect fewer than , people in the US and no more than 5 in 10, people within the general population in Europe.
Independently of the numbers, a rare disease occurs in a small number of people compared to other diseases prevalent in the general population. Documented rare diseases range between 5, and 8,, thus complicating the findings for appropriate pharmacological treatments, owing to the low number of cases for each pathology and its distribution across countries The majority of rare diseases are life-threatening and genetic in origin, and most of them affect children, resulting in significant developmental problems or death.
Therefore, treatments for rare diseases remain an unmet medical need. Needless to say, the severe adverse effects of long-term and high-dose GC therapy warrant the search of new pharmacological tools that could help avoid GC use while affording the same anti-inflammatory and immunosuppressive effects.
A brief description of examples of GC treatments for some rare diseases follows. Insulin autoimmune syndrome, a rare and systemic disease, is characterized by spontaneous episodes of hyperinsulinemic hypoglycemia caused by high titers of serum insulin autoantibodies.
Self-remission occurs often in the affected individual; however, high-dose GC therapy is required and has resulted in successful outcomes because of its autoimmune origin. Other therapies are available, from immunosuppressive agents, such as azathioprine, to monoclonal antibodies-based therapies, such as rituximab an anti-CD20 antibody which targets IgG producer B cells Another systemic inflammatory orphan disease is relapsing polychondritis, which can be considered a syndrome, because it is frequently associated with other autoimmune conditions, including systemic vasculitis, RA, and spondyloarthritis.
It is characterized by an inflammatory infiltrate, IgG deposits, and islands of cartilage with fibrosis. High-dose steroid therapy represents the first line of treatment only in life-threatening cases, followed by a switch to less toxic drugs in the maintenance phase, such as azathioprine. Non-steroidal anti-inflammatory drugs NSAIDs are also used in cases involving the nose, external ear, or joints.
Biologicals including tocilizumab an anti-IL-6 antibody , abatacept a CTLA4 fusion protein , and TNF inhibitors can be used in patients who do not respond to standard therapies 39 , Some rare diseases affect the skin, and sometimes, also other organs.
Autoimmune bullous disorders encompass autoimmune diseases with high morbidity and mortality. Aberrant IgG and IgA autoantibody production directed against adhesion molecules of the epidermis or the dermal-epidermal basement membrane zone leads to a loss of skin adhesion.
In pemphigus, IgG autoantibodies react against epidermal adhesion complexes of keratinocytes, whereas in pemphigoid diseases, loss of adhesion is typical of the basement membrane zone. The result of the action of these autoantibodies is the occurrence of mucosal or cutaneous blisters and erosions. First-line treatment involves systemic corticosteroids that may be combined with immunosuppressive agents, such as azathioprine, which help reduce the risk of relapse As in other autoimmune diseases that involve autoantibody production by B cells, the anti-CD20 antibody rituximab has been found to be efficacious to such an extent that it has been recently considered as a first-line treatment The evidence, in well-controlled trials, for their benefit in curing diseases or improving outcome often does not exist.
However, the outcome for patients since steroids were introduced is far better than the results of the natural progression of these diseases. When prescribing steroids, an adequate dose must be used for long enough to achieve an effect.
The patient must be aware of the risks of therapy and the potential benefits. Care must be taken to prevent, minimise and appropriately treat complications of steroid therapy. In many cases, additional immunosuppressive drugs will be required to control immune aggression and inflammation or, in the long term, minimise corticosteroid usage. There should be a plan to minimise the dose in long-term maintenance therapy if this is required. Giving high-dose corticosteroid therapy for a few days to a critically ill patient, or for a few weeks in a patient with a condition such as asthma which should settle, is relatively safe.
Patients with chronic incurable diseases such as systemic lupus erythematosus or nephritis need a clear plan of when, how much and for how long corticosteroid therapy is required. Sites on the basic glucocorticoid structure hydrocortisone that are chemically modified to produce the common therapeutic agents are numbered and the chemical groups added are in bold.
