steroid treatment for temporal arteritis

budesonide asthma steroid

Miami's independent source of local news and culture. Athletes and bodybuilders have been using steroids to increase muscle mass for a long time. Many men, particularly those who participate in sports or who are interested in bodybuilding, use steroids to achieve quick results. Many steroids are sold illegally and come with a slew of negative side effects. So, what are some other safe and legitimate alternatives to steroid abuse? Are you trying to bulk up or lose weight with a legal steroid? Researchers have recently created safe, and legal steroids that can be used daily with no negative side effects.

Steroid treatment for temporal arteritis steroid cream potency chart

Steroid treatment for temporal arteritis

In GCA medical treatment is required for induction and maintenance of remission. Glucocorticoids: Glucocorticoids remain the cornerstone of treatment in GCA since their discovery in the s[ 11 ]. They should be prescribed immediately after the diagnosis of GCA is suspected, and in most cases are able to provide complete symptomatic relief within h[ 12 ].

Despite their importance, there are no clinical trials comparing different glucocorticoid dosing regimens. These guidelines were based on an extensive literature review of the available evidence, including published data from randomised controlled trials, and full consensus by expert opinion. The BSR guidelines advise prednisolone 40 to 60 mg at least 0.

Daily dosing is more effective than alternate day dosing, but single or divided daily doses have shown comparable results[ 14 ]. Larger studies are needed to address this issue[ 16 ]. A degree of controversy exists regarding induction treatment by either high-dose pulsed IV methylprednisolone or oral prednisolone in GCA patients with visual symptoms.

There are patients who despite being given high doses of IV methylprednisolone still develop visual loss. This might be explained by the latent period of up to 5 d between starting treatment and controlling the arteritic process in the wall of the posterior ciliary arteries; as well as by the decreased perfusion pressure in the vascular bed of the optic nerve head that makes it very prone to ischaemia due to any minor fall of the systemic blood pressure[ 18 ].

Another proposed explanation is that glucocorticoids may have a pro-coagulant effect by enhancing platelet activation[ 19 ], but this needs further confirmation. Although conflicting data exist[ 18 , 20 - 22 ], most clinicians, especially ophthalmologists, will prescribe IV steroids when presented with a patient with GCA with acute visual impairment. Adapted from Ness et al[ 17 ].

Other immunosuppressive therapy: The key to successful induction therapy is to initiate glucocorticoids as quickly as possible, given their rapid onset of action. Other immunosuppressive treatments prescribed at presentation of the disease have been tried, particularly with the aim of allowing a faster withdrawal of steroids or help controlling severe manifestations of the disease; however, results have been conflicting and generally disappointing[ 23 - 25 ].

Nevertheless, when a patient has an unacceptable high-risk of glucocorticoid-related side effects, such as concomitant severe osteoporosis and poorly controlled high blood pressure or diabetes mellitus, it might be feasible to add another immunosuppressive e. Glucocorticoids: Glucocorticoid reduction should be considered only in the absence of clinical symptoms, signs and laboratory abnormalities suggestive of active disease.

Nevertheless, the BSR[ 13 ] has proposed a standard tapering scheme after 1 mo of treatment: reducing by 10 mg of prednisolone every 2 wk to 20 mg, then another 2. There are no reliable predictors to determine treatment duration. Different studies have shown different treatment durations[ 28 - 30 ], but typically 2 to 3 years are necessary for the patients to be weaned off glucocorticoids without any clinical features of active disease.

In some cases, particularly when the disease is recurrent or there is secondary adrenal insufficiency, the treatment duration may exceed 5 years[ 31 , 9 ]. Other immunosuppressive therapy: The search for an effective disease-modifying agent for the treatment of GCA has proven elusive. Few clinical trials have been performed; the number of patients enrolled is limited and the duration of follow up is often short. A number of drugs have been studied, with disappointing results to date.

However, given the significant burden of morbidity associated with long term glucocorticoid treatment, current BSR guidelines for the management of GCA recommend consideration of the early introduction of methotrexate or alternative immunosuppressant therapy following a relapse[ 13 ] and EULAR guidelines for the management of large vessel vasculitis recommend that an immunosuppressant agent should be considered for use in large vessel vasculitis as adjunctive therapy[ 9 ].

Of the limited available evidence, methotrexate may be of benefit in the management of GCA. Three prospective randomised double blind placebo controlled trials have addressed this issue. In , Spiera et al[ 23 ] randomised 21 patients with newly diagnosed GCA to high dose corticosteroids plus methotrexate up to 20 mg once weekly or placebo.

At study completion there were no differences between the methotrexate and placebo groups with regard to cumulative steroid dose, relapse or adverse events[ 24 ]. In a similar study, in the same year, Jover et al[ 26 ] randomised 42 patients to high dose corticosteroid and methotrexate 10 mg per week or placebo.

Adverse events were similar in the two groups. In , Hoffman et al[ 32 ] randomised 98 patients with newly diagnosed GCA to glucocorticoids plus either methotrexate up to a maximum of 15 mg once weekly or placebo. No differences were observed in cumulative steroid exposure or in the number of adverse events between the methotrexate and placebo treated groups. One patient in the methotrexate treated group relapsed vs five patients in the placebo group. A subsequent meta-analysis of individual patient data from these three trials demonstrated a modest reduction in relapse and glucocorticoid exposure in the methotrexate treated groups.

