eMedicine Specialties > Rheumatology > Vasculitis

Giant Cell Arteritis: Treatment & Medication

Author: Mythili Seetharaman, MD, Consulting Staff, Einstein Arthritis Center, Albert Einstein Medical Center, St Christopher's Hospital for Children
Coauthor(s): Stephen A Paget, MD, Chair, Division of Rheumatology, Chief, Department of Medicine, Hospital for Special Surgery; Professor, Department of Internal Medicine, Division of Rheumatology, Weill-Cornell University; Evan Leibowitz, MD, Fellow, Department of Internal Medicine, Division of Rheumatology, Valley Hospital
Contributor Information and Disclosures

Updated: Nov 14, 2008

Treatment

Medical Care

Both polymyalgia rheumatica and giant cell arteritis (GCA) are clinical diagnoses, with laboratory tests and temporal artery biopsies functioning as supporting, not definitive, data. Thus, the diagnosis should not be held hostage to the finding of an elevated ESR or positive temporal artery biopsy results in the setting of a clinical picture that overwhelmingly supports the diagnosis. Thus, do not withhold corticosteroid therapy pending the results of a temporal artery biopsy, as such an action could leave a patient with giant cell arteritis open to developing irreversible vision loss.

  • Corticosteroid therapy is discussed as follows:
    • Prednisone is the preferred therapy for giant cell arteritis and polymyalgia rheumatica. The starting dose is usually 60-80 mg/d for giant cell arteritis and 10-15 mg/d for polymyalgia rheumatica. Start patients on parenteral methylprednisolone at doses of 250-1,000 mg intravenously daily for 3 days when acute visual changes secondary to giant cell arteritis are present. Alternate-day therapy is not effective in preventing vision loss.
    • Do not offer empirical treatment with high-dose steroid regimens appropriate for giant cell arteritis to patients with polymyalgia rheumatica who do not have symptoms of giant cell arteritis or who do not demonstrate histologic arteritis. On the other hand, do not delay treatment in patients with visual symptoms or signs (eg, amaurosis fugax, partial or complete visual loss) when giant cell arteritis is strongly suggested. The confirmatory biopsy can be performed after treatment is started, without major alteration in the diagnostic histology for up to 10 days.
    • Usually, symptoms of giant cell arteritis (eg, polymyalgia rheumatica, headache, lethargy) disappear in 36-72 hours. The ESR elevation and ischemic manifestations (eg, temporal headache, jaw claudication, localized temporal artery inflammation) diminish in several days. The temporal artery pulse may not return, and visual loss may be permanent.
    • A prompt and dramatic clinical response to low-dose prednisone (<15 mg/d) is a key feature of polymyalgia rheumatica, and most symptoms resolve in 48-72 hours.
    • After 2-4 weeks, the ESR, anemia, and thrombocytosis usually normalize. If the patient shows no significant improvement in a week, consider an alternative diagnosis, which may include one of the aforementioned disorders or a companion systemic disorder (eg, giant cell arteritis that may require a higher steroid dose).
  • Even in patients with known giant cell arteritis, do not use steroids to treat large vessel disease without evidence that vasculitis, rather than atheromatous disease, is responsible. Because cases of aortic aneurysms caused by giant cell arteritis may develop many years after the patient no longer requires steroid therapy, follow-up chest radiographs and thoracic or abdominal ultrasound may be needed over time.
  • In refractory cases of polymyalgia rheumatica or giant cell arteritis that require persistent doses of prednisone of more than 5-10 mg/d or in those patients who develop significant steroid-related adverse effects, consider using other anti-inflammatory agents, such as methotrexate20 (RA doses of 15-25 mg/wk PO) or azathioprine21 (2 mg/kg/d PO), as potentially steroid-sparing disease-controlling drugs. These agents may suppress rheumatic symptoms but do not reduce the risk of blindness if giant cell arteritis is present. The newer tumor necrosis factor antagonists are being evaluated in clinical trials for the treatment of giant cell arteritis. Initial studies of infliximab have not shown impressive disease-controlling or steroid-sparing effects.22
  • Recent retrospective but impressive data support the use of low-dose aspirin in patients with giant cell arteritis for prevention of visual loss and stroke.23

Surgical Care

The temporal artery biopsy site should be monitored.