Clear therapeutic goals can be set such as reduction in proteinuria, reduction in weakness and muscle enzymes, improved blood counts or lung function studies. The risks and complications of long-term corticosteroid therapy should be discussed with the patient and minimised by attempts to lower the dose or use adjunct immunosuppression to spare steroid usage.
Alternate day therapy may be of use to minimise adverse effects, particularly to allow maximal bone growth in children. Minimising symptoms in chronic inflammatory conditions Classical examples of this are rheumatoid arthritis and polymyalgia rheumatica. The place of steroids in rheumatoid arthritis remains vexed see 'The role of corticosteroids in rheumatology' Aust Prescr ; In these diseases, the aim should be to use the minimum dose required to gain symptomatic relief.
A typical starting dose is Corticosteroids are also used for intra-articular injections of painful joints.
Saving lives and saving organs Very high-dose therapy might be indicated for several days in critically ill patients with an aggressive acute presentation or a life- or organ-threatening relapse. Experience with treating organ allograft rejection showed that daily doses of 1 g of intravenous methylprednisolone could be given safely. The infusion has to be given slowly as it can induce an anaphylactoid reaction. This regimen has been utilised in a variety of other non-transplant situations, often with a lower daily dose of mg or mg for days.
In acute relapses of multiple sclerosis and optic neuritis, a short course of parenteral treatment can significantly shorten the time the patient is symptomatic. In the Optic Neuritis trial 1 , the only benefit was seen in the group given intravenous methylprednisolone. April 3, Share this article. Facebook Twitter LinkedIn. Steroids as an Ongoing Treatment for Autoimmune Conditions.
AutoimmuneMom Psoriasis. Steroids are a common treatment for autoimmune conditions, especially skin conditions, but are they really safe to use on an ongoing basis for decades, even in low doses found in hydrocortisone creams? If I do use steroid treatments, is it safer to get a higher-level dosage e. Will this help with side effects? Will you combine steroids with other immunosuppressants to treat my disease?
If so, which ones, and what are the pros and cons? The newest group of drugs—biologic response modifiers, or disease-modifying drugs—includes etanercept, belimumab, and infliximab. These drugs are effective at stopping inflammation and the damage it causes in certain autoimmune diseases, such as rheumatoid arthritis.
All of these drugs have many side effects and often interact with other medications. The risk of infection increases with use of any drug that suppresses the immune system. For some autoimmune diseases, supplements such as insulin, thyroid hormone, and vitamins are used to control symptoms that result from tissue or organ destruction.
For many patients, the symptoms and treatment of autoimmune diseases are life-altering. These are chronic conditions that can be a difficult burden for patients and their families.
When the immune system malfunctions in this way, it can cause a wide variety of chronic diseases. Although there is no specific cure for most autoimmune diseases, drug treatments are available to counteract the faulty immune reaction and the symptoms that result. Drugs used to treat autoimmune diseases are potent and effective, but they are often expensive and can cause significant side effects and serious drug interactions.
In autoimmune diseases, a faulty immune system mistakes healthy tissues or organs for foreign, potentially harmful invaders.
More than 80 diseases are considered to be caused by this defective immunity, including type 1 diabetes, rheumatoid arthritis, multiple sclerosis, psoriasis, and lupus. Millions of people in the United States—most of them female—have these conditions. The specific cause of autoimmune diseases is not clear, but it is thought that exposure to a drug or infectious agent such as viruses or bacteria triggers the immune system to attack healthy tissues.
Symptoms of autoimmune diseases depend on the tissues or organs the immune system attacks. Common tissues or organs affected by these diseases include the joints, muscles, connective tissues, nerves, blood vessels, skin, pancreas, and thyroid. Early symptoms of many autoimmune diseases include feelings of tiredness, illness, or weakness.
These symptoms are general and may continue for an extended period before medical help is sought. Most autoimmune diseases eventually cause symptoms that are related to the tissues damaged by the immune system. Examples are joint pain and swelling in rheumatoid arthritis, muscle spasms and weakness in multiple sclerosis, abdominal pain and diarrhea in inflammatory bowel disease, and scaly skin plaques in psoriasis. Depending upon the disease, the diagnosis is made by combining information from the medical history and physical examination with blood tests.
