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Sock's Rheumatoid Arthritis Links - RA

Management RA
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Some people have RA for only a few months, or a year or two. Then it goes away without causing damage. Other people have times when the symptoms get worse (flares), and times when they get better (remissions). Others have a severe form of the disease that can last for many years or a lifetime. This form of the disease can cause serious joint damage and also may have extra-articular features (EAFs) involvement

The damage to the joints caused by RA is thought to be caused by the interaction of many inflammatory cells and chemicals. Cytokines,like tumour necrosis factor,IL-ra alpha etc., are secreated by synovial fibroblasts and other cells resulting in pain,and inflammation TNF may also be responsible for influencing other inflammatory compounds including interleukins (IL-1), collagenase,and prostaglandins

Complete remission is defined as the absence of :
1) symptoms of active inflammatory joint pain (in contrast to mechanical joint pain).
2) morning stiffness.
3) fatigue.
4) synovitis on joint examination.
5) progression of radiographic damage on sequential radiographs.
6) elevated erthrocyte sedimintation rate or (ESR),or C-reactive protein (CRP) level.
If complete remission is not achieved,the management goals are to control disease activity,alleviate pain,maintain function for essential activities of daily living,and work,maximize quality of life,and slow the rate of joint damage.

Typical symptoms: *Pain,swelling,limited motion,warmth,and tightness around involved joints,most commonly,including the hands,and wrists,feet and ankles, elbows,shoulders, neck, knees,and hips,usually in a symmetric pattern, over time,joints may form deformities.
*Generalized fatigue,soreness,stiffness,and aching,particularily in the early morning,and afternoon (described as morning stiffness,and afternoon fatigue).
*Lumps or rheumatoid nodules below the skin (moderate-severe RA)
*Weight loss.
*Low grade fever,and sweats.
*Sleep difficulties.
*Weakness,and loss of mobility.
*Depression (may worsen existing disease or provoke it as a new problem).

Rheumatoid arthritis is an autoimmune disorder of unknown etilogy characterized by symmetric,erosive synovitis and in some cases,extraarticular involvement. The utimate goals in managing RA are to prevent or control joint damage,prevent loss of function,and decrease pain. The initial steps in the management of RA are to establish the diagnosis,perform a baseline evaluation,and estimate the prognosis. A rheumatology consultation and principal direction is a preference.
RA affects 1% of the adult population. This low prevalence means that the average physician often develop little experience with its diagnosis or management. Disability from RA  causes major economic loss and can have a major impact on families.
Treatment begins with educating the patient about the disease and the risks and benefits of existing treatment modalities. Patients will benefit from consultation with,physical therapists,occupational therapists and social workers should the need arise. Nonsteriodal antiinflammatory drugs (NSAIDs),glucorticoid are used for control of symptoms. The majority of patients,with newly diagnosed RA should be started on disease-modifying antirheumatic drugs (DMARDs) therapy within 3 months of diagnosis.
Since DMARDs control,rather then cure RA,the management of RA is an on-going process,and patients should be periodically reassessed for evidence of disease or limitation of function with significant alteration of joint anatomy.
Reconstructive surgery can be done at any point in the course of RA to restore or improve quality of life and relieve pain when other therapy fails. Some patients have resistant disease and experience a progressive course despite exhaustive trials of DMARDs,whether used alone or in combination.
While the utimate goal  is to induce remission,this occurs infrequently. Complete remission is defined as the absence of the following: 1)symptoms of active inflammatory joint pain (in contrast to mechanical joint pain),2)morning stiffness,3)fatigue,4)synovits on joint examination,5)progression of radiographic damage on sequential radiographs,and 6)elevation of the erthrocyte sedimentation rate (ESR) or C-reactive protein (CRP) levels.
If complete remission is not achieved,the management goals are to control disease activity,alleviate pain,maintain function of activities of daily living and work,and maximize quality of life. Achieving these goals challenges the management skills of the rheumatologist to determine the most efficacious combination of pharmacologic therapy,which may include NSAID,DMARD(s),low-dose predisone,local injection of glucocorticoid,rehabilitation support, and analgesics. Although adequate pain relief is an important goal with a chronic disease like RA,every effort should be made to avoid narcotic analgesic dependency.