However, adverse events remained similar between the groups[ 33 ]. Azathioprine is often considered as a potential steroid- sparing agent in GCA. Evidence supporting its use is limited. Only one double blind randomised placebo controlled trial was performed, which included 31 patients with GCA or PMR, or both not differentiated randomly assigned in a double blind fashion to either a standard glucocorticoid treatment schedule plus placebo or standard treatment plus azathioprine mg once daily.

However, the maintenance steroid dose was low in both arms at week 52, and the differences observed 1. Two small cases series have suggested that leflunomide has a steroid sparing effect in patients with PMR and GCA[ 35 , 36 ]. Adizie et al[ 36 ] demonstrated the efficacy of leflunomide in patients with difficult to treat disease.

However, these results require replication in prospective randomised placebo controlled trials. A number of retrospective studies have looked at cyclophosphamide use in patients with GCA, particularly in those who were steroid resistant, dependent or toxic and who had failed either methotrexate or azathioprine. However, substantial treatment related adverse events observed limits it routine use[ 37 - 40 ]. Neither hydroxychloroquine nor cyclosporine have demonstrated any benefit in clinical trials in the management of GCA[ 41 - 43 ].

Neither the infliximab nor the adalimumab studies met their primary endpoints and the infliximab trial was stopped prematurely following the interim analysis[ 25 , 45 ]. Nevertheless, patients on etanercept did have a statistically significant lower cumulative steroid dose after 1 year; however, given that only 17 patients in total were enrolled in this study, firm conclusions cannot be made[ 46 ].

More recently, treatment with tocilizumab, a monoclonal IL-6 receptor blocker, has shown potential in a number of case studies and case series in the treatment of patients with PMR and GCA in terms of improvement of clinical symptoms and reduction in the acute phase response[ 47 - 50 ]. GiACTA is a multicentre, randomised, double-blind, placebo controlled trial designed to test the ability of tocilizumab to maintain disease remission in GCA and is currently ongoing[ 51 ].

Antiplatelet agents: The use of antiplatelet agents in GCA is controversial. There are no randomised controlled trials that have evaluated the use of aspirin as an adjuvant treatment in GCA. However, in addition to its antiplatelet effects, aspirin may have a disease modifying effect in GCA.

Other studies have not demonstrated any clinical benefit from the use of aspirin[ 55 , 56 ]. Some of the discrepant findings may be explained by a higher burden of ischaemic heart disease in some cohorts, which is of itself associated with a higher risk of developing a subsequent ischaemic event. Statins : Statins are inhibitors of 3-hydroxymethylglutaryl coenzyme A reductase, the most powerful class of lipid lowering drugs to date, widely used in medical practice.

Apart from their lipid lowering effect, additional pleotropic effects have been discovered, which include anti-inflammatory and immunomodulatory properties. Moreover they restore endothelial cell function and decrease muscle cell proliferation in the vessel wall, which in turn prevents intimal hyperplasia[ 57 , 58 ]. Given the pathophysiology of the disease, statins could influence the inflammatory process in GCA, since some of the inflammatory pathways may be shared with atherosclerosis.

By contrast, in another retrospective study of patients GCA and controls , patients receiving statins were less likely to develop GCA; however, these drugs did not appear to modify the clinical presentation or disease course in patients who actually developed GCA[ 60 ].

To date there are no formal recommendations on the use of statins in patients with GCA. Bone protection: The treatment of GCA requires both long-term and high dose glucocorticoid therapy. Calcium in isolation appears to have little effect in preventing bone loss in patients starting glucocorticoids[ 63 ] although when combined with vitamin D, it is an appropriate adjunctive treatment[ 64 ].

Bisphosphonates are indicated in accordance with local guidelines. Gastrointestinal protection: Given the high doses and long term duration of glucocorticoid therapy in patients with GCA, gastrointestinal protection is recommended with proton pump inhibitors, especially if concomitant risk factors are present such as NSAID use, and older age[ 13 , 66 ]. However, in clinical practice it is often advisable to discontinue NSAID use apart from low dose aspirin whilst the patient is receiving glucocorticoids.

Advances in immunology have revealed that a number of molecules are important modulators in the pathophysiology of GCA. Mice lacking the interleukin 1 receptor antagonist IL-1ra gene developed large vessel vasculitis[ 67 ], suggesting that IL-1 inhibition could be a therapeutic option in patients with GCA. However, randomized control trials are needed to determine the true efficacy and safety of this drug. Activated T-cells are believed to have a critical role in the development of large-vessel vasculitis.

However, most patients with LV-GCA improve with medical treatment alone, making the need for surgical interventions uncommon. The risk of aortic aneurysm is higher in patients with GCA when comparing with the general population twofold increased risk in the United Kingdom[ 72 ] , and the aneurysms are more likely to occur late in the disease course.

Given there are no validated guidelines on surgical repair of aneurysms in patients with GCA, most strategies are based on the recommendations of atherosclerosis-related aneurysms. In addition, revascularization procedures e. Although narrowing of important arteries, such as the subclavian artery, may compromise distal tissue viability, the development of extensive collateral circulation over time is usually sufficient to maintain adequate tissue viability, even when ischaemic symptoms, such as limb claudication or loss of large vessel pulses, are observed.

