eMedicine Specialties > Emergency Medicine > Rheumatology
Temporal Arteritis: Treatment & Medication
Updated: Sep 8, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
Patients generally do not present via emergency medical services, and no particular prehospital interventions are warranted.
Emergency Department Care
Optimal care of patients with temporal arteritis in the emergency department involves maintaining a high index of suspicion and a low threshold to treat.
Treatment consists of corticosteroids. Although corticosteroids are the only proven treatment of temporal arteritis, few studies exist regarding dosing protocols. It is generally agreed that patients with suspected temporal arteritis should be started on oral prednisone 60 mg/day in the emergency department, with a temporal artery biopsy performed as an outpatient procedure scheduled within 1 week.
Improvement of systemic symptoms typically occurs within 72 hours of initiation of therapy. Patients should be counseled that corticosteroid therapy may be lengthy (1-2 y) and can lead to the typical complications associated with long-term steroid use. Recent data suggest that initial high-dose intravenous corticosteroid administration is beneficial in reducing temporal arteritis remission rates.4 However, further study is warranted before this is routinely practiced.
Consultations
An ophthalmologist should be consulted for a complete, dilated ocular examination to rule out other causes of vision loss, particularly when the diagnosis is uncertain.
A rheumatologist or internist should direct follow-up care for these patients, monitor remissions and recurrence, and manage complications associated with long-term corticosteroid therapy.
Medication
Systemic steroids should be started. Oral steroids are effective. Intravenous steroids may be administered if visual deficit is established or if the patient requires admission for other reasons.
Glucocorticoids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects.
Prednisone (Deltasone, Sterapred, Orasone)
DOC in treatment of temporal arteritis. Useful in treatment of inflammatory and allergic reactions by reversing increased capillary permeability and suppressing PMN activity.
In prolonged treatment, taper over 1-2 wk.
Adult
1-2 mg/kg/d PO
Pediatric
4-5 mg/m2/d
Alternatively, administer 1-2 mg/kg PO qd
Coadministration with estrogens may decrease prednisone 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 with coadministration of diuretics
Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease; use with caution in patients with diabetes
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; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Methylprednisolone (Solu-Medrol, Medrol, Depo-Medrol)
Decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability.
Adult
125-250 mg IV loading dose, followed by 0.5-1 mg/kg/dose q6h, not to exceed 3 d
Pediatric
2 mg/kg IV loading dose, followed by 0.5-1 mg/kg/dose q6h, not to exceed 3 d
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; use with care in patients with diabetes
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
Immunosuppressants
These agents suppress key factors of the immune system involved in immune reactions.
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 qd for 6-8 wk; increase by 0.5 mg/kg q4wk until response or dose reaches 2.5 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 MTX 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 monitor liver, renal, and hematologic function; pancreatitis rarely associated
Methotrexate (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/IM; not to exceed 20 mg
Pediatric
Not established
Oral aminoglycosides may decrease absorption and blood levels of concurrent oral 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
X - Contraindicated; benefit does not outweigh risk
Precautions
Monitor CBCs monthly and monitor 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 occurs; fatal reactions reported when administered concurrently with NSAIDs
More on Temporal Arteritis |
| Overview: Temporal Arteritis |
| Differential Diagnoses & Workup: Temporal Arteritis |
 Treatment & Medication: Temporal Arteritis |
| Follow-up: Temporal Arteritis |
| Multimedia: Temporal Arteritis |
| References |
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References
Wiszniewska M, Devuyst G, Bogousslavsky J. Giant cell arteritis as a cause of first-ever stroke. Cerebrovasc Dis. 2007;24(2-3):226-30. [Medline].
Hunder GG, Bloch DA, Michel BA, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum. Aug 1990;33(8):1122-8. [Medline].
Karahaliou M, Vaiopoulos G, Papaspyrou S, et al. Colour duplex sonography of temporal arteries before decision for biopsy: a prospective study in 55 patients with suspected giant cell arteritis. Arthritis Res Ther. 2006;8(4):R116. [Medline].
[Best Evidence] Mazlumzadeh M, Hunder GG, Easley KA, et al. Treatment of giant cell arteritis using induction therapy with high-dose glucocorticoids: a double-blind, placebo-controlled, randomized prospective clinical trial. Arthritis Rheum. Oct 2006;54(10):3310-8. [Medline].
Mahr AD, Jover JA, Spiera RF, et al. Adjunctive methotrexate for treatment of giant cell arteritis: an individual patient data meta-analysis. Arthritis Rheum. Aug 2007;56(8):2789-97. [Medline].
Barrier J, Bignon JD, Soulillou JP, et al. Increased prevalence of HLA-DR4 in giant-cell arteritis. N Engl J Med. Jul 9 1981;305(2):104-5. [Medline].
Bongartz T, Matteson EL. Large-vessel involvement in giant cell arteritis. Curr Opin Rheumatol. Jan 2006;18(1):10-7. [Medline].
Cantini F, Niccoli L, Storri L, et al. Are polymyalgia rheumatica and giant cell arteritis the same disease?. Semin Arthritis Rheum. Apr 2004;33(5):294-301. [Medline].