Given the chronic waxing and waning course of RA,a longitudinal treatment plan needs to be developed,and the patient should be involved in developing the plan. The discussion should should address disease prognosis and treatment options,taking into account the costs,adverse effects,expected time for response,the patient's risk factors and comorbid conditions,monitoring requirements of pharmacologic agents and patient preferences.
 Expectations for treatment and potential barriers for carrying out the recommended plan should be discussed.Psychosocial factors,such as illness beliefs and perceived self-efficacy,have been shown to affect patient outcomes. Programs such as the Arthritis Self-management are available as a guide.
The initial evaluation of the patient with RA should document symptoms of active disease (i.e.,presence of joint pain,duration of morning stiffness,degree of fatigue),functional status,objective evidence of disease activity (i.e., synovitis,as assessed by tender and swollen joint count,and the ESR or CRP level),mechanical joint problems (i.e.,loss of motion, erepitus, instability, malignment,and or deformity),the presence of extraarticular disease,and the presence of radiographic damage.
The presence of comorbid conditions should be also assessed. The patient's  and physicians's global assessment of disease activity and a quantitative assessment of pain using a visual analog scale or other validated measure of function or quality of life are useful parameters to follow during the course of the disease. This baseline information greatly facilitates assessment of disease progression and response to treatment.
Baseline laboratory evaluations should include a complete blood cell count (with white blood cell differential and platelet counts),rheumatoid factor (RF) measurement,and measurement of ESR or CRP. Evaluation of renal and hepatic function is necessary,since many antirheumatic agents cause renal or hepatic toxicity and may be contraindicated if these organs are impaired (Bun test is useful for kidney test).
Since the hands and feet are so frequently involved in RA,radiographs of these joints as well as other affected joints establish a baseline for future assessment of structural damage. Arresting and preventing structural damage is a primary goal of therapy,and radiographic studies of major involved joints may be needed periodically.
Selection of the treatment regimen requires an assessment of prognosis. Poor prognosis is SUGGESTED by earlier age (not always) at disease onset,higher titer of RF,elevated ESR,and swelling of >20 joints. Extraarticular manife stations of RA,such as rheumatoid nodules,Sjogren's syndrome,episcleritis and scleritis (eye),intestinal lung disease,pericardial involvement (heart),systemic vasculitis (blood),and Felty's syndrome,may also indicate a worse prognosis.
The ACR criteria for 20% clinical improvement (the ACR 20) require a 20% improvement in the tender and swollen joint count,as well as a 20% improvement in 3 of the following 5 parameters: patient's global assessment, physician's global assessment of pain,degree of disability,and level of acute-phase reaciant.
These criterias have been expanded to include criteria for 50% and 70% improvement measures (i.e.,ACR 50,ACR 70). Other criteria,such as the Paulus criteria have also been employed. More recently,radiographic progression (e.g.,the Sharp score) has been utilized as a out come measure.
Optimal management of RA involves more than pharmacologic therapy. Early in the course of the disease patients with polyarticular,RF positive have a >70% probability of developing joint damage or erosion within 2 years of the onset of disease. (Recent studies with magnetic resonance imaging have detected erosions occuring as early as 3 months that was not detected by ordinary radiographic studies).
Since studies have demonstrated that treatment with DMARDs may alter the disease course in patients with recent-onset RA,particularily those with unfavorable prognostic factors,aggressive treatment should be initiated as soon as the diagnosis is established.
At each follow-up visit,the physician must access whether the disease is active or inactive. Symptoms of inflammatory (as contrasted with mechanical) joint disease,which include prolonged morning stiffness,duration of fatigue,and active snovitis on joint examination,indicate active disease and accessitate consideration of changing the treatment program.
Occassionally,findings of the joint examination alone may not adequately reflect disease activity and structural damage;therefore,periodic measurement of ESR or CRP level and functional status,as well as radiographic examinations of involved joints should be performed. Functional status such as the Arthritis Impact Measurement Scales or the Health Assessment Questionnaire.  It is important to determine whether a decline in function is the result of inflammation,mechanical damage,or both,treatment strategies will differ accordingly.
The American College of Rheumatology (ACR) has developed criterias for defining improvement and clinical remission in RA. These criterias have become accepted for outcome assessment in clinical practise. The patient will need to become involved in the process of making decisions about treatment.