There have been some case reports of successful revascularization surgery, but with common restenosis[ 74 - 76 ]. When necessary, surgical treatment should be performed in the quiescent phase of the disease and in experienced centres[ 9 ]. Aortic structural damage in GCA is associated with a trend towards increased mortality of any cause [ 77 ]; however, the comparison between surgical outcomes in GCA and other causes of aortic disease has not been evaluated.

Not all patients with GCA respond to therapy in the same way, but there are no valid biomarkers to assess treatment response. Several potential molecular and imaging biomarkers have been investigated. Changes in the conventional inflammatory markers CRP and ESR do not consistently reflect disease activity[ 78 ]; however, they are still the laboratory tests used routinely to monitor the effects of therapy.

Additionally, circulating pentraxin 3 PTX3 and vascular endothelial growth factor VEGF levels have been recognized to be significantly increased in patients with very recent optic nerve ischaemia[ 80 ], with VEGF levels responding well to treatment[ 81 ]. Antibodies against ferritin have also been suggested as potential activity markers for GCA, particularly in patients without cranial artery involvement[ 82 ]. However, further studies with larger series are warrant to understand the potential role of these serum markers in the assessment of GCA.

Imaging techniques, especially for patients with extracranial involvement, have an important role in monitoring patients with GCA. Ultrasound: Three meta-analyses have reported the high value and validity of ultrasound in diagnosing GCA[ 83 - 85 ], and we have recently completed patient recruitment for a large multicentre study looking at ultrasound as a diagnostic tool for GCA - TABUL study Temporal Artery Biopsy vs ULtrasound in diagnosis of GCA [ 86 ]; however, the role of ultrasound as a measure of disease activity is still unclear.

In small case series and case reports, abnormal ultrasound appearances have been reported to resolve within 2 d of starting glucocorticoids[ 87 ] or alternatively, to persist for 11 wk despite treatment[ 88 ], allowing correlation of imaging changes with clinical response. In the TABUL study, we performed a cross-sectional analysis of patients with GCA and positive ultrasound halo dark area around arterial wall ; the size of the halo was found to be smaller in patients who had received more days of glucocorticoid treatment, as well as correlating with the presence of ischaemic symptoms, supporting the early use of ultrasound as a potential prognostic marker and monitoring tool[ 89 ].

Ultrasound of the left temporal artery showing a dark halo arrows around the vessel wall of the parietal branch compatible with vascular inflammation. These imaging modalities can be used in patients with GCA, not only to verify extra-cranial involvement, but also to evaluate temporal arteries.

High-resolution MRI of the cranium has been reported to detect biopsy-positive GCA with high sensitivity[ 91 , 92 ], but future research is needed to validate this technique for diagnosis of cranial GCA. Although it has great value for assessing aortitis and potential associated aneurysms and stenoses, MRI has failed to correlate well with clinical measures of disease activity[ 93 - 95 ]. In addition, false-positives may occur due to increased mural contrast enhancement as a result of vascular remodelling.

When compared to MRI, it appears to be more sensitive in detecting early vascular inflammation and correlates better with changes in disease activity over time[ 93 , 97 , 98 ]. However, like MRI, the relationship between PET findings and the prediction of disease activity or relapse is also inconsistent[ 93 , 97 ], which can be partly explained by the lack of standardized and validated criteria for disease activity in large vessel vasculitis.

Whole body positron emission tomography-computerised tomography scan of a patient with large vessel vasculitis, showing increased fluorodeoxyglucose uptake in the ascending and abdominal aorta arrows. The main limitations of this modality are: the lack of a uniform definition of vascular inflammation based on the FDG uptake; inability to provide information regarding wall structure or luminal flow; inability to visualize the temporal arteries; the use of large amounts of ionizing radiation typically MSv per scan ; and the limited access to this technique by most health institutions.

This imaging modality has been proposed to evaluate response to treatment in Takayasu patients[ 99 ], but to our knowledge the same has not been considered in GCA. Chest radiograph: The main use for regular chest radiographs in patients with GCA is to monitor for potential aortic aneurysms. Although the BSR recommends its performance at least every 2 years[ ], we have recently demonstrated that the risk of aneurysm development as a result of GCA is actually quite low[ 72 ]; if an aneurysm is suspected, more advanced imaging modalities described above should additionally be obtained in order to confirm the diagnosis and evaluate possible treatment measures.

The frequency for patient follow-up should be guided by their clinical manifestations and adverse advents. The BSR recommends follow-up during the first year at weeks 0, 1, 3, 6, then months 3, 6, 9, 12 and if new symptoms or adverse effects occur[ 13 ]. Screening for aortic aneurysms and monitoring bone density may be indicated in high risk individuals e. Despite the severe consequences of untreated GCA, such as blindness, there is no consensus on the optimal therapeutic strategies for this disease.

Early initiation of glucocorticoid treatment is essential; however, the value of additional steroid-sparing synthetic or biologic agents to avoid the common glucocorticoid adverse effects or obtain quicker remission is still uncertain. We do not know how many and which synthetic DMARDs should be used before considering a biologic agent, because there are no valid and specific biomarkers to assess therapy response in GCA.

Potential biomarkers which require further validation include circulating levels of IL-6 and VEGF as well as imaging assessments, such as ultrasound. Further investigation is needed to establish the role of these biomarkers, which can assist in the development and testing of innovative targeted therapies whose effects can be more reliably measured. Conflict-of-interest: The authors have no conflicts of interest. Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers.

