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Show The Immunopathology of Giant Cell Arteritis: Diagnostic and Therapeutic Implications We read with great interest the article "The immuno-pathology of giant cell arteritis: diagnostic and ther-apeutic implications" by Weyand et al (1) and commend the authors on their comprehensive review of giant cell arteritis (GCA) immunopathogenesis and excellent discus-sion of potential new therapeutic targets. Due to the adverse effects of steroids and lack of therapeutic response in some patients with GCA, clinicians have investigated the use of steroid-sparing agents, including anti-tumor necrosis factor (anti-TNF)-a agents, for GCA treatment. Case reports on the use of anti-TNF-a antibodies for GCA and one small placebo-controlled trial investigating the use of etanercept in GCA patients have been promising (2-7). However, occurrences of GCA despite use of anti-TNF-a antibodies have been reported in the literature (8,9). We add to these reports with a patient who developed arteritic anterior ischemic optic neuropathy secondary to biopsy-proven GCA despite use of etanercept, an anti-TNF agent. A 59-year-old Caucasian woman with rheumatoid arthritis treated with etanercept and leflunomide was referred for evaluation of sudden peripheral vision loss in her right eye. She reported a 2-week history of intermittent bilateral blurred vision and transient binocular vertical diplopia. She noted transient obscurations of vision during the week before her loss of vision. She also reported a 1-month history of bilateral jaw claudication, low-grade fevers and malaise, a 3-week history of daily global headaches, and weight loss of 15 lbs over the previous 6 weeks. She had been taking leflunomide for 2.5 years and etanercept for 1.5 years. Etanercept was discontinued for 3 weeks due to her low-grade fever and malaise and was restarted 1 week before her vision loss. On examination, her best-corrected visual acuity was 20/25 in each eye. Her color vision was slightly decreased in the right eye and full in the left eye (13/14 and 14/14 Hardy-Hand- Rittler plates, respectively). A right afferent pupillary defect was present. Automated visual field 24-2 SITA Standard testing demonstrated dense superior altitudinal and inferior arcuate defects in her right eye. Her left visual field was normal. Fundus examination revealed pallid optic disc edema with associated peripapillary hemorrhage in the right eye and a normal appearing disc in the left eye (Fig. 1). The right superficial temporal artery pulse was not palpable. Laboratory workup was notable for an erythrocyte sedimentation rate of 106 mm/hr and a C-reactive protein of 55.1 mg/L (normal: 0-10 mg/L). The patient was immediately treated with 100 mg of prednisone and a right temporal artery biopsy performed the same day demonstrated active GCA. She was subsequently admitted and treated with methylprednis-olone (250 mg intravenously 4 times a day) for 3 days and aspirin (81 mg) daily. At 1-month follow-up, her best-corrected FIG. 1. Right optic disc demonstrates pallid edema while the left disc is normal. 100 Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 95-104 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. visual acuity was 20/20 in each eye, and repeat Humphrey visual field was stable. Her right optic disc was diffusely pale with minimal residual edema. Given the paucity of cases, the potential role of TNF-a antagonists in the treatment of GCA is unclear. Interestingly, vasculitis has been reported to occur with use of TNF antag-onists, mainly in the form of leukocytoclastic vasculitis (10-12). One postulated mechanism for the development of vasculitis during the use of anti-TNF agents is direct drug toxicity to the vasculature. Other mechanisms include deposi-tion of anti-TNF/TNF immune complexes in the vessel wall with induction of a type III hypersensitivity reaction, reaction of autoantibodies with endothelial cells, paradoxical increased vulnerability to granulomatous vasculitis due to TNF defi-ciency, and a TNF antagonist-induced switch from a Th1 to a Th2 