If treatment doesn not fully control the disease,the patient may struggle emotionally as well as physically in adjusting to the chronic disease,its flares and the concomitant loss of function. Rheumatologist,other physicians and their staff pay important roles in educating the patient and the patient's family about the disease and providing longitudinal supportive care.
Other health professionals FAMILIAR with RA,including nurses,physical therapists,occupational therapists health educators,health psychologists,and orthopedic surgeons may also be involved in an interdisciplinary team approach in the overall care.
Instruction in joint protection,conservation of energy,and a home program of joint range of motion and strengthening exercises are important in achieving the treatment goal of maintaining joint function. Physical and occupational therapy may help help the patient who is comprimised in activities of daily living.
Regular participation in dynamic and even (light) aerobic conditioning exercise  programs improves joint mobility,muscle strength,aerobic fitness and function and psychological well being,without increasing fatigue,or joint symptoms.
Pharmacologic therapy for RA often consists of combinations of NSAIDs, DMARDs,and/or glucocorticoids. The dosing schedules,efficacy and toxicity of these medications are important part of therapy and  the patient must be knowledgeable  in the management and treatment of RA. Know when therapy is working and when it is not.

Every drug,every medication has its own set of possible side effects,its own set of issues,and expectations on it's suitabilility and effiacy to the individual patient's needs. It may take time,it doesn't mean you have to suffer pain during the time lag that is required to determine it's effectiveness. That's were perhaps,steriods like Predisone come into play.
The initial drug treatment of RA usually involves the use of salicylates. NSAIDs,or selective cyclooxygenase 2 (COX-2) inhibitor to reduce joint pain and swelling and to improve joint function. These agents have analgesic and antiinflammatory properties. These agents have analgesic and antiinflammatory properties but do not alter the course of the disease or prevent joint destruction. Thus,they should not be used as the sole treatment of RA
Choice of available agents is based on considerations of efficacy, safety, convenience,and cost. Some salicylates and all available nonsalicylate NSAIDs inhibit the production of prostaglandins by inhibiting one or both of the cycloogenase enzyme isoforms,COX-1 and COX-2,COX-1 is produced constitutively and is present in many cells,including platelets,cells of the gastric and intestinal mucosa,and endothelial cells. Production of COX-2 can be increased many times over,particularily by cells at sites of inflammation.
Data suggest that although selective COX-2 inhibitors have a significantly lower risk of serious adverse gastrointestinal (GI) effects than do nonselective NSAIDs, they are no more effective than nonselective NSAIDs,and may cost as much as 15-20 times per month of treatment than generic NSAIDs.
Patients with RA are nearly twice as likely as patients with osteoarthritis to have a serious complication from NSAID treatment. Risk factors for the development of NSAID-associated gastroduodenal ulcers include advanced age,history of ulcer,concomitant use of corticosteriods or anticoagulants,higher dosage of NSAID,use of mutiple NSAIDs,or a serious underlying disease.
Advanced age is defined as 75 years or older. The following approaches may be considered for patients with RA who would benefit from an NSAID but who are at risk of serious adverse GI effects; use of low-dose predisone instead of an NSAID,use of which is effective in decreasing NSAID-associated gastroduodenal ulceration,include high-dose H2 blockers,proton-pump inhibitors,and oral prostaglandin analogs.
While symptoms of dyspepsia are often improved with H2 blockers,one study showed that asymptomatic patients with RA who were both receiving both NSAIDs and low-dose H2 blockers were at higher risk of GI complications than those receiving NSAIDs alone. Therefore,routine use of h2 blockers to prevent dyspepsia or to protect against NSAID-induced gastropathy is not recommended.
In two recent large trials comparing highly selective COX-2 agents with traditional NSAIDs,the patients in the selective COX-2 agent group had significantly fewer GI events. There are several caveats,however. If antiplatelet therapy is indicated (e.g.,as risk reduction for cardiovascular disease),an agent such as a nonacetylated salicylate,use of a highly selective COX-2 inhibitor,or use of a combination of an NSAID and a gastroprotective agent.
Gastroprotective agents,low-dose aspirin should be used because unlike nonselective NSAIDs,he selective COX-2 inhibitors have no effect on platelet adhesion or aggregation. The addition of low-dose aspirin may partially ameliorate the benefit of less GI toxicity with highly selective COX-2 agents.