Peer-review started: January 20, First decision: January 30, Article in press: April 2, National Center for Biotechnology Information , U. World J Clin Cases. Published online Jun Author information Article notes Copyright and License information Disclaimer. Author contributions: All authors contributed to the writing of this review manuscript.

Published by Baishideng Publishing Group Inc. All rights reserved. This article has been cited by other articles in PMC. Abstract Glucocorticoids remain the cornerstone of medical therapy in giant cell arteritis GCA and should be started immediately to prevent severe consequences of the disease, such as blindness. Keywords: Giant cell arteritis, Therapy, Disease management, Glucocorticoids, Immunosuppressive agents. Open in a separate window.

Figure 1. Induction Glucocorticoids: Glucocorticoids remain the cornerstone of treatment in GCA since their discovery in the s[ 11 ]. Table 1 Eye manifestations in giant cell arteritis. Maintenance Glucocorticoids: Glucocorticoid reduction should be considered only in the absence of clinical symptoms, signs and laboratory abnormalities suggestive of active disease. Future therapies Advances in immunology have revealed that a number of molecules are important modulators in the pathophysiology of GCA.

Molecular markers Changes in the conventional inflammatory markers CRP and ESR do not consistently reflect disease activity[ 78 ]; however, they are still the laboratory tests used routinely to monitor the effects of therapy. Imaging Imaging techniques, especially for patients with extracranial involvement, have an important role in monitoring patients with GCA.

Figure 2. Figure 3. Follow-up The frequency for patient follow-up should be guided by their clinical manifestations and adverse advents. Footnotes Conflict-of-interest: The authors have no conflicts of interest. References 1.

Kale N, Eggenberger E. Diagnosis and management of giant cell arteritis: a review. Curr Opin Ophthalmol. Schmidt WA. Role of ultrasound in the understanding and management of vasculitis. Ther Adv Musculoskelet Dis. Nosology of primary vasculitis. Curr Opin Rheumatol. Giant cell arteritis: epidemiology, diagnosis, and management.

Curr Rheumatol Rep. Polymyalgia rheumatica and giant-cell arteritis. Prednisolone combined with adjunctive immunosuppression is not superior to prednisolone alone in terms of efficacy and safety in giant cell arteritis: meta-analysis. Clin Rheumatol. Current understanding and management of giant cell arteritis and polymyalgia rheumatica. Patients with polymyalgia rheumatica usually have similar nonspecific systemic symptoms, proximal muscle pain and stiffness, and an elevated ESR.

The diagnosis is based on the clinical findings. Both disorders are treated with corticosteroids: high dosages for giant cell arteritis prednisone in a dosage of 40 to 60 mg per day and lower dosages for polymyalgia rheumatica prednisone in a dosage of 10 to 20 mg per day.

Symptom relief in response to treatment is rapid and reinforces the diagnosis. After normalization of the ESR, the corticosteroid is tapered, with the patient monitored closely for symptom recurrence. Most patients require corticosteroid therapy for two to three years and experience one or more treatment complications. Giant cell arteritis and polymyalgia rheumatica are closely related clinical conditions that are sometimes considered to represent different manifestations of the same underlying disease process.

Substantial impairment of function can occur with polymyalgia rheumatica, and blindness is a serious complication of giant cell arteritis. Because family physicians encounter both of these conditions in their practices, they should have a systematic approach to diagnosis and treatment. Giant cell arteritis and polymyalgia rheumatica are rare in persons less than 50 years of age. The incidence of each disorder increases with age, and both conditions are approximately two times more common in women than in men.

Prevalences vary considerably in different ethnic and racial groups. Both disorders occur more often in whites than in blacks, Hispanics or Asians. In the United States, the reported annual incidence of giant cell arteritis ranges from 0. Clinically, considerable overlap exists between the two conditions.

Approximately one half of patients with giant cell arteritis meet diagnostic criteria for polymyalgia rheumatica, and 15 to 25 percent of patients with polymyalgia rheumatica have concurrent giant cell arteritis or will develop manifestations of the disorder in the future.

Little is known about causative factors for giant cell arteritis or polymyalgia rheumatica. The most prevalent speculation is that these disorders result from immunologic responses to infectious triggers in genetically susceptible persons. Giant cell arteritis, also known as temporal arteritis or cranial arteritis, is a vasculitis of the large and medium arteries of the head and neck. Arteries below the aortic arch and veins are rarely involved. Microscopically, the inflammation of arterial walls is often patchy and segmental, and it is characterized by the infiltration of mononuclear cells and the presence of giant cells.

In polymyalgia rheumatica, pathologic findings are variable and may be minimal or absent. There is no consistent pathology of muscle. Vasculitis may be present, and lymphocytic synovitis is sometimes found in large joints. The American College of Rheumatology criteria for the classification of giant cell arteritis. Arthritis Rheum ;—8. Approximately two thirds of patients with giant cell arteritis have new-onset headache. This headache is often present on a daily basis and is quite bothersome.

The headache may be generalized, but it is more commonly unilateral and localized to the temporal area. When headache is absent or mild, the index of suspicion for the disorder is frequently low, and the diagnosis may be delayed for weeks or even months. Patients with giant cell arteritis often have a variety of other symptoms, such as malaise, fatigue, low-grade fever, anorexia, weight loss, myalgias or arthralgias.