Blood tests that assess immune-system function include complete blood count, C-reactive protein, antinuclear antibody, autoantibody, and erythrocyte sedimentation rate. Treatment goals include the control of symptoms, whenever possible, by controlling the autoimmune reaction that caused the disorder. In many autoimmune diseases, symptoms can go into remission with the proper drug therapy. Treatments aim to avoid symptom flare-ups.
Drugs used to treat autoimmune disorders include anti-inflammatory agents such as prednisone, methylprednisolone, and dexamethasone. Other potent drugs that suppress the immune system but are not corticosteroids include sirolimus, methotrexate, and cyclophosphamide.
The newest group of drugs—biologic response modifiers, or disease-modifying drugs—includes etanercept, belimumab, and infliximab. These drugs are effective at stopping inflammation and the damage it causes in certain autoimmune diseases, such as rheumatoid arthritis. All of these drugs have many side effects and often interact with other medications.
The risk of infection increases with use of any drug that suppresses the immune system. For some autoimmune diseases, supplements such as insulin, thyroid hormone, and vitamins are used to control symptoms that result from tissue or organ destruction. For many patients, the symptoms and treatment of autoimmune diseases are life-altering.
These are chronic conditions that can be a difficult burden for patients and their families. There is no known prevention for these diseases because it is not understood how they develop. With continued research, scientists may someday understand how genetics and exposure to an infection or environmental toxin work together to spur the immune system to mistakenly attack healthy tissue and organs.
Featured Issue Featured Supplements. US Pharm. Early Symptoms Are Vague, but Later Symptoms Are Specific to the Damage In autoimmune diseases, a faulty immune system mistakes healthy tissues or organs for foreign, potentially harmful invaders.
Symptoms and Diagnosis of Autoimmune Diseases Symptoms of autoimmune diseases depend on the tissues or organs the immune system attacks. Treatment Goals and Methods Treatment goals include the control of symptoms, whenever possible, by controlling the autoimmune reaction that caused the disorder.
Living With Autoimmune Disease For many patients, the symptoms and treatment of autoimmune diseases are life-altering. Related Content. All rights reserved. Reproduction in whole or in part without permission is prohibited.
localhost › article › autoimmune-disease. Corticosteroids can be used to induce a remission or reduce the morbidity in autoimmune diseases. Although high doses can be given for short periods. High-Dose Prednisone for Treatment of Autoimmune Pancreatitis in a Patient with Coronavirus Disease (COVID) due to Infection with Severe Acute. Most autoimmune diseases are responsive to corticosteroids administered in dosages sufficient to shut off the inflammatory process. Steroid therapy for the management of various immune and inflammatory conditions is a tremendous weapon in the fight to control patients'. Finally, from the economic point of view, care for a patient with a rare disease is much more expensive that for patients suffering from a common pathology. People with lupus should never smoke due to their increased risk of cardiovascular disease. However, as their name suggests, immunosuppressive work to suppress the immune system, so when taking these drugs, it is important to watch out for infection and notify your doctor at any sign of illness. Eye Exams Finally, since medications can increase your risk of cataracts and aggravate glaucoma, try to get an eye exam twice a year.RIS file. Corticosteroids can be used to induce a remission or reduce the morbidity in autoimmune diseases. Although high doses can be given for short periods, the aim is to achieve specific targets with the minimum effective dose. Patients who require long-term treatment should be advised about the adverse effects of corticosteroids, particularly the risk of adrenal insufficiency, osteoporosis and cataracts. What are corticosteroids? All corticosteroid drugs are chemical modifications of natural glucocorticosteroids see 'Corticosteroids - mechanisms of action' Aust Prescr ; Prednisone and prednisolone are commonly used.
They only differ from cortisone and hydrocortisone by the addition of a double bond in the 1,2 position Fig. To become active, prednisone must be converted to prednisolone by changing the keto group to hydroxyl.