Moreover,the use of a highly selective COX-2 agent has been reported to be associated with a higher rate of thrombotic events (including more myocardial infarctions) compared with traditional NSAIDs. Use of NSAIDs and selective COX-2 inhibitors should be avoided in conditions associated with diminished intravascular volume of edema,such as congestive heart failure,nephrotic syndrome,or cirrhosis,and in patients with serum creatinine levels  <2.5mg/dl.
All patients with RA are candidates for DMARD therapy. Although NSAIDs and glucocorticoids may alleviate symptoms,joint damage may continue to occur and to progress. DMARDs have the potential to reduce or prevent joint damage,preserve joint integrity and function,and utimately,reduce the total costs of health care and maintain economic productivity of the patient with RA.
 The initiation of DMARD therapy should not be delayed beyond 3 months for any patient with an established diagnosis,who,despite adequate treatment with NSAIDs,has ongoing joint pain,significant morning stiffness or fatigue,active synovitis,persistent elevation of the ESR or CRP level,or radiographic joint damage,DMARD treatment should be started promptly to prevent or slow further damage.
The DMARDs commonly used in RA include hydroxychloroquine (HCQ), sulfasalazine (SSZ),methotrexate (MTX), leflunomide, etanercept ,anakinra (Il-1 inhibitor),humira and infliximab. Those used less infrequently include azathioprine (AZA),D-penicillame (D-Pen),gold salts,minocycline and cyclosporine. Many studies have demonstrated the benefit of DMARD therapy in RA. The outcome of these trials include control of the signs and symptoms of joint involvement,changes in functional status and quality of life,retardation of radiographic evedince of erosions.
Treatment considerations include costs of the medication and monitoring (including physician visits,and laboratory costs) time until expected benefit and its frequency and potential seriousness of adverse reactions. The physician should also access patient factors,such as likelihood of compliance,comorbid diseases,severity and prognosis of the patient's disease,and the confidence of the physician's own training and familiarity in administeration and monitoring of the drug.
 Because of these many considerations the services of a rheumatologist is often essential component of the overall management plan when initiating DMARD therapy.
For women of childbearing age,effective contraception is required when most DMARDs are prescribed. The drug regimen will need to be modified if pregnancy or breastfeeding is contemplated.
Based on consideration of safety convience and cost,many rheumatologists select HCQ or SSZ first,but for the patient with very active disease or with indicators of prognosis,MTX or combination therapy would be preferred.
If a patient with RA  has not achieved remission or a satisfactory response to the initial trial of DMARD(s),and if a rheumatologist has not been involved in the patient's care,a rheumatology consultation should be obtained. MTX as monotherapy or as a component of combination therapy should be instituted in patients whose treatment has not yet included MTX .
For patients in whom MTX is contraindicated or have failed to achieve satisfactory disease control either because of lack of efficacy (in doses up to 25mg/wk) or intolerance,treatment with bilogic agents or with other DMARDs, either alone or in combination is indicated.
In the last decade,a number of studies have documented the symptomatic benefit of HCQ and SSZ,particularily for patients with early,milder disease. Although HCQ alone does not  slow radiographic damage,early treatment with HCQ has a significant impact on long-term patient outcome. Rash,abdominal cramps and diarrhea are common side effects.
HCQ is generally well tolerated and requires no routine laboratory  monitoring,although patients need periodic opthalmologic examinations for early detection of reversible retinal toxicity. The risk of retinal toxicity is increased when the dose exceeds 6mg/kg. The length of time to benefit may vary from 1 month to as long as 6 months.
SSZ may act more quickly than HCQ,with benefit sometimes as early as 1 month after beginning therapy. More importantly,SSZ has shown in clinical trials  to retard radiographic progression of RA. SSZ is usually ,well  tolerated,with most side effects,which include nausea,mouth sores,and abdominal discomfort,occurring in the first few months of therapy.
The incidence of these side effects is lessened by starting at a low dosage and then gradually increasing the dosage. Leukopenia is an occasional,more serious side effect that may occur at any time,and periodic laboratory monitoring is therefore necessary. Clinical response should be apparent within 4 months,and the need for a change in therapy may be determined at that time
A trial was conducted which consisted of HCQ,and SSZ without increased toxicity (double-DMARD theapy). In another study the efficacy of a 3 DMARD combination without the occurence of additional toxicity was confirmed in a randomized trial. In this latter trial,patients with early disease were studied and the treatment regimen included low-dose predisone in a subset of patients.