They may also have various visual symptoms, including blurring and scotomas. The onset of these symptoms may be abrupt or insidious. Jaw claudication in patients more than 50 years of age has fairly high specificity but only moderate sensitivity 45 to 50 percent for giant cell arteritis. Physical Findings. In patients with giant cell arteritis, the physical findings are highly variable and frequently nonspecific. Nonetheless, the physical examination is important for detecting signs of neoplasm, infection, connective tissue disease and other conditions that can produce the nonspecific symptoms.

Fever and documented weight loss may be present but frequently are absent. Tenderness of one or both temporal arteries or of the adjacent scalp is often present. Temporal artery pulsations may be decreased or absent, but the classic finding of a nonpulsatile nodular temporal artery is uncommon. The funduscopic examination is usually normal but may show pallor or edema of the optic disc. Patients with giant cell arteritis have few, if any, objective findings relating to muscles or joints.

However, findings of coexisting osteoarthritis are often present. Muscle strength is normal. Laboratory Findings. The erythrocyte sedimentation rate ESR is the most important laboratory test in the evaluation of patients with suspected giant cell arteritis. The ESR is almost always elevated, frequently to greater than mm per hour. Occasionally, the ESR may be as low as 40 or 50 mm per hour; rarely, it may be normal.

A mild normocytic, normochromic anemia is frequently present. The white blood cell count is usually normal but may be mildly elevated. The serum alkaline phosphatase level may be mildly elevated. Less commonly, mild elevation of aminotransferase levels is present. Temporal Artery Biopsy. If the clinical picture is confusing, a temporal artery biopsy is crucial to establish the diagnosis of giant cell arteritis. Because of the patchy distribution of the inflammation, an arterial segment at least 3 cm long preferably 5 cm long should be obtained for examination.

Biopsy of the temporal artery is a simple, low-risk procedure, and complications are rare. The role of temporal artery biopsy is less clear when the findings of the history, physical examination and laboratory tests strongly indicate the diagnosis of giant cell arteritis. Some authorities recommend pathologic confirmation of the diagnosis in all patients because of the potentially serious side effects of long-term corticosteroid therapy.

According to the ACR criteria, giant cell arteritis can be diagnosed without a biopsy. The issue is complicated by the fact that biopsies are not always positive, even when giant cell arteritis is present. Color Duplex Ultrasonography. The use of color duplex ultrasonography of the temporal arteries is under investigation as a diagnostic tool for giant cell arteritis. The sensitivity and specificity of this technique may prove to be sufficiently high to obviate the need for biopsy in some patients.

One set of diagnostic criteria for polymyalgia rheumatica is presented in Table 2. The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication. In patients with polymyalgia rheumatica, symptoms may develop abruptly or insidiously. The most common symptom is aching pain involving large proximal muscle groups. Morning stiffness is often present.

Initially, the pain may be unilateral or bilateral. As the condition progresses, pain is almost always bilateral, involves the neck, shoulders, back, hips and thighs, and increasingly interferes with physical function. Muscle pain is frequently accompanied by malaise, fatigue and a low-grade fever. Some patients experience swelling of their hands and feet. On physical examination, patients may have a low-grade fever.

Weight loss may be present. Proximal muscles may be tender, but muscle strength is good. The tender points characteristic of fibromyalgia are absent. Occasionally, patients have evidence of synovitis and peripheral edema. As in giant cell arteritis, the most sensitive laboratory finding is an elevated ESR. However, as many as 20 percent of patients with polymyalgia rheumatica have a normal or only mildly elevated ESR. Patients with polymyalgia rheumatica may have the nonspecific laboratory abnormalities found in giant cell arteritis.

The serum creatine kinase level is normal, which helps differentiate the disorder from polymyositis and primary muscle disorders. Differential Diagnosis. The differential diagnosis of polymyalgia rheumatica includes malignancy, acute and chronic infections, thyroid disorders, depression, osteoarthritis, rheumatoid arthritis and polymyositis.

The ESR is also increased in many of these conditions. The history, physical examination and laboratory evaluation should focus on distinguishing polymyalgia rheumatica from these disorders. A trial of a corticosteroid given in a low dosage may be helpful, because rapid relief of symptoms is characteristic of polymyalgia rheumatica.

Coexisting Giant Cell Arteritis. As many as one fourth of patients with polymyalgia rheumatica may have coexisting giant cell arteritis. Thus, the question arises: Should a patient with polymyalgia rheumatica and no objective signs of temporal arteritis undergo temporal artery biopsy to assess the possible presence of giant cell arteritis?

Although this question continues to be debated in the literature, the general consensus seems to be that a temporal artery biopsy is not necessary in this setting. Virtually all patients with giant cell arteritis or polymyalgia rheumatica are treated.

Thus, the natural history of either condition is not well understood. Early experiences suggest that the disorders are self-limited and run their course in one to three years. Giant cell arteritis has several serious complications, most notably blindness, which may occur in 10 to 15 percent of untreated or inadequately treated patients.

