eMedicine Specialties > Ophthalmology > Hematologic & Cardiovascular Disorders

Giant Cell Arteritis: Treatment & Medication

Author: Manolette R Roque, MD, MBA, President and CEO, Service Chief of Ocular Immunology and Uveitis, Refractive Surgery, EYE REPUBLIC Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines; Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, St. Luke's Medical Center Global City; Senior Eye Surgeon, The LASIK Surgery Clinic
Coauthor(s): Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, Eye Republic Ophthalmology Clinic; Elisabetta Miserocchi, MD, Fellow in Immunology and Uveitis Service, Department of Ophthalmology, Harvard Medical School; C Stephen Foster, MD, FACS, FACR, FAAO, Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution
Contributor Information and Disclosures

Updated: Oct 23, 2008

Treatment

Medical Care

The universally accepted treatment of GCA is high-dose corticosteroid therapy.15,113,114,115,116,117,118,119,38,120,121,122,123,124,125,126,127 The major justification for the use of corticosteroids is the impending danger of blindness in untreated patients. The goals of treatment are to reverse the disease and to prevent further progression. This is of utmost importance, especially in the ophthalmic arteries, to prevent blindness. In individuals presenting with visual symptoms, there is a 22-fold increased chance of visual improvement if therapy is started within the first day. Damage may be irreversible if treatment is delayed beyond 48 hours.

Using constitutional symptoms, vascular symptoms, and the ESR findings as guidelines, the physician is usually able to gradually taper off the corticosteroids to a maintenance dose for 2 years.

  • A hallmark paper by Birkhead and colleagues showed that corticosteroids often were effective in preventing blindness in patients with GCA.15 High-dose glucocorticoid therapy is recommended in all patients with GCA.
  • Initially, high doses of corticosteroids may be given at 1-2 mg/kg/d for one month or until the disease activity is suppressed adequately.
  • Sequential ESR determination may assist in determining the success of the high-dose corticosteroid therapy. Once the signs of clinical inflammation are suppressed and the ESR is maintained at a low level, corticosteroids may be tapered slowly.
  • No agreement exists as to the length of treatment with corticosteroids for GCA. It may be reasonable to maintain the patient on treatment for 2 years to lessen the chances for relapses. Even then, relapses have been reported.128
  • The author uses a cyclosporine-azathioprine or cyclosporin-methotrexate combination as a steroid-sparing recipe for steroid-resistant cases. This alternative recipe may be beneficial in patients with steroid-resistant symptoms, and these immunosuppressives may be useful as glucocorticoid-sparing agents in patients requiring protracted treatment.
  • Nesher and colleagues reported that the addition of low-dose acetylsalicylic acid (ASA) decreases the incidence of cerebrovascular accidents and visual loss in a retrospective analysis of 175 patients diagnosed with GCA between 1980 and 2000.129 This therapy should be initiated in every patient diagnosed with GCA who does not have contraindications to ASA.
  • The disastrous nature of the disease occasionally may require the administration of treatment prior to a definitive superficial TAB. It is generally believed that the results of a superficial TAB will not be altered if the procedure is performed within 7-10 days of initiating corticosteroid therapy.

Surgical Care

Aside from the performance of a superficial TAB, usually no further surgical intervention is necessary in the management of patients with GCA.

Surgery, ideally performed while the GCA is inactive and in the absence of steroid therapy, may be necessary in as many as 41% of patients with thoracic aortic aneurysms.

Consultations

Patients with GCA are in need of an experienced team of physicians to ensure quality care.130

  • Rheumatologist
    • Immediate consultation with a rheumatologist is suggested when initiating high-dose steroid therapy for presumed GCA prior to a superficial TAB. Therapy should not be delayed if consultation is not available immediately.
    • Rheumatologic consultation also is indicated to consider the need for steroid therapy when cranial artery biopsy results are negative, but the clinical presentation strongly suggests GCA.
    • The occasional patient with GCA who does not respond adequately to steroid therapy requires a referral for reconsideration of the diagnosis and for other forms of immunosuppressive therapy (eg, azathioprine, cyclophosphamide, dapsone).
  • Neuro-ophthalmologist/ocular immunologist: Urgent ophthalmologic evaluation is needed if visual impairment is reported. If it is not available, one can proceed directly to hospitalization for immediate institution of high-dose parenteral corticosteroid therapy.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