O'Dell and associates demonstrated the triple DMARD combination of MTX, SSZ and HCQ has been shown to be superior ro the double-DMARD combinations of MTX plus SSZ or MTX plus HCQ in both early and advanced RA,without a increase of toxicity.
The combinations of infliximab,etanercept or lefluenomide wit MTX have all been studied in patients who had a partial response to MTX,and the combinations were found to be beneficial. The use of combination therapy continues to evolve.
Many rheumatologists select MTX as the initial DMARD,especially for those patients whose RA is more active. Because of its favourable efficacy and toxicity profile,low cost,and established tract record in the treatment of RA,MTX has become the standard by which new DMARDs are evaluated.
Randomized clinical trials have established the efficacy of MTX in RA, particularily in those patients with more severe disease. Longitudinal observational studies,and randomized controlled trials shows that MTX retards the progression of radiographic erosions.
Observational studies indicate that more than 50% of patients who take MTX continue the drug beyond 3 years which is longer than any other DMARD. RA patients taking MTX are more likely to discontinue treatment because of adverse reactions than because of lack of efficacy.
Stomatitis,nausea,diaarhea,and perhaps,alopecia caused by MTX may decrease the concomitant folic acid or folinic acid treatment without significant loss of efficacy. Relative contraindictions for MTX therapy are preexisting liver disease,renal impairement,significant lung disease,or alcohol abuse.
Since the most frequent adverse reaction to MTX is elevation of liver enzyme levels their function must be monitored but the risk of liver toxicities is low, based on clinical trials.  In the ACR guidlines for monitoring liver toxicity in patients receiving MTX,a liver biopsy should be performed on patients who develop abnormal findings on liver function tests that persist during treatment or after discontinuation of the drug.
Rare but potentially serious pulmonary toxicity may occur at any time with any dosage of MTX. Lymphoproliferative disorders may rarely occur in patients taking MTX,but the relatioship is unclear,some of these cases have regressed or resolved with discontinuation of MTX. Since MTX is potentially teratogenic appropriate contraceptive measures during MTX treatment are recommended.
Clinical trials have established leflunomide as an alternative to MTX as monotherapy,especially for patients who cannot tolerate MTX or are experiencing an inadequate respose to MTX. The reduction in RA disease activity and in the rate of radiographic progression achieved by leflunomide appears to be equivalent to a modest dose of MTX  Leflunomide is also beneficial in combination therapy with MTX,in the absence of a complete clinical respose with full doses of MTX.
Five percent of patients receiving leflunomide and up to 60% of patients taking MTX receiving MTX and leflunomide have elevated liver enzyme levels. Since enterohepatic recirculation play a large role in leflunomide metabolism, leflunomide has a long half-life. Without the recommended washout protocol with cholestyramine resin,elimination of the drug could take as lon as 2 years.
Leflunomide is a potent teratogen and women taking leflunomide and undergo cholestyramine washout before attempting conception. Obstructive biliary disease,liver disease,biral hepatitis,severe immunodeficiency,inadequate birth control,and rifampin therapy (which raises leflunomide serum levels) are all contradictions to the use of leflunomide.
Recently,randomized double-blind,placebo-controlled trials have demonstrated the efficacy of minocycline in improving the clinical parameters of RA. Importantly,one trial showed showed long-term benefit of minocycline ana decrease in radiographic progress ion in a subset of patients who were positive for the HLA shared epitope (HLA-DR4+) Early mild RA patients.
According to the ACR,further research is necessary to define the exact role of tetracyclines in the treatment of RA. Dermatologists have used it on teen-agers for acne treatment. A report came out recently,that a patient had been treated with the medication for acne and developed Lupus-like-symptoms,and warnings against using this medication for skin problems.
Cyclosporine is beneficial as monotherapy and has short-term efficacy similar to that of D-Pen. The use of cyclosporine,however,has been limited by its toxicity,especially hypertension and dose-related loss of renal function The 20% loss of renal function appears to be dose-related,reversible,but not entirely with discontinuation. Dose calculation to avoid renal toxicity is more critical with cyclosporine than any other DMARD.
