Rheumatoid Arthritis and Ankylosing Spondylitis Treatment

Glucocorticoids (steroids)

steroid therapy for rheumatoid arthritis

Corticosteroids like prednisone, have many drug interactions; examples include: Studies have demonstrated that it can also be carefully combined with methotrexate in patients with no preexisting liver disease, as long as the liver function tests are carefully monitored. Other toxicities that are common include mild diarrhea, GI upset and alopecia and hair thinning sometimes of sufficient severity to cause cessation of the drug. Ruffing has been a member of the Arthritis Center since , currently serving as the Nurse Manager. Biologics More Related Topics. When given by intravenous infusion it is used once per month after initial doses at baseline, 2 weeks, and 4 weeks.

Advertisement

Causes of SI joint pain include osteoarthritis, abnormal walking pattern, and disorders that can cause SI joint inflammation including gout, rheumatoid arthritis, psoriasis, and ankylosing spondylitis. Major side effects include severe rash and effects on renal function. Prednisone and other corticosteroids Weigh the benefits and risks of corticosteroids, such as prednisone, when choosing a medication. Infusion reactions have been seen in clinical trials that are typically mild. Respiratory infections including pneumonia were more common in clinical trials in patients with underlying COPD, thus extreme caution is suggested in this population.

For these people, steroid therapy may eliminate the need for kidney dialysis or transplant. Low doses of steroids may provide significant relief from pain and stiffness for people with conditions including rheumatoid arthritis. Temporary use of higher doses of steroids may help a person recover from a severe flare-up of arthritis.

Injecting steroids into one or two areas of inflammation allows doctors to deliver a high dose of the drug directly to the problem area. When doctors give steroids by mouth or IV, they cannot be sure an adequate amount will eventually reach the problem area. In addition, the risk of side effects is much higher with oral or IV steroids.

Steroids often are injected directly into joints to treat conditions such as rheumatoid arthritis , gout , or other inflammatory diseases. They also can be injected into an inflamed bursa or around tendons near most joints in the body. Some people report relief from osteoarthritis when steroids are injected directly into swollen or painful joints.

Steroid injections into a specific area are generally well tolerated and are less likely than other forms of steroid drugs to produce serious side effects. Also, the injections may help avoid the need for oral steroids or increased doses of oral steroids, which could have greater side effects. Steroid injections can be added to a treatment program that may already include anti-inflammatory pain medications NSAIDs , physical therapy , occupational therapy, or supportive devices such as canes and braces.

Whether one or more of these treatment methods are used depends on the nature of the problem. For example, in an otherwise healthy person, tendinitis may be adequately treated with only a steroid injection into the inflamed area.

However, in a person with rheumatoid arthritis , injections are generally a small part of a multifaceted treatment approach. Steroids should not be injected when there is infection in the area to be targeted or even elsewhere in the body, because they could inhibit the natural infection-fighting immune response. Also, if a joint is already severely destroyed, injections are not likely to provide any benefit. If someone has a potential bleeding problem or is taking anticoagulants often referred to as blood thinners , steroid injections may cause bleeding at the site.

For these people, injections are given with caution. Frequent steroid injections, more often than every three or four months, are not recommended because of an increased risk of weakening tissues in the treated area. Steroid injections are one of the most effective ways to decrease pain and improve function, yet they generally do not cure the illness. Not everyone will develop side effects and side effects vary from person to person. If steroid injections are infrequent less than every three to four months , it is possible that none of the listed side effects will occur.

Side effects are more common with a higher dose and longer treatment. Side effects are much more common with oral drugs. Other effects and adverse events include glaucoma, cataracts, obesity, facial hair growth, moon face, and growth retardation in children. This medicine also causes psychiatric problems, for example: Serious side effects include reactions to diabetes drugs, infections, and necrosis of the hips and joints. Corticosteroids like prednisone, have many drug interactions; examples include: Prednisone is available as tablets of 1, 2.

It's use during the first trimester of pregnancy may cause cleft palate. This medicine is secreted in breast milk and can cause side effects in infants who are nursing. You should not stop taking prednisone abruptly because it can cause withdrawal symptoms and adrenal failure. Talk with your doctor, pharmacist, or other medical professional if you have questions about beta-blockers.

Talk with your doctor, pharmacist, or other medical professional if you have questions about prednisone. If you notice other effects not listed above, contact your doctor or pharmacist. In the US -Call your doctor for medical advice about side effects. In Canada - Call your doctor for medical advice about side effects. You may report side effects to Health Canada at How are steroids given? How do steroids work?

What conditions are treated with steroids? What are the benefits of steroids? Why are steroids injected? What conditions including arthritis are treated with steroid injections? What are the expected benefits of steroid injections? What role do steroid injections play in an overall treatment program? When should steroid injections not be used?

