Share this article on:

Throat Pain as a Presenting Symptom of Giant Cell Arteritis

Ling, Jeanie D. BS; Hashemi, Nafiseh MD; Lee, Andrew G. MD

Journal of Neuro-Ophthalmology: December 2012 - Volume 32 - Issue 4 - p 384
doi: 10.1097/WNO.0b013e318270ffaf
Letter to the Editor

Baylor College of Medicine, Houston, Texas

Department of Ophthalmology, The Methodist Hospital, Houston, Texas

Department of Ophthalmology, The Methodist Hospital, Houston, Texas

Department of Ophthalmology, Neurology, and Neurosurgery, Weill Cornell Medical College, New York, New York

Department of Ophthalmology (Adjunct Professor) Baylor College of Medicine, Houston, Texas

Department of Ophthalmology, The University of Texas Medical Branch, Galveston, Texas

Department of Ophthalmology (Adjunct Professor) The University of Iowa Hospitals and Clinic, Iowa City, Iowa

The authors report no conflict of interest.

We read with great interest the state-of-the-art review on giant cell arteritis (GCA) by Weyand (1). We recently saw a 76-year-old man who presented with severe throat pain to the point where he had difficulty swallowing. He was treated with doxycycline for “strep throat”, although swabs and culture were not performed. He failed to improve and developed hoarseness and unintentional weight loss of 10–15 pounds. Three months after developing a sore throat, the patient experienced jaw claudication without headache, scalp tenderness, or night sweats. Two months later, he had several episodes of transient monocular vision loss in the left eye, reporting “snowflakes” in the superior left visual field. Five days later, he experienced abrupt vision loss in the left eye. His medical and surgical histories, medication use, and review of systems otherwise were negative.

Neuro-ophthalmic examination revealed visual acuity of 20/40, right eye, because of a cataract, and hand motions, left eye. There was a left relative afferent pupillary defect, ocular motility was normal, and funduscopy showed right optic disc hyperemia and the left disc had pallid edema. Fluorescein angiography confirmed bilateral optic disc leakage while choroidal and retinal filling times were normal.

Erythrocyte sedimentation rate (ESR) was 84 mm/h. The patient was treated with intravenous methylprednisolone (1,000 mg) and then switched to 80 mg of oral prednisone per day. A temporal artery biopsy revealed chronic inflammation, histiocytes, and giant cells within the vessel wall with destruction of the internal elastic lamina.

Over the next 2 weeks, the patient’s sore throat, hoarseness, and jaw claudication resolved. His visual acuity remained unchanged and after 6 weeks of treatment, his ESR was 5 mm/h, and he was clinically stable.

Our patient presented with respiratory tract symptoms that, we believe, were due to inflammation of branches of external carotid arteries (ascending pharyngeal arteries) causing reversible ischemic injury to pharyngeal tissue. Larson et al (2) reported that 9% of GCA patients present with prominent respiratory symptoms, such as cough, sore throat, and hoarseness, whereas respiratory tract symptoms are the initial complaints among 4% of the patients with GCA (3). These symptoms usually resolve quickly with steroid treatment. Other respiratory symptoms of GCA include nonproductive cough, changes in voice, fatigue and pain in the tongue, and dyspnea with orthopnea (3–6). Aortitis might also produce hoarseness in GCA from involvement of the recurrent laryngeal nerve (7).

Our patient’s initial presentation of isolated throat pain resulting from GCA is unusual (8,9). Subsequently, he developed more classic manifestations of the disorder, including jaw claudication and arteritic anterior ischemic optic neuropathy. Our case serves as a reminder to the clinician of the diverse clinical presentations of GCA.

Back to Top | Article Outline


1. Weyand C, Liao YJ, Goronzy JJ. The immunopathology of giant cell arteritis: Diagnostic and therapeutic implications. J Neuroophthalmol. 2012;32:259–265.
2. Larson TS, Hall S, Hepper NGG, Hunder GG. Respiratory tract symptoms as a clue to giant cell arteritis. Ann Int Med. 1984;101:594–597.
3. Hunder GG. Clinical features of GCA/PMR. Clin Exp Rheumatol. 2000;18(suppl 20):S6–S8.
4. Nelson DA. Speech pathology in giant cell arteritis. Ann Otol Rhinol Laryngol. 1989;98