Many medications may increase cyclosporine levels and thus increase the risk of nephro-toxicity. Therfore cyclosporine treatment is primarily confined to patients with refractory RA. Cyclosporine plus MTX was found to be more effective than MTX alone,but long-term followup revealed the development of hypertension and elevated creatinine levels.
AZA,a purine analog myelosuppresant,has demonstrated benefits in controlling RA,but is rarely used. D-Pen is effective,but its use is limited,in part,by an incosistent dosing schedule and high level of adverse events.
Prosoba column (recirculate- clean -blood) was reported to be efficacious in a portion of patient with severe refractory RA. Given the difficulty and cost of administeration -weekly treatments for 12 weeks,the limited duration of the response,and the high frequency of side effects,this treatment should be considered only,for patients with refractory RA,where other treatments has failed.
Convential treatment with a single DMARD often fails to adequately control clinical symptoms or to prevent disease progression. As a result rheumatologists are increasingly prescribing combination DMARD therapy.
Controversy remains about whether to initiate this type of treatment in a sequential "step-up" approach in patients with persistently active disease in whom single agents have failed or whether to initiate combination therapy early in the disease course and then apply a "step-down" approach once adequate disease control is attained. In either case,rheumatogology referral is needed for patients being considered for initiation of combination therapy.
The development of genetically engineered biologic agents that selectively block cytokines (anticytokine therapy) in the short term represents a major advance in the treatment of RA. The most clinically effective anticytokine agents studied to date are antagonists to TNF-alpha,an essential mediator of the cytokine inflammatory cascade in RA.
Three anti-TNF alpha agents are available in the U.S.,etanercept,a recombiant soluable TNF-Fe fusion protein;infliximab,a chimeric (mouse-human) anti-TNF monoclonal antibody;Humira (wholly human) has recently been approved by the FDA for Treatment of RA patients.
Randomized trials have demonstrated that patients treated with etanercept alone or with infliximab plus MTX have less radiographic progression after 1  year than patients treated with MTX alone. In the trial of patients with early RA,the symptoms and signs of RA improved more rapidly with etanercept treatment than with MTX treatment over the first 6 months,with comparable efficacy of the two agents at 12 months.
Those trials have demonstrated the efficacy of etanercept and infliximab in improving clinical symptoms and signs in patients with RA,according to the ACR20,ACR50,and ACR70 improvement criterias. Patients with early RA and those with active RA in whom previous DMARD therapy have failed showed improvement with etanercept therapy. both etanercept and infliximab have been shown to beneficial when used in combination with MTX in patients with ongoing active RA despite adequate doses of MTX alone.
Infliximab is currently recommended for use only with concomitant MTX therapy. In the trials of etanercept and infliximab,many patients improved rapidly.even during the early 2 weeks.
Although data from randomized trials have not shown an increased frequency of adverse effects such as serious infections or malignancies for either anti-TNF agents,concerns about the long-term safety of these agents coninue. TNF-alpha plays an important role in host production against infection and tumour genesis.
 Postmarketing experience with etanercept and infliximab shows deaths and hospitalizations from serious infections in patients treated with these agents. Most of the few patients who died while being treated with TNF-alpha had significant chronic infections or risk factors for infections.
Anti-TNF-alpha agents should therefore be used with caution in patients with any susceptibility to infection or a history of tuberculosis,should be avoided in patients with significant chronic infections,and should be discontinued temporarily in all patients with acute infection.
Postmarketing surveillance has yielded reports of septis,tuberculosis,atypical mycibacterial infections,fungal infections,other opportunistic infections, demyelinating disorders,and aplastic anemia. Risk of latent tuberculosis should be assessed prior to initiation of a TNF-alpha antagonist. While the follow up period with these new agents is relatively short (5 years),thus far,there have been no demonstrated increases in the incedencance of malignancy in patients treated with etanercept ot infliximab compared with the expected rates in the general polulation.
At this time,there appears to be no need for routine laboratory monitoring with the TNF-alpha agents,but people shold be alerted to report any signs or symptoms of infection.