Consultations

  • Consultation with a rheumatologist is helpful.
  • Consultation with an ophthalmologist may be useful to help exclude other causes of visual disturbances and to perform temporal artery biopsy.
  • Consultation with vascular surgeon may be useful to perform temporal artery biopsy.
  • Consultation with neurologist is helpful for excluding other causes of headache.

Medication

Corticosteroid therapy for giant cell arteritis (GCA) is started at high doses with gradual tapering, using clinical manifestations and the ESR to gauge disease activity. In general, prednisone is a safe treatment in patients with the clinical presentation of pure polymyalgia rheumatica, preventing the need for high-dose steroid therapy or routine biopsy. However, instruct all patients with polymyalgia rheumatica to call their physician immediately if they develop headache, visual symptoms, or other manifestations of giant cell arteritis.

The transition from polymyalgia rheumatica to giant cell arteritis is uncommon but can occur within 12-14 months after initial diagnosis. In general, administering low-dose corticosteroids for polymyalgia rheumatica enables protection from visual loss. Some physicians have advocated treating all patients with polymyalgia rheumatica with high-dose corticosteroids to prevent complications of occult giant cell arteritis. This approach leads to unnecessary treatment-related toxicity and is not generally recommended.

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.


Prednisone (Deltasone, Meticorten, Orasone)

DOC; steroids have many physiologic, molecular, and cellular effects. They regulate many CNS, metabolic, and anti-inflammatory functions. With regard to autoimmune diseases, they inhibit many inflammatory and immune pathways. Steroids are potent anti-inflammatory drugs.

Adult

Giant cell arteritis: 40-60 mg PO qd or divided bid
Polymyalgia rheumatica: 10-15 mg PO qd or divided bid
Intravenous solu-Medrol in high doses for acute visual loss or visual symptoms
Attempt using minimal effective dose; do not stop abruptly; taper gradually

Pediatric

Not established; giant cell arteritis and polymyalgia rheumatica are extremely rare in pediatric patients

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia when coadministered with diuretics

No absolute contraindication; documented hypersensitivity; severe bacterial, viral, fungal infection; active peptic ulcer disease; diabetes mellitus

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; weight gain, hyperglycemia, edema, cataracts, avascular necrosis, myopathy, dyspepsia, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, and infections may occur with glucocorticoid use


Methylprednisolone (Medrol, Solu-Medrol, Depo-Medrol)

Slightly more potent than prednisone. Same effects as prednisone and decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Four mg of methylprednisolone is equivalent to 5 mg of prednisone.

Adult

Acute visual changes secondary to giant cell arteritis: 80-100 mg/d IV; taper to prednisone 60 mg/d PO over 7-10 d

Pediatric

Not established; giant cell arteritis and polymyalgia rheumatica are extremely rare in pediatric patients

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when coadministered with diuretics

No absolute contraindication; documented hypersensitivity; severe bacterial, viral, fungal infection; active peptic ulcer disease; diabetes mellitus

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hyperglycemia, edema, avascular necrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myopathy, and infections are possible complications of glucocorticoid use; all patients should be treated with optimal doses of calcium and vitamin D and bisphosphonates to prevent osteoporosis

Immunosuppressive agents

These agents may have anti-inflammatory properties in giant cell arteritis and result in steroid sparing in relatively resistant cases.


Methotrexate (Folex PFS, Rheumatrex)

Inhibits dihydrofolate reductase. The precise mechanism of action in giant cell arteritis is unknown but may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Adjust dose gradually to attain satisfactory response.

