Which medications in the drug class Corticosteroids are used in the treatment of Giant Cell Arteritis (Temporal Arteritis)?

Updated: Sep 10, 2020
  • Author: Mythili Seetharaman, MD; Chief Editor: Herbert S Diamond, MD  more...
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These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli and inhibit the synthesis of tumor necrosis factor (TNF)-alpha, interleukin-2 (IL-2), IL-6, and interferon (IFN)-gamma. In addition, glucocorticoids modulate serum and leukocyte-bound levels of cell adhesion molecules.

Corticosteroid therapy for GCA is started at high doses with gradual tapering, using clinical manifestations and the erythrocyte sedimentation rate (ESR) to gauge disease activity. An initial dose of 40-60 mg/d of prednisone (or equivalent) in a single or divided dose is adequate in the vast majority of cases. This dose is usually given for 2-4 weeks until all reversible signs and symptoms have resolved and levels of acute-phase reactants are back to normal. The dose is then gradually reduced every 1-2 weeks by a maximum of 10% of the total daily dose.

Most patients are treated for 1-2 years, but some with a prolonged or relapsing course may require low doses of steroids for several years. Clinical flares usually occur when the prednisone is reduced to 5-10 mg/d.

Prednisone (Rayos)

The drug of choice in GCA, prednisone is an oral corticosteroid that must be metabolized in the liver to its active metabolite, prednisolone. Prednisone decreases inflammation by suppressing migration of polymorphonuclear neutrophils (PMNs) and reversing increased capillary permeability.

Typical patients require prednisone for 1-2 y with daily initial doses of 40-60 mg. In acute neurologic syndrome or rapidly worsening neurologic status—whether visual loss, mononeuritis multiplex, or acute encephalopathy—treatment may begin with IV pulses over several days.

A patient with GCA who has a relapse may require only a modest dose increment to control flare in symptoms. Following initiation of treatment, ESR may be expected to drop within days and become normal in 1-2 wk. All neurologic deficits can improve, but irreversible end-organ infarction may preclude clinically significant gains in some patients.

Neurovascular complications may occur during initial tapering of corticosteroid dosage (often around 1 mo after beginning treatment), underscoring the need for ESR monitoring and the importance of small steroid decrements. The doses described below are suggested for general consideration. Tailor dosing regimens to medical circumstances confronting patient.

Prednisolone (Flo-Pred, Prelone, Millipred, Orapred)

Prednisolone decreases inflammation by suppressing migration of PMNs and reducing capillary permeability.

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

Methylprednisolone decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability. This agent is slightly more potent than prednisone; 4 mg of methylprednisolone is equivalent to 5 mg of prednisone.

Dexamethasone (Baycadron)

Dexamethasone is a glucocorticoid that acts as an immunosuppressant by stimulating the synthesis of enzymes needed to decrease the inflammatory response. It also acts as an anti-inflammatory agent by inhibiting the recruitment of leukocytes and monocyte-macrophages into affected areas via inhibition of chemotactic factors and factors that increase capillary permeability.

Dexamethasone is readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.

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