In addition to absense of long-term safety data,the disadvantages of TNF-alpha agents are the need for parenteral administeration and the high cost of these medications. Not all patients with RA respond to anti-TNF-alpha therapy,and disease flares occur after therapy is discontinued
Low-dose oral glucocorticoids (>10 mg of predisone daily or the equivalent)and local injections of glucococorticoids are highly effective for relieving symptoms in patients with active RA. A patient disabled by active polyarthritis may experience marked and rapid improvement in functional status within a matter of days,following initiation of low-dose glucococorticoids.
Frequently disabling synovitis recurs when glucococorticoids are discontinued, even in patients who are receiving combination therapy with one or more DMARDs. therefore,many patients with RA are functionally dependant on glucocorticoids and continue them long-term.
Predisone for "bridging" purposes,(e.g.,before DMARDs come into play) can be especially effective in therapy. Physicians,generally,use enough predisone, for the shortest possible time,and yet,be effective-without causing long-term adverse effects.
Recent evidence suggests that low-dose glucocorticoids slow the rate of joint damage (IL-1) and therefore,appear to have disease-modifyuing potential.Joint damage may increase on discontinuation of glucocorticoids.,but usually, therapy  is balanced out so that the negatives are kept to a minimum.with adequate compensation in-between,and in the long term treatment of RA..
The benefits of low-dose systemic glucocorticoids,however,should always be weighed against their adverve effects when used long-term. The possible adverse effects of long-term therapy with steriods include osteoporosis, hypertension,weight gain,fluid retention,hyperglycemia,cataracts,and skin fragility,as well as the potential for premature atherosclerosis.
These adverse effects should be considered and should be discussed in detail with the patient before glucocorticoid therapy is begun Generally,for long-term disease control the glucocorticoid dosage should be kept to a minimum. For the majority of patients with RA,this means >10 mg of predisone per day.
RA is associated with an increased risk of osteoporosis regardless of glucocortoid therapy. Patients taking glucocortoids as low as 5mg/cay have an increased risk of osteoporosis,an densitometry to assess bone loss should be performed at regular intervals for the duration of glucococorticoid treatment.
Glucocorticoid-treated patients should receive 1,500 mg of elemental calcium per day (including diet and supplementary) and 400-800 IU of vitamin D per day. Hormone replacement therapy should be considered for postmenopausal women in whom such treatment is contraindicated. Antiresorptive agents, especially bisosphonates,prevent bone loss,and these agents should be considered at the time glucococorticoid therapy is initiated.
Gludocorticoid injection of joints and periarticular structures is safe and effective when administered by a experienced physician Injecting one or a few of the most-involved joints early in the course of RA may provide local and even systemic relief. The effects are sometimes dramatic,but temporary.
Improvement from an intraarticular injection of glucocorticoid helps to istill confidence that treatment can be effective. A patient who has a disease flare in only one or a few joints can be treated successfully by injecting the particular joint(s),without requiring a major change in the regimen They will enable the patient to participate in rehabilitation programs to restore joint function.
Not all joint flares in RA are caused by the disease. Joint infection or microcrystalline arthritis must be considered and ruled out before local glucococorticoid ijections are given. In general,the same joint should not be injected more than once within 3 months. The need for repeated injections in the same joint indicates the need to reassess the adequecy of the overall treatment program.
In patients who have unacceptable levels of pain,loss of range of motion,or limitation of function because of structual joint damage,surgical procedures should be considered. Surgical procedures for RA include,carpel tunnel release,synovectomy,resection of the metatarsal heads,total joint arthroplasty and joint fusion.
New prosthesis materials and cements for fixing joint prostheses have greatly advanced the prevention of aseptic loosening and  have increased the longevity of total joint prostheses in patients with RA that requires them.

We're all self-managers, and there are two ways of looking at that. If you choose to be a self-manager and you make a deliberate choice and create a mindset that you will take control of the management of your disease, you will likely turn into being a good manager. Most individuals use one to three coping skills, and sometimes denial is that coping skill, but if you deny that you have disease, that is a rather poor thing because you are still a self-manager, you're just a poor self-manager, and you're not making interventions that can help you and your health over time. Overcoming the grief and the feelings of loss, and accept that "Yes, I have this probably incurable disease," but quickly coming around to the idea that, "Well, I'm going to do whatever it takes so I can live as full life as I can and that this is more of an inconvenience to me rather than a life-changing illness.