The glucocorticoid activity of prednisone and prednisolone is fold greater than hydrocortisone Table 1. The addition of a 6a-methyl group to prednisolone creates methylprednisolone, which has times the activity of hydrocortisone. How do corticosteroids act in autoimmunity?
Corticosteroids induce a transient lymphocytopenia by altering lymphocyte recirculation. They also induce lymphocyte death. The most important immunosuppressive effect of corticosteroids is on T cell activation, by inhibition of cytokine and effect or molecule production. In this action, they are similar to cyclosporin, although the intracellular pathways by which the two classes of drug achieve this effect are quite separate. Starting treatment with corticosteroids Corticosteroids are widely used for a variety of inflammatory and non-inflammatory conditions that are not a result of hydrocortisone deficiency.
The evidence, in well-controlled trials, for their benefit in curing diseases or improving outcome often does not exist. However, the outcome for patients since steroids were introduced is far better than the results of the natural progression of these diseases.
When prescribing steroids, an adequate dose must be used for long enough to achieve an effect. The patient must be aware of the risks of therapy and the potential benefits. Care must be taken to prevent, minimise and appropriately treat complications of steroid therapy. In many cases, additional immunosuppressive drugs will be required to control immune aggression and inflammation or, in the long term, minimise corticosteroid usage.
There should be a plan to minimise the dose in long-term maintenance therapy if this is required. Giving high-dose corticosteroid therapy for a few days to a critically ill patient, or for a few weeks in a patient with a condition such as asthma which should settle, is relatively safe. Patients with chronic incurable diseases such as systemic lupus erythematosus or nephritis need a clear plan of when, how much and for how long corticosteroid therapy is required.
Sites on the basic glucocorticoid structure hydrocortisone that are chemically modified to produce the common therapeutic agents are numbered and the chemical groups added are in bold. Clear therapeutic goals can be set such as reduction in proteinuria, reduction in weakness and muscle enzymes, improved blood counts or lung function studies. The risks and complications of long-term corticosteroid therapy should be discussed with the patient and minimised by attempts to lower the dose or use adjunct immunosuppression to spare steroid usage.
Alternate day therapy may be of use to minimise adverse effects, particularly to allow maximal bone growth in children. Minimising symptoms in chronic inflammatory conditions Classical examples of this are rheumatoid arthritis and polymyalgia rheumatica. The place of steroids in rheumatoid arthritis remains vexed see 'The role of corticosteroids in rheumatology' Aust Prescr ; In these diseases, the aim should be to use the minimum dose required to gain symptomatic relief.
A typical starting dose is Corticosteroids are also used for intra-articular injections of painful joints. Saving lives and saving organs Very high-dose therapy might be indicated for several days in critically ill patients with an aggressive acute presentation or a life- or organ-threatening relapse. Experience with treating organ allograft rejection showed that daily doses of 1 g of intravenous methylprednisolone could be given safely.
The infusion has to be given slowly as it can induce an anaphylactoid reaction. This regimen has been utilised in a variety of other non-transplant situations, often with a lower daily dose of mg or mg for days.
In acute relapses of multiple sclerosis and optic neuritis, a short course of parenteral treatment can significantly shorten the time the patient is symptomatic. In the Optic Neuritis trial 1 , the only benefit was seen in the group given intravenous methylprednisolone. The group given oral prednisone had an increased risk of new episodes of optic neuritis in either eye. In general, oral treatment with prednisone should not be used in multiple sclerosis.
In patients who present with aggressive vasculitis such as Wegener's granulomatosis, polyarteritis nodosa, Good pasture's syndrome and idiopathic rapidly progressive glomerulonephritis, daily pulses of methylprednisolone can be used to try to control the immune injury. In these diseases, corticosteroids should be combined with other immunosuppressive drugs, e. These drugs take days to weeks to work, whilst the corticosteroids will start to have an effect in hours.