What are the side effects of steroid injections? What are the possible side effects of oral steroids? Does everyone develop side effects to steroids? How can steroid side effects be minimized?

Who should not take steroids? How do I know if steroid treatment is right for me? Agency for Healthcare Research and Quality: A Guide for Adults. Related Article Rheumatoid Arthritis Quiz: Patient Comments Steroids to Treat Arthritis - Experience Please share your experience with taking steroids to treat arthritis. Post Steroids to Treat Arthritis - Side Effects What side effects did you experience due to steroid treatment of arthritis? When joints are inflamed they can develop stiffness, warmth, swelling, redness and pain.

There are over types of arthritis, including osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, lupus, gout, and pseudogout.

Cortisone injections are used to treat small areas of inflammation or widespread inflammation throughout the body. There is minimal pain from these injections, and relief from the pain of inflammation occurs rapidly. Buildup of uric acid crystals in a joint causes gouty arthritis. Symptoms and signs include joint pain, swelling, heat, and redness, typically of a single joint. Gout may be treated with diet and lifestyle changes, as well as medication.

Methylprednisolone Medrol, Depo-Medrol, Solu-Medrol is a medication prescribed to patients to suppress inflammation from a variety of conditions and diseases. Side effects, drug interactions, dosage, and pregnancy safety information should be reviewed prior to taking this medication.

Osteoarthritis is a type of arthritis that is caused by the breakdown and eventual loss of the cartilage of one or more joints. See a picture of Osteoarthritis and learn more about the health topic. Rheumatoid arthritis RA is an autoimmune disease that causes chronic inflammation of the joints, the tissue around the joints, as well as other organs in the body. Because it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease.

Sacroiliac joint SI dysfunction is a general term to reflect pain in the SI joints. Causes of SI joint pain include osteoarthritis, abnormal walking pattern, and disorders that can cause SI joint inflammation including gout, rheumatoid arthritis, psoriasis, and ankylosing spondylitis. Treatment includes oral medications, cortisone injections, and surgery. Medications are also available to treat dry eye and dry mouth. Systemic lupus erythematosus is a condition characterized by chronic inflammation of body tissues caused by autoimmune disease.

Lupus can cause disease of the skin, heart, lungs, kidneys, joints, and nervous system. When only the skin is involved, the condition is called discoid lupus.

When internal organs are involved, the condition is called systemic lupus erythematosus SLE. Vasculitis arteritis, angiitis is a general term for a group of uncommon diseases which feature inflammation of the blood vessels.

Each form of vasculitis has its own characteristic pattern of symptoms. The new onset of psoriasis has also been seen. Abatacept is the first of a class of agents known as T-cell costimulatory blockers. T lymphocytes become activated due to an unknown stimulus but likely involving the interaction between antigen presented in the context of the Class II Major Histocompatability Complex molecule on the surface of antigen presenting cells.

T cells recognize antigens as foreign and if they receive a second stimulus, will become active, proliferate, traffic to inflamed sites, and secrete proinflammatory cytokines including TNF.

One of the important second signals for T cell activation is mediated by the molecules CD80 and CD86 found on antigen presenting cells and the CD28 molecule on the T cell surface. When abatacept binds to CD28 on the T cell surface, it prevents the second signal from being delivered, thus turning down the T cell response. Additional effects are decreasing the production of T cell derived cytokines including TNF. Abatacept is administered either via IV or subcutaneously. When given by intravenous infusion it is used once per month after initial doses at baseline, 2 weeks, and 4 weeks.

The medication is administered over a period of approximately 30 minutes to one hour. Responses are typically seen within 3 months. In clinical trials, patients with initial responses continued to show improvements through the first year. These have ranged from mild to severe. Respiratory infections including pneumonia were more common in clinical trials in patients with underlying COPD, thus extreme caution is suggested in this population.

Opportunistic infections have been seen, though only a few cases of TB have been seen to date. TB screening is recommended. Malignancies have been seen in clinical trials but the rates appear to be similar for those expected in patients with rheumatoid arthritis. Infusion reactions have been seen in clinical trials that are typically mild. B cells are an important inflammatory cell with multiple functions in the immune response.

They serve as antigen presenting cells, directly interact with T-cells and others, can secrete cytokines, and differentiate into antibody-forming plasma cells.

The depletion of B cells has been shown to be effective in reducing signs and symptoms of RA and in slowing radiographic progression. One B cell depleting agent, Rituximab, is currently available for the treatment of rheumatoid arthritis.

Ritxuimab causes a rapid and sustained depletion of circulating B cells in the circulation with clinical improvements in many patients. Clinical trials have demonstrated that Rituximab is effective in decreasing signs and symptoms and in slowing radiographic progression in RA patients who have failed other DMARD therapies.

