Purpose High-dose corticosteroids (CS) are the mainstay of treatment for giant cell arteritis (GCA). A usually required long-term treatment with CS, ranging from 1 to 5 years or more, frequently leads to serious side effects in about 60% of patients. There are few reports of treatment of refractory or steroid dependent GCA with tumor necrosis factor a (TNFa) inhibitors, including infliximab and etanercept. We report a case of a refractory GCA treated successfully with adalimumab, a fully human recombinant IgG1 anti-TNFa monoclonal antibody.
Case Report A 70-year-old white female was admitted with a 2-week history of fatigue, night sweats, headache, jaw claudication, intermittent bilateral vision loss, unstable angina, and dyspnea in March 2005. Her physical examination was significant for blood pressure of 174/78, tender temporal arteries, and temporal visual field defect in the right eye. Significant laboratory values on admission included a normocytic normochromic anemia, thrombocytosis, an erythrocyte sedimentation rate of 69 mm/hr, and C-reactive protein 11.54 mg/dL. A temporal artery biopsy was diagnostic of GCA. She was treated with intravenous methylprednisolone 1 g daily for 3 days followed by prednisone 60 mg daily that resulted in resolution of her symptoms. She also underwent percutaneous coronary angioplasty with stent placement. Methotrexate (MTX) was added as a steroid-sparing agent. On tapering prednisone to 40 mg daily she developed cough, pleuritic chest pain, and dyspnea. A CT of chest revealed ground glass opacification in both lung fields suggestive of pneumonitis related to MTX, which was discontinued. She received another course of IV methylprednisolone due to flare of GCA manifested by decreased vision, constitutional symptoms, and elevated acute-phase reactants. Due to development of steroid-induced diabetes, she was placed on adalumimab as a steroid-sparing agent in September 2005. Prednisone was subsequently tapered to 20 mg daily within 2 months with no recurrent symptoms or increase in acute-phase reactants.
Discussion and Conclusion GCA is characterized by infiltration of the vessel wall by macrophages, giant cells, and T lymphocytes, with production of several cytokines responsible for the acute-phase response. TNFa has been demonstrated in up to 60% of the cells in all areas of inflamed arteries by immunohistochemical techniques; hence it could play a pivotal role in the pathogenesis of GCA. There is no conclusive evidence of the a inhibitors in resistant GCA should be studied in larger, controlled studies.
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