Patients with giant cell arteritis are also at increased risk for the development of aortic aneurysms, primarily involving the thoracic aorta. Giant cell arteritis may also be associated with an increased risk of stroke. One study 12 suggested that patients with giant cell arteritis are at higher risk of death from cardiovascular disease during the first year after the onset of symptoms.

In contrast, other studies 13 , 14 indicate that long-term survival in patients who are adequately treated for giant cell arteritis is comparable to that in unaffected persons of similar age. Polymyalgia rheumatica generally is not associated with the serious complications of giant cell arteritis.

However, untreated patients with this disorder often feel miserable and have impaired quality of life. With appropriate treatment, survival is similar to that in unaffected persons of the same age. The overlap between polymyalgia rheumatica and late-onset seronegative rheumatoid arthritis has been discussed in the literature.

Giant cell arteritis and polymyalgia rheumatica are treated with corticosteroids. High dosages 40 to 60 mg per day of prednisone are used for giant cell arteritis, and low dosages 10 to 20 mg per day of prednisone are used for polymyalgia rheumatica. Therapy is primarily based on empiric experiences because few randomized clinical trials are available to guide treatment decisions.

Evidence from one clinical trial 17 indicated that daily dosing is superior to every-other-day dosing. The use of high dosages of corticosteroids in the treatment of giant cell arteritis is based on the need to suppress vascular inflammation and decrease the risk of blindness. In the absence of good evidence from clinical trials, numerous regimens are used.

Several of these approaches are summarized in Table 3. Prednisone in a dosage of 40 to 60 mg per day until the ESR is normal and the patient is asymptomatic. Decrease the dosage by 2. Decrease the dosage by 10 percent every 2 weeks to a dosage of 10 mg per day; then decrease the dosage by 1 mg per day every 4 weeks.

Monitor the patient for symptom recurrence throughout the steroid taper; monitor the ESR every 4 weeks for 2 to 3 months, then every 8 to 12 weeks until 12 to 18 months after the cessation of therapy. Patients diagnosed as having giant cell arteritis should be started immediately on 40 to 60 mg of prednisone given once a day or in divided doses. Rapid initiation of therapy is thought to minimize the risk of blindness.

The initiation of corticosteroid therapy within one to two weeks before temporal artery biopsy does not appear to change the characteristic pathologic findings. Symptoms usually resolve quickly, often within two to three days of the initiation of the corticosteroid. Most authorities recommend continuing the high dosage of prednisone until the ESR has declined to a normal level.

Once the ESR has normalized, a steroid taper is begun. One approach is to reduce the prednisone dosage by 2. Many patients have at least one recurrence of disease activity during the course of the taper. Recurrences should result in an increase in the dosage followed by a slower taper.

Flexibility should be maintained with respect to the steroid taper, and patients should be managed individually. Most patients with giant cell arteritis require at least two years of corticosteroid therapy. A few patients remain on a low dosage of corticosteroid indefinitely. Patients diagnosed as having polymyalgia rheumatica should be started on 10 to 20 mg of prednisone a day Table 4.

Some evidence indicates that the incidence of relapse may be lower with a starting dosage of 20 mg per day than with 10 mg per day. Prednisone in a dosage of 10 to 20 mg per day until the ESR is normal and the patient is asymptomatic.

HIVES AFTER STEROID TREATMENT

PEOPLE WHO TAKE STEROIDS

Thank steroids and depo provera the purpose

Tenderness of one or both temporal arteries or of the adjacent scalp is often present. Temporal artery pulsations may be decreased or absent, but the classic finding of a nonpulsatile nodular temporal artery is uncommon. The funduscopic examination is usually normal but may show pallor or edema of the optic disc. Patients with giant cell arteritis have few, if any, objective findings relating to muscles or joints.

However, findings of coexisting osteoarthritis are often present. Muscle strength is normal. Laboratory Findings. The erythrocyte sedimentation rate ESR is the most important laboratory test in the evaluation of patients with suspected giant cell arteritis. The ESR is almost always elevated, frequently to greater than mm per hour.

Occasionally, the ESR may be as low as 40 or 50 mm per hour; rarely, it may be normal. A mild normocytic, normochromic anemia is frequently present. The white blood cell count is usually normal but may be mildly elevated. The serum alkaline phosphatase level may be mildly elevated. Less commonly, mild elevation of aminotransferase levels is present. Temporal Artery Biopsy. If the clinical picture is confusing, a temporal artery biopsy is crucial to establish the diagnosis of giant cell arteritis.

Because of the patchy distribution of the inflammation, an arterial segment at least 3 cm long preferably 5 cm long should be obtained for examination. Biopsy of the temporal artery is a simple, low-risk procedure, and complications are rare. The role of temporal artery biopsy is less clear when the findings of the history, physical examination and laboratory tests strongly indicate the diagnosis of giant cell arteritis.

Some authorities recommend pathologic confirmation of the diagnosis in all patients because of the potentially serious side effects of long-term corticosteroid therapy. According to the ACR criteria, giant cell arteritis can be diagnosed without a biopsy. The issue is complicated by the fact that biopsies are not always positive, even when giant cell arteritis is present.

Color Duplex Ultrasonography. The use of color duplex ultrasonography of the temporal arteries is under investigation as a diagnostic tool for giant cell arteritis. The sensitivity and specificity of this technique may prove to be sufficiently high to obviate the need for biopsy in some patients.