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


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

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Adult

1-2 mg/kg/d PO qd or divided bid, followed by gradual reduction to lowest level that will maintain clinical response

Pediatric

0.5-1.7 mg/kg/d or 5-25 mg/m2/d PO/IV/IM qd or divided bid

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

Documented hypersensitivity; viral, fungal or tubercular skin 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

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Immunosuppressant agents

Inhibit key steps in the immune system responsible for inflammatory reactions.


Cyclosporine (Sandimmune, Neoral)

Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft-vs-host disease for a variety of organs. For children and adults, base dosing on ideal body weight.
Available dosage strengths include 25 mg, 50 mg, 100 mg/mL.

Adult

2-10 mg/kg/d PO qd or divided bid/tid

Pediatric

Administer as in adults

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease cyclosporine concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase cyclosporine toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin

Documented hypersensitivity; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UV-B radiation in psoriasis since it may increase risk of cancer

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

Precautions

Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin, and liver enzymes; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO


Methotrexate (Folex PFS, Rheumatrex)

Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness).
Adjust dose gradually to attain satisfactory response.

Adult

0.3 mg/kg/wk PO; not to exceed 25 mg/wk PO/IM/SC

Pediatric

Not established

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral methotrexate (MTX); charcoal lowers MTX levels; coadministration with etretinate may increase hepatotoxicity of MTX; folic acid or its derivatives contained in some vitamins may decrease response to MTX
Probenecid, NSAIDs, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, can increase MTX plasma levels; may decrease phenytoin plasma levels; 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); renal insufficiency

Pregnancy

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

Precautions

Monitor CBCs monthly, and liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); MTX has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood counts occur; fatal reactions reported when administered concurrently with NSAIDs


Azathioprine (Imuran)

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

Adult

1 mg/kg/d PO for 6-8 wk; increase by 0.5 mg/kg q4wk until response or dose reaches 4 mg/kg/d

Pediatric

Initial dose: 2-5 mg/kg/d PO/IV
Maintenance dose: 1-2 mg/kg/d PO/IV

Toxicity increases with allopurinol; concurrent use with ACE inhibitors may induce severe leukopenia; may increase levels of methotrexate metabolites and decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine

Documented hypersensitivity; low levels of serum thiopurine methyl transferase (TPMT)

Pregnancy

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

Precautions

Increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur; check TPMT level prior to therapy and follow liver, renal, and hematologic function; pancreatitis rarely associated

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
Multimedia: Giant Cell Arteritis
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

giant cell arteritis, GCA, temporal arteritis, cranial arteritis, Horton's disease, Horton disease, Horton arteritis, Horton's arteritis, granulomatous arteritis, polymyalgia rheumatica, vasculitis, migraine headache

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Contributor Information and Disclosures

Author

Manolette R Roque, MD, MBA, President and CEO, Service Chief of Ocular Immunology and Uveitis, Refractive Surgery, EYE REPUBLIC Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines; Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, St. Luke's Medical Center Global City; Senior Eye Surgeon, The LASIK Surgery Clinic
Manolette R Roque, MD, MBA is a member of the following medical societies: American Academy of Ophthalmic Executives, American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, American Society of Ophthalmic Administrators, American Uveitis Society, International Ocular Inflammation Society, Philippine Medical Association, Philippine Ocular Inflammation Society, and Philippine Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.

Coauthor(s)

Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, Eye Republic Ophthalmology Clinic
Disclosure: Nothing to disclose.

Elisabetta Miserocchi, MD, Fellow in Immunology and Uveitis Service, Department of Ophthalmology, Harvard Medical School
Disclosure: Nothing to disclose.

C Stephen Foster, MD, FACS, FACR, FAAO, Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution
C Stephen Foster, MD, FACS, FACR, FAAO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Kilbourn Gordon III, MD, FACEP, Urgent Care Physician
Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians & Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong
Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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