T-lymphocyte response (11). Whether any of these proposed mechanisms of vascular destruction underlie the development of GCA during use of TNF-a antagonists is un-known. While on long-term treatment with etanercept except for a 3-week drug holiday, our patient developed symptoms that, in retrospect, were most likely due to GCA. Although we cannot exclude the gap in therapy as a precipitating event of the patient's ischemic optic neuropathy, we believe this most likely was due to natural evolution of her disease process. Katharine Liegel, MD Steven Feldon, MD, MBA Zoë Williams, MD Department of Ophthalmology, Flaum Eye Institute, University of Rochester Medical Center, Rochester, New York Supported, in part, by an unrestricted grant from Research to Prevent Blindness. The authors report no conflicts of interest. ACKNOWLEDGMENTS The authors thank Haodong Xu, MD, of the Department of Pathology, University of Rochester Medical Center. REFERENCES 1. Weyand C, Liao YJ, Goronzy J. The immunopathology of giant cell arteritis: diagnostic and therapeutic implications. J Neuroophthalmol. 2012;32:259-265. 2. Tan A, Holdsworth J, Pease C, Emery P, McGonagle D. Successful treatment of resistant giant cell arteritis with etanercept. Ann Rheum Dis. 2003;62:373-374. 3. Uthman I, Kanj N, Atweh S. Infliximab as monotherapy in giant cell arteritis. Clin Rheumatol. 2006;25:109-110. 4. Airó P, Antonioli CM, Vianelli M, Toniati P. Anti-tumour necrosis factor treatment with infliximab in a case of giant cell arteritis resistant to steroid and immunosuppressive drugs. Rheumatology (Oxford). 2002;41:347-349. 5. Martínez-Toboada VM, Rodríguez-Valverde V, Carreño L, López- Longo J, Figueroa M, Belzunegui J, Mola EM, Bonilla G. A double-blind placebo controlled trial of etanercept in patients with giant cell arteritis and corticosteroid side effects. Ann Rheum Dis. 2008;67:625-630. 6. Cantini F, Niccoli L, Salvarani C, Padula A, Olivieri I. Treatment of longstanding active giant cell arteritis with infliximab: report of four cases. Arthritis Rheum. 2001;44:2933-2935. 7. Andonopoulos AP, Meimaris N, Daoussis D, Bounas A, Giannopoulos G. Experience with infliximab (anti-TNFa monoclonal antibody) as monotherapy for giant cell arteritis. Ann Rheum Dis. 2003;62:1116. 8. Leydet-Quilici H, Luc M, Armingeat T, Pham T, Lafforgue P. Giant cell arteritis during adalimumab treatment for rheumatoid arthritis. Joint Bone Spine. 2007;74:303-304. 9. Seton M. Giant cell arteritis in a patient taking etanercept and methotrexate. J Rheumatol. 2004;31:1467. 10. Mohan N, Edwards ET, Cupps TR, Slifman N, Lee JH, Siegel JN, Bruan MM. Leukocytoclastic vasculitis associated with tumour necrosis factor-a blocking agents. J Rheumatol. 2004;31:1955-1958. 11. Jarrett S, Cunnane G, Conaghan PG, Bingham SJ, Buch MH, Quinn MA, Emery P. Anti-tumour necrosis factor-a therapy-induced vasculitis: case series. J Rheumatol. 2003;30:2287-2291. 12. Cunnane G, Warnock M, Eye KH, Daikh DI. Accelerated nodulosis and vasculitis following etanercept therapy for rheumatoid arthritis. Arthritis Rheum. 2002;47:445-449. Radiation Optic Neuropathy After Proton Beam Therapy for Optic Nerve Sheath Meningioma I enjoyed reading the recent article regarding radia-tion optic neuropathy after proton beam therapy for optic nerve sheath meningioma by Siddiqui et al (1). The authors state "magnetic resonance imaging revealed enhancement of the right optic nerve consistent with radiation optic neuropathy." It is my experience that the optic nerve enhancement, as pictured in Figure 3B, also can result from a multitude of etiologies including extension of optic nerve sheath meningioma (2). Often it is difficult to differentiate the 2 on the fat-suppressed gadolinium-enhanced orbital magnetic resonance imaging. So, how do we know that the optic nerve enhancement was indeed from the radiation and not from progression of the optic nerve sheath meningioma? Michael Vaphiades, DO Departments of Ophthalmology, Neurology, and Neurosurgery, Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 95-104 101 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