One set of diagnostic criteria for polymyalgia rheumatica is presented in Table 2. The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication. In patients with polymyalgia rheumatica, symptoms may develop abruptly or insidiously. The most common symptom is aching pain involving large proximal muscle groups. Morning stiffness is often present. Initially, the pain may be unilateral or bilateral.

As the condition progresses, pain is almost always bilateral, involves the neck, shoulders, back, hips and thighs, and increasingly interferes with physical function. Muscle pain is frequently accompanied by malaise, fatigue and a low-grade fever. Some patients experience swelling of their hands and feet.

On physical examination, patients may have a low-grade fever. Weight loss may be present. Proximal muscles may be tender, but muscle strength is good. The tender points characteristic of fibromyalgia are absent. Occasionally, patients have evidence of synovitis and peripheral edema. As in giant cell arteritis, the most sensitive laboratory finding is an elevated ESR.

However, as many as 20 percent of patients with polymyalgia rheumatica have a normal or only mildly elevated ESR. Patients with polymyalgia rheumatica may have the nonspecific laboratory abnormalities found in giant cell arteritis. The serum creatine kinase level is normal, which helps differentiate the disorder from polymyositis and primary muscle disorders.

Differential Diagnosis. The differential diagnosis of polymyalgia rheumatica includes malignancy, acute and chronic infections, thyroid disorders, depression, osteoarthritis, rheumatoid arthritis and polymyositis. The ESR is also increased in many of these conditions.

The history, physical examination and laboratory evaluation should focus on distinguishing polymyalgia rheumatica from these disorders. A trial of a corticosteroid given in a low dosage may be helpful, because rapid relief of symptoms is characteristic of polymyalgia rheumatica. Coexisting Giant Cell Arteritis. As many as one fourth of patients with polymyalgia rheumatica may have coexisting giant cell arteritis. Thus, the question arises: Should a patient with polymyalgia rheumatica and no objective signs of temporal arteritis undergo temporal artery biopsy to assess the possible presence of giant cell arteritis?

Although this question continues to be debated in the literature, the general consensus seems to be that a temporal artery biopsy is not necessary in this setting. Virtually all patients with giant cell arteritis or polymyalgia rheumatica are treated. Thus, the natural history of either condition is not well understood.

Early experiences suggest that the disorders are self-limited and run their course in one to three years. Giant cell arteritis has several serious complications, most notably blindness, which may occur in 10 to 15 percent of untreated or inadequately treated patients.

Patients with giant cell arteritis are also at increased risk for the development of aortic aneurysms, primarily involving the thoracic aorta. Giant cell arteritis may also be associated with an increased risk of stroke. One study 12 suggested that patients with giant cell arteritis are at higher risk of death from cardiovascular disease during the first year after the onset of symptoms.

In contrast, other studies 13 , 14 indicate that long-term survival in patients who are adequately treated for giant cell arteritis is comparable to that in unaffected persons of similar age. Polymyalgia rheumatica generally is not associated with the serious complications of giant cell arteritis. However, untreated patients with this disorder often feel miserable and have impaired quality of life.

With appropriate treatment, survival is similar to that in unaffected persons of the same age. The overlap between polymyalgia rheumatica and late-onset seronegative rheumatoid arthritis has been discussed in the literature. Giant cell arteritis and polymyalgia rheumatica are treated with corticosteroids.

High dosages 40 to 60 mg per day of prednisone are used for giant cell arteritis, and low dosages 10 to 20 mg per day of prednisone are used for polymyalgia rheumatica. Therapy is primarily based on empiric experiences because few randomized clinical trials are available to guide treatment decisions. Evidence from one clinical trial 17 indicated that daily dosing is superior to every-other-day dosing. The use of high dosages of corticosteroids in the treatment of giant cell arteritis is based on the need to suppress vascular inflammation and decrease the risk of blindness.

In the absence of good evidence from clinical trials, numerous regimens are used. Several of these approaches are summarized in Table 3. Prednisone in a dosage of 40 to 60 mg per day until the ESR is normal and the patient is asymptomatic. Decrease the dosage by 2. Decrease the dosage by 10 percent every 2 weeks to a dosage of 10 mg per day; then decrease the dosage by 1 mg per day every 4 weeks.

Monitor the patient for symptom recurrence throughout the steroid taper; monitor the ESR every 4 weeks for 2 to 3 months, then every 8 to 12 weeks until 12 to 18 months after the cessation of therapy. Patients diagnosed as having giant cell arteritis should be started immediately on 40 to 60 mg of prednisone given once a day or in divided doses. Rapid initiation of therapy is thought to minimize the risk of blindness.

The initiation of corticosteroid therapy within one to two weeks before temporal artery biopsy does not appear to change the characteristic pathologic findings. Symptoms usually resolve quickly, often within two to three days of the initiation of the corticosteroid. Most authorities recommend continuing the high dosage of prednisone until the ESR has declined to a normal level.

Once the ESR has normalized, a steroid taper is begun. One approach is to reduce the prednisone dosage by 2. Many patients have at least one recurrence of disease activity during the course of the taper. Recurrences should result in an increase in the dosage followed by a slower taper. Flexibility should be maintained with respect to the steroid taper, and patients should be managed individually.