The agent is currently approved in the US, however, only in patients who have failed TNF antagonists. Rituximab is a chimeric monoclonal antibody that binds to the CD20 molecule on the B cell surface leading to the removal of B cells from the circulation. A single course of ritximab 2 infusions of mg each given 2 weeks apart leads to a rapid and sustained depletion of B lymphocytes in the peripheral blood.

This effect is sustained for 6 months to 1 year or even longer. The levels of the autoantibody rheumatoid factor decrease, but the levels of other antibodies typically remain within the normal range after the first infusion, but may drop with subsequent courses. Effects from rituximab are not seen for up to 3 months after an infusion. Effects however may last 6 months and up to 2 years following a single infusion course.

The currently approved dose is mg administered intravenously over hours with two doses given 2 weeks apart. Patients receive intravenous corticosteroids 30 minutes prior to each infusion. The optimal time for readministration is not yet clear.

Doses of mg have also been studied and appear to have similar clinical efficacy in patients who have failed to respond to DMARDS. Infusion reactions are seen in patients who receive Rituximab infusions.

These may include hives, itching, swelling, difficualty breathing, fever, chills, and changes in blood pressure. These are usually mild and respond to slowing the infusion rate or additional medication such as antihistamines but may be severe. These are reactions were the most common with the first infusion. As with other immunomodulatory therapies, infections may be increased in patients who are receiving rituximab. Rituximab may lead to the reactivation of viral infections that were dormant including hepatitis B.

Cases of progressive multifocal leukoencephalopathy PML , a severe and potentially fatal brain infection, have been seen in patients with autoimmune disease who receive rituximab though this condition has also been seen in patients with autoimmune diseases who are not administered rituximab. Immunizations should be completed before starting therapy with rituximab and live virus vaccinations avoided.

Repeat administration of rituximab has been associated with decreases in levels of IgG and IgM antibodies with subsequent courese. Whether these decreases are clinically important is under study. Tocilizumab is the first approved drug in a class of IL-6 inhibitors. Clinical studies have shown that tocilizumab is effective in decreasing signs and symptoms and in slowing radiographic progression in RA patients who have failed other DMARD therapies.

Tocilizumab binds specifically to both soluble and membrane-bound IL-6 receptors and has been shown to inhibit ILmediated signaling through these receptors. IL-6 is a pleiotropic pro-inflammatory cytokine produced by a variety of cell types including T- and B-cells, lymphocytes, monocytes and fibroblasts.

IL-6 has been shown to be involved in diverse physiological processes such as T-cell activation, induction of immunoglobulin secretion, initiation of hepatic acute phase protein synthesis, and stimulation of hematopoietic precursor cell proliferation and differentiation.

IL-6 is also produced by synovial and endothelial cells leading to local production of IL-6 in joints affected by inflammatory processes such as rheumatoid arthritis. As with other biological DMARDs, an increase risk of infection and serious infection is present with tocilizumab. Because of a risk of GI perforation, patients with a history of diverticulitis should not receive tocilizumab. Monitoring for any of these side effects should be considered every 4 to 8 weeks while on therapy.

IL-1 is another proinflammatory cytokine implicated in the pathogenesis of RA. IL-1 receptor antagonist IL1ra is an endogenous blocker of the cytokine. Evidence supporting an anti-inflammatory role of IL-1ra in vivo is demonstrated by the observation that IL-1ra deficient mice spontaneously develop autoimmune diseases similar to rheumatoid arthritis as well as vasculitis. IL1 has effects on cartilage degradation leading to damage as well as inhibiting repair, and is a potent stimulus to osteoclasts leading to bone erosion.

Other agents have been studied as well in RA. The dose should be administered at approximately the same time each day. An autoinjection system is available for the medication.

The most commonly observed side effect in all of the clinical trials with anakinra is injection site reactions, occurring in approximately two-thirds of patients. These reactions are present as erythema, itching, and discomfort and typically resolve over one to two months. In some patients these reactions can be severe leading to drug discontinuation. Opportunistic infections including tuberculosis are less common with anakinra than with TNF antagonists.

Mild to moderate decreases in absolute neutrophil counts were seen more commonly in anakinra treated patients in clinical trials, some severe. The rate of malignancies reported for anakinra was not increased relative to expected rates in the general population. Patients receiving infused biological agents including may develop a clinical syndrome of fever, chills, body aches, and headache associated with the infusion of biologics.

The symptoms can often be reduced or prevented by slowing the infusion rate, administration of diphenhydramine, acetaminophen, and sometimes corticosteroids before the infusion. Injection site reactions may be seen with injectable biologics. These are typically mild and generally do not result in drug discontinuation. Because the potential of high toxicity, these agents are typically utilized for life-threatening extra-articular manifestations of RA such as systemic vasculitis or with severe articular disease that is refractory to other therapy.