For this reason, high-dose corticosteroids are required immediately to control disease and, later, the immunosuppressant allows minimisation of the steroid dosage. In this situation, the risk of disease progression outweighs the risk of the high-dose steroids. Hazards associated with such therapy are reduced resistance to infection, especially bacterial, and relapse of latent infection such as Herpes simplex and zoster , as well as Pneumocystis carinii and Helicobacter pylori.
There is also a risk of acute myocardial ischaemia in pre-disposed patients. Minimising corticosteroid toxicity Toxicity relates to cumulative dose, so all therapy must aim to find the minimum dose which will maintain the desired therapeutic effect.
Adjunctive therapy with a corticosteroid sparing immunosuppressive drug should be considered early rather than after irreversible complications have occurred. Cardiovascular disease Patients should be closely monitored for glucose intolerance and hyperlipidaemia. Dietary restriction to avoid weight gain should begin immediately, together with exercises to minimise muscle weakness.
Blood pressure should be monitored as hypertension may develop because of the mineralocorticoid activity of the drugs. Patients on steroids have accelerated atherosclerosis and all risk factors should be reduced, especially smoking. There is an increased risk of acute vascular events, including myocardial infarction, shortly after starting high-dose steroids.
Relative receptor affinity compared to hydrocortisone for budesonide is over 50x and for fluticasone x. Infection and vaccination Corticosteroids are relatively contraindicated in patients with uncontrolled infection. All patients with a risk of prior exposure to tuberculosis should be assessed. If previous infection is confirmed and they have not received a curative course of antimycobacterial drugs, they should be treated.
Patients on steroids are at increased risk of infection, and symptoms such as fever and pain may be masked by the steroids.
Bacterial infections, such as urinary and respiratory infections, are the most common. Opportunistic infections should also be considered e. Pneumocystis carinii. Immunisation with standard vaccines such as influenza should be undertaken, although the protective effect may be reduced.
Live vaccines, including BCG, measles, rubella and chicken pox are contraindicated. Peritonitis should be considered in patients with minor abdominal symptoms as clinical signs may be masked. Osteoporosis Corticosteroids accelerate bone loss. Screening for osteoporosis and therapies for bone loss prevention should be considered in all patients who require long-term corticosteroids.
Preventative therapy includes calcium, vitamin D and a bisphosphonate, as well as hormone replacement therapy in postmenopausal women. Others Other major adverse effects are aseptic necrosis of bone, psychosis, sleep disturbance, skin fragility and poor wound healing. The eyes should be checked for glaucoma and cataracts.
Hypothalamic-pituitary-adrenal suppression Inhibition of the hypothalamic-pituitary-adrenal axis may lead to adrenal insufficiency when steroids are ceased after long-term use. It requires corticosteroid supplements in episodes of severe acute illness.
Therapy for under 3 weeks or with less than 10 mg of prednis ol one is unlikely to suppress the hypothalamic-pituitary-adrenal axis. This axis will be suppressed in anyone with Cushingoid features. Low early morning cortisol levels, after omitting therapy for 24 hours, suggest suppression. Evening doses of steroids increase the risk of suppression. Alternate day therapy probably does not reduce the risk.
Patients should be advised of the risk of adrenal insufficiency and wear a bracelet indicating their corticosteroid usage. For major illnesses and surgical procedures, a short course of corticosteroids should be started. Stopping corticosteroid therapy In autoimmune disease, clear end-points should be set before starting therapy. Corticosteroids may improve mood and give patients a feeling of general well-being unrelated to the effect on the disease being treated.
Subjective assessments can therefore be misleading. Objective clinical parameters should be used to monitor the need for continuing or restarting therapy e. Therapy should be tapered off. For example, with prednis ol one, the dose is reduced in steps of 2. At that point, switch to alternate day therapy and reduce in 2. This minimises the impact on mood and lessens the drop in general well-being.
Reasonable care is taken to provide accurate information at the time of creation. This information is not intended as a substitute for medical advice and should not be exclusively relied on to manage or diagnose a medical condition. NPS MedicineWise disclaims all liability including for negligence for any loss, damage or injury resulting from reliance on or use of this information. Read our full disclaimer. This website uses cookies.
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