Aortitis Medication

Updated: Dec 18, 2014
  • Author: Masato Okada, MD, FACP, FACR, FAAAAI; Chief Editor: Uchechukwu Sampson, MBBS, MPH, MBA, MSc  more...
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Medication Summary

No reliable method exists for determining the activity of arteritis. According to vascular specimens obtained at the time of bypass surgery and sequential angiographic studies, active vasculitis is present in approximately 50% of patients who lack symptoms of active inflammation or have a normal ESR. To prevent progression of vascular lesions and to reduce the necessity of surgical procedures in the later stage, careful monitoring of disease activity with sequential imaging studies and more prolonged immunosuppressive treatments may be necessary.

As the prognosis of patients with Takayasu arteritis improves, prevention of atherosclerotic disorders becomes more important. Treatment of hypertension and congestive heart failure should be instituted if these complications occur, and serum cholesterol and homocysteine levels should be monitored, especially if the patients require long-term corticosteroid therapy.



Class Summary

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

Prednisone (Deltasone, Orasone, Sterapred)

Mainstay of therapy. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Daily doses should be given to patients with active Takayasu arteritis. As many as 75% of patients respond favorably to this regimen, but remaining patients, and patients who relapse with tapering, must receive immunosuppressants. Maximum reduction should be 10% of daily amount per week. Long-term low-dose therapy may be necessary to prevent progression of arterial stenoses. Complications include aseptic necrosis of hip, corticosteroid dependence, and ulcers.



Class Summary

A substantial percentage of patients with aortitis or other forms of vasculitis require additional immunosuppressive agents (eg, cyclophosphamide, methotrexate, mycophenolate mofetil).

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).

Weekly doses thought to be less toxic than daily doses of cyclophosphamide. In one study of 16 patients whose disease was resistant to corticosteroid therapy, weekly methotrexate (mean dose 17.1 mg; range 10-25 mg) produced remissions in 81%. Relapse occurred in 44% when corticosteroids were tapered to or near discontinuation. Reinstitution of corticosteroids led to remission, and 3 of 7 patients in this group successfully stopped glucocorticoid therapy.

Mycophenolate (CellCept)

Inhibits purine synthesis and proliferation of human lymphocytes. Promising published case report of 3 patients with resistant disease treated with mycophenolate mofetil. Reduced toxicity makes this regimen an attractive alternative.

Cyclophosphamide (Cytoxan)

Chemically related to nitrogen mustards. As alkylating agent, mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.


Anti-tumor Necrosis Factor Agents

Class Summary

These agents are disease modifying drugs.

Etanercept (Enbrel)

Soluble p75 TNF receptor fusion protein (sTNFR-Ig). Inhibits TNF binding to cell surface receptors, which, in turn, decreases inflammatory and immune responses.

Infliximab (Remicade)

Chimeric IgG1k monoclonal antibody that neutralizes cytokine TNF-a and inhibits its binding to TNF-a receptor. Reduces infiltration of inflammatory cells and TNF-a production in inflamed areas. Used with methotrexate in patients who have had inadequate response to methotrexate monotherapy.



Class Summary

Empiric antimicrobial therapy should cover all likely pathogens in the context of the clinical setting.

Minocycline (Dynacin, Minocin)

Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma.