Giant Cell Arteritis Medication

  • Author: Mythili Seetharaman, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: May 23, 2012
 

Medication Summary

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.

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Corticosteroids

Class Summary

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

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Prednisone (Sterapred)

 

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.

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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.

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Immunosuppressive agents

Class Summary

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

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Azathioprine (Imuran, Azasan)

 

Imidazolyl derivative of 6-mercaptopurine. Many biological effects are similar to those of parent compound. Both compounds are eliminated rapidly from blood and are oxidized or methylated in erythrocytes and liver. No azathioprine or mercaptopurine is detectable in urine 8 h after taken.

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. The mechanism whereby azathioprine affects autoimmune diseases unknown. Works primarily on T cells. Suppresses hypersensitivities of cell-mediated type and causes variable alterations in antibody production. Immunosuppressive, delayed hypersensitivity, and cellular cytotoxicity tests are suppressed to a greater degree than antibody responses. Works very slowly; may require 6-12 mo of trial prior to effect. Up to 10% of patients may have idiosyncratic reaction, disallowing use. Do not allow WBC count to drop below 3000/µL or lymphocyte count to drop below 1000/µL.

Available in tab form for PO administration or in 100-mg vials for IV injection.

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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.

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Antiplatelet agents

Class Summary

Low-dose aspirin decreases the rate of visual loss and strokes in patients with giant cell arteritis.[41]

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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.

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Contributor Information and Disclosures
Author

Mythili Seetharaman, MD  Consultant Rheumatologist, OAA, Allentown, PA; Clinical Assistant Professor, Thomas Jefferson University Hospital; 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: Abbott pharmaceuticals Honoraria Speaking and teaching

Coauthor(s)

Stephen A Paget  MD, Physician in Chief Emeritus, Joseph P Routh Professor of Medicine, New York Hospital Weill Cornell Medical College; Program Director, Cornell Arthritis and Multipurpose Arthritis and Musculoskeletal Diseases Center (MAMDC), Hospital for Special Surgery

Stephen A Paget 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: Crescendo bioscience Consulting fee Consulting

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.

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Lawrence H Brent, MD  Associate Professor of Medicine, Jefferson Medical College of 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 for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

Alex J Mechaber, MD, FACP  Senior 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  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh 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: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

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