It is a purine analog that can cause bone marrow suppression and lowering of blood cell counts white blood cells, red blood cells, and platelets particularly in patients with renal insufficiency or when used concomitantly with allopurinol or ACE inhibitors. Increased risk of secondary malignancy due to azathioprine is controversial.

Screening for levels of the enzyme thiopurine methyltransferase TPMT is recommended before initiating therapy with azathioprine. Certain individuals have deficiencies in this enzyme that metabolizes azathioprine with a concomitantly increased risk of toxicitiy for the medication. Side effects include nausea, and alopecia.

Blood tests to monitor blood counts and liver function tests are necessary for patients on azathioprine. Studies have demonstrated that cyclosporine can be combined with methotrexate in RA patients to capture clinical responses. It is an immunosuppressive agent approved for use in preventing renal and liver transplant rejection and also has activity in psoriasis and other autoimmune diseases. Cyclosporine inhibits T cell function by inhibiting transcription of interleukin Main toxicities include infection and renal insufficiency.

Increase in blood pressure is common and may require treatment. Careful monitoring of renal function and blood pressure is needed for the entire time a patient is taking cyclosporine.

Numerous medication interactions may affect blood levels of cyclosporine and lead to more toxicity. The package insert contains important information concerning these medication interactions. Cyclosporine increases risks of infection and may also increase the risk of malignancies including lymphoma.

It is used in the treatment of other autoimmune conditions including lupus and vasculitis. Cyclophosphamide is an alkylating agent with serious toxicities including bone marrow suppression, hemorrhagic cystitis, premature ovarian failure, infection and secondary malignancy particularly an increased risk of bladder cancer.

Blood counts must be carefully monitored with this medication. Like gold it is a relatively toxic drug that has limited utility due to issues of tolerability and efficacy that is not as robust as other currently available agents. Major side effects include severe rash and effects on renal function. Careful monitoring of kidney function is required with this drug.

Patients may develop a lupus like illness or other autoimmune diseases when taking d-Penicillamine. Gold is effective in the treatment of rheumatoid arthritis when it is given intramuscularly. Gold compounds are rarely used now due to their numerous side effects and monitoring requirments, their limited efficacy, and very slow onset of action. A number of mechanisms have been postulated, but how gold works in patients with rheumatoid arthritis remains unknown. Myochrysine or Solganal therapy is started at 10 mg intramuscularly, 25mg is then given the second week, then 50mg is given weekly until a response has occurred or until a total of 1 g has been given.

If there is a favorable response, therapy is tapered to 50mg every 2 weeks for 3 months, then every 3 weeks for 3 months and then finally to a maintenance monthly dose. No response after a total of 1g should be considered a treatment failure. Monthly gold should be continued indefinitely. Prior to each gold injection, patients should have a complete blood count and urine test for protein. The most common reaction is a rash, which can vary from a simple pruritic erythematous patch to a severe exfoliative dermatitis.

Ulcerations and mucositis of the mouth, tongue, and pharynx can occur. If a mild mucocutaneous eruption occurs, therapy should be interrupted. If the eruption abates, therapy can be restarted at a mg weekly, titrating upwards to 50mg weekly with careful monitoring for further rash.

Iamges: steroid therapy for rheumatoid arthritis

steroid therapy for rheumatoid arthritis

Sulfasalazine is also used in the treatment of inflammatory bowel disease and spondyloarthropathies. Rituximab may lead to the reactivation of viral infections that were dormant including hepatitis B. Whether these decreases are clinically important is under study.

steroid therapy for rheumatoid arthritis

These medicines can be taken by mouth orally. Related Article Rheumatoid Arthritis Quiz: Pain and joint mobility may be improved by a surgical approach.

steroid therapy for rheumatoid arthritis

Guide to Understanding Cancer. Acne Blurred vision Cataracts or glaucoma Easy bruising Difficulty sleeping High blood pressure Increased appetite, weight gain Increased growth of body steroid therapy for rheumatoid arthritis Insomnia Lower resistance to infection Muscle weakness Nervousness, restlessness Osteoporosis Stomach irritation or bleeding Sudden mood swings Swollen, puffy face Water retention, swelling Worsening of diabetes Please note: It may take 6 weeks to 3 months to see the effects of sulfasalazine. TNF is one of the critical cytokines that mediate joint damage and destruction due to its activities on many cells in the joint as well as effects on other organs and body systems. However, rheumtoid with all drugs some people will have side-effects. How dbol gh side effects I know if rhumatoid treatment is steroid therapy for rheumatoid arthritis for me?