Carroll SC, Gaskin BJ, Danesh-Meyer HV. Giant cell arteritis. Clin Experiment Ophthalmol. Mar 2006;34(2):159-73; quiz 194. [Medline].
Cid MC, Font C, Oristrell J, et al. Association between strong inflammatory response and low risk of developing visual loss and other cranial ischemic complications in giant cell (temporal) arteritis. Arthritis Rheum. Jan 1998;41(1):26-32. [Medline].
Cornblath WT, Eggenberger ER. Progressive visual loss from giant cell arteritis despite high-dose intravenous methylprednisolone. Ophthalmology. May 1997;104(5):854-8. [Medline].
De Silva M, Hazleman BL. Azathioprine in giant cell arteritis/polymyalgia rheumatica: a double-blind study. Ann Rheum Dis. Feb 1986;45(2):136-8. [Medline].
Eberhardt RT, Dhadly M. Giant cell arteritis: diagnosis, management, and cardiovascular implications. Cardiol Rev. Mar-Apr 2007;15(2):55-61. [Medline].
Fardet L, Flahault A, Kettaneh A, et al. Corticosteroid-induced clinical adverse events: frequency, risk factors and patient's opinion. Br J Dermatol. Jul 2007;157(1):142-8. [Medline].
Gabriel SE, Espy M, Erdman DD, et al. The role of parvovirus B19 in the pathogenesis of giant cell arteritis: a preliminary evaluation. Arthritis Rheum. Jun 1999;42(6):1255-8. [Medline].
Gonzalez-Gay MA. Genetic epidemiology. Giant cell arteritis and polymyalgia rheumatica. Arthritis Res. 2001;3(3):154-7. [Medline].
Haugeberg G, Bie R, Nordbo SA. Temporal arteritis associated with Chlamydia pneumoniae DNA detected in an artery specimen. J Rheumatol. Jul 2001;28(7):1738-9. [Medline].
Hellmann DB. Temporal arteritis: a cough, toothache, and tongue infarction. JAMA. Jun 12 2002;287(22):2996-3000. [Medline].
Horton BT, et al. Arteritis of temporal vessels: report of 7 cases. Proc Staff Meet Mayo Clin. 1937;12:548-53.
Hunder GG. Giant cell arteritis and polymyalgia rheumatica. Med Clin North Am. Jan 1997;81(1):195-219. [Medline].
Imrich R, Bosak V, Rovensky J. Polymyalgia rheumatica and temporal arteritis: the endocrine relations and the pathogenesis. Review. Endocr Regul. Sep 2006;40(3):83-9. [Medline].
Parikh M, Miller NR, Lee AG, et al. Prevalence of a normal C-reactive protein with an elevated erythrocyte sedimentation rate in biopsy-proven giant cell arteritis. Ophthalmology. Oct 2006;113(10):1842-5. [Medline].
Regan MJ, Wood BJ, Hsieh YH, et al. Temporal arteritis and Chlamydia pneumoniae: failure to detect the organism by polymerase chain reaction in ninety cases and ninety controls. Arthritis Rheum. Apr 2002;46(4):1056-60. [Medline].
Rodriguez-Pla A, Bosch-Gil JA, Echevarria-Mayo JE, et al. No detection of parvovirus B19 or herpesvirus DNA in giant cell arteritis. J Clin Virol. Sep 2004;31(1):11-5. [Medline].
Salvarani C, Cantini F, Boiardi L, et al. Polymyalgia rheumatica and giant-cell arteritis. N Engl J Med. Jul 25 2002;347(4):261-71. [Medline].
Unwin B, Williams CM, Gilliland W. Polymyalgia rheumatica and giant cell arteritis. Am Fam Physician. Nov 1 2006;74(9):1547-54. [Medline].
Wagner AD, Wittkop U, Prahst A, et al. Dendritic cells co-localize with activated CD4+ T cells in giant cell arteritis. Clin Exp Rheumatol. Mar-Apr 2003;21(2):185-92. [Medline].
Watts RA, Gonzalez-Gay MA, Lane SE, et al. Geoepidemiology of systemic vasculitis: comparison of the incidence in two regions of Europe. Ann Rheum Dis. Feb 2001;60(2):170-2. [Medline].
Weyand CM, Goronzy JJ. Arterial wall injury in giant cell arteritis. Arthritis Rheum. May 1999;42(5):844-53. [Medline].
Weyand CM, Goronzy JJ. Medium- and large-vessel vasculitis. N Engl J Med. Jul 10 2003;349(2):160-9. [Medline].
Weyand CM, Hicok KC, Hunder GG, et al. The HLA-DRB1 locus as a genetic component in giant cell arteritis. Mapping of a disease-linked sequence motif to the antigen binding site of the HLA-DR molecule. J Clin Invest. Dec 1992;90(6):2355-61. [Medline].
Further Reading
Keywords
TA, temporal arteritis, GCA, giant cell arteritis, cranial arteritis, vasculitis, systemic vasculopathy, temporal-located headaches, ischemic optic neuritis, headache, cephalgia, impaired vision, vision loss, jaw claudication, sixth nerve palsy, afferent pupillary defect, temporalarteritis, ophthalmic emergency, blindness, arteritic ischemic optic neuropathy