Most patients with giant cell arteritis require at least two years of corticosteroid therapy. A few patients remain on a low dosage of corticosteroid indefinitely. Patients diagnosed as having polymyalgia rheumatica should be started on 10 to 20 mg of prednisone a day Table 4. Some evidence indicates that the incidence of relapse may be lower with a starting dosage of 20 mg per day than with 10 mg per day. Prednisone in a dosage of 10 to 20 mg per day until the ESR is normal and the patient is asymptomatic.

Decrease the dosage by 1 to 2. Monitor the patient for symptom recurrence throughout the steroid taper; monitor the ESR every 4 weeks for 2 to 3 months, then every 8 to 12 weeks until 12 months after the cessation of therapy. Information frmo reference 1. The response to corticosteroid therapy is usually rapid and dramatic. If a patient suspected of having polymyalgia rheumatica does not improve greatly within three to four days after the initiation of treatment, the diagnosis should be reconsidered.

If patients respond to treatment, the initial corticosteroid dosage should be continued until the ESR normalizes. This usually occurs in approximately four weeks. At that time, a slow steroid taper is initiated if the initial prednisone dosage was 15 or 20 mg per day. The approach varies but generally involves decreasing the dosage by 1 to 2.

Patients started on 10 mg per day of prednisone should probably remain on this dosage for one to two months after the ESR has normalized. Patients with polymyalgia rheumatica who develop clear evidence of giant cell arteritis should be treated with a corticosteroid in the high dosage appropriate for giant cell arteritis. Attempts have been made to treat polymyalgia rheumatica with high dosages of non-steroidal anti-inflammatory drugs NSAIDs. Adequate control of symptoms is occasionally achieved with these agents.

Patients who are treated for giant cell arteritis or polymyalgia rheumatica are at high risk for one or more complications of long-term corticosteroid therapy. Many patients have suppression of the hypothalamic-pituitary-adrenal axis, and life-threatening adrenal insufficiency may develop after abrupt cessation of corticosteroid therapy. For this reason, prednisone is slowly tapered over an extended period from the dosage of 10 mg per day to the cessation of therapy.

Also, patients who are receiving a low dosage should be given a higher dosage when they have an infection, when they must undergo surgery or when they have other periods of increased physiologic stress. Patients with giant cell arteritis or polymyalgia rheumatica may be at increased risk for serious complications of corticosteroids because of advanced age and coexisting diseases.

Osteoporosis, increased susceptibility to infection, impaired wound healing, hyperglycemia, hypertension, cataracts, glaucoma and psychiatric disorders are among the complications that may cause serious problems in these patients. A Mayo Clinic study 20 found that at least one complication occurred in 65 percent of patients with polymyalgia rheumatica who were treated with a corticosteroid alone and in 80 percent of patients with the disorder who were treated with a corticosteroid and an NSAID.

In addition, the risk of developing diabetes mellitus or incurring a vertebral, femoral neck or hip fracture was two to five times greater in these patients than in control subjects matched by age and gender. Because of higher corticosteroid dosages, complications are even more common in patients with giant cell arteritis. The toxicity of corticosteroids has led to efforts to identify alternative or adjunctive treatments that reduce exposure to these drugs in patients with giant cell arteritis or polymyalgia rheumatica.

Unfortunately, no other treatment has been found to approach the efficacy of corticosteroids. Supplementation of calcium calcium carbonate in a dosage of 1 to 1. Therapeutic decisions regarding giant cell arteritis and polymyalgia rheumatica must address the balance of benefits and risks. Both disorders cause significant morbidity that affects quality of life. Corticosteroids constitute the most effective therapy for these conditions.

Patients should be informed about the potential benefits and risks of corticosteroid therapy and should participate in treatment decisions. Already a member or subscriber? Log in. She received her master of science in nursing degree from the University of Illinois—Peoria. TONY D. Medical Clinic. He received his master of science in nursing degree from the University of North Carolina, Chapel Hill. Address correspondence to Robert L. Blake, Jr. Reprints are not available from the authors.

In giant cell arteritis, the vessels most involved are those of the head, especially the temporal arteries located on each side of the head. For this reason, the disorder is sometimes called temporal arteritis. However, other blood vessels, including large ones like the aorta, can become inflamed in giant cell arteritis.

Standard treatment involves high doses of corticosteroids that are tapered over time. The efficacy and safety of subcutaneous injected under the skin Actemra for giant cell arteritis were established in a double-blind, placebo-controlled study with patients with giant cell arteritis. The primary efficacy endpoint was the proportion of patients achieving sustained remission from Week 12 through Week Sustained remission was defined as the absence of symptoms of giant cell arteritis, normalization of inflammatory laboratory tests, and tapering the use of prednisone a steroid drug.

A greater proportion of patients receiving subcutaneous Actemra with standardized prednisone regimens achieved sustained remission from Week 12 through Week 52 as compared to patients receiving placebo with standardized prednisone regimens. The cumulative prednisone dose was lower in treated patients with Actemra relative to placebo. The overall safety profile observed in the Actemra treatment groups was generally consistent with the known safety profile of Actemra.

Actemra carries a Boxed Warning for serious infections. Patients treated with Actemra who develop a serious infection should stop that treatment until the infection is controlled. Live vaccines should be avoided during treatment with Actemra. Actemra should be used with caution in patients at increased risk of gastrointestinal perforation.

Hypersensitivity reactions, including anaphylaxis and death, have occurred.