Adult

7.5-25 mg PO or SC qwk

Pediatric

Not established; giant cell arteritis and polymyalgia rheumatica are extremely rare in pediatric patients

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral methotrexate; charcoal lowers levels; coadministration with etretinate may increase hepatotoxicity; indomethacin and phenylbutazone can increase plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides (including TMP-SMZ) may increase effects and toxicity; may increase plasma levels of thiopurines

Documented hypersensitivity; alcoholism, hepatic insufficiency, documented immunodeficiency syndromes, preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia)

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBC counts monthly and liver and renal function every 1-3 mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated levels [eg, dehydration]); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue use if significant drop in blood counts; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly (possibility of increased toxicity with NSAIDs including salicylates has not been studied)

Antiplatelet agents

Low-dose aspirin decreases the rate of visual loss and strokes in patients with giant cell arteritis.23


Aspirin (Ecotrin, Bayer Aspirin)

Odorless white powdery substance available in 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.
Stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives. Acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.
Irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to PGI2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregate). Platelet-inhibition lasts for life of cell (approximately 10 d). May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. Reduces likelihood of myocardial infarction. Also very effective in reducing risk of stroke. Early administration of aspirin in patients with AMI may reduce cardiac mortality in first month.

Adult

81-325 mg/d PO

Pediatric

Not established; giant cell arteritis and polymyalgia rheumatica are extremely rare in pediatric patients

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs; simultaneous administration of other NSAIDs may decrease the cardioprotective and stroke preventive effects

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; because of the association of aspirin with Reye syndrome, do not use in children (<16 y) with viral infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants

More on Giant Cell Arteritis

Overview: Giant Cell Arteritis
Differential Diagnoses & Workup: Giant Cell Arteritis
Treatment & Medication: Giant Cell Arteritis
Follow-up: Giant Cell Arteritis
References
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Further Reading

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Keywords

giant cell arteritis, temporal arteritis, GCA, cranial arteritis, polymyalgia rheumatica, PMR, occult giant cell arteritis, aching syndrome, Horton disease, Horton's disease, intimal hyperplasia, vasculopathy, ischemic optic retinopathy, stenotic lesions, ischemic optic retinopathy, vision loss, visual defects, fever of unknown origin, systemic vasculitis, granulomatous arteritis, limb claudication

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Contributor Information and Disclosures

Author

Mythili Seetharaman, MD, Consulting Staff, Einstein Arthritis Center, Albert Einstein Medical Center, St Christopher's Hospital for Children
Mythili Seetharaman, MD is a member of the following medical societies: American College of Rheumatology and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Stephen A Paget, MD, Chair, Division of Rheumatology, Chief, Department of Medicine, Hospital for Special Surgery; Professor, Department of Internal Medicine, Division of Rheumatology, Weill-Cornell University
Stephen A Paget, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, and New York Academy of Sciences
Disclosure: Nothing to disclose.

Evan Leibowitz, MD, Fellow, Department of Internal Medicine, Division of Rheumatology, Valley Hospital
Evan Leibowitz, MD is a member of the following medical societies: Alpha Omega Alpha and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

John Varga, MD, Professor, Department of Internal Medicine, Division of Rheumatology, Northwestern University
John Varga, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, Central Society for Clinical Research, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Lawrence H Brent, MD, Associate Professor of Medicine, Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center
Lawrence H Brent, MD is a member of the following medical societies: American Association of Immunologists, American College of Physicians, and American College of Rheumatology
Disclosure: Genentech Honoraria Speaking and teaching; Genentech Grant/research funds Other; Amgen Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Immunology Honoraria Speaking and teaching

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; Merck, Amgen, Biogen, Zimmer, Wyeth, Johnson&Johnson, Stryker, Medtronic, Zimmer.Abbott,  Ownership interest Other; West Penn Allegheny Health System Consulting fee Consulting; Alpharma Honoraria Consulting; Proctor&Gamble Grant/research funds Independent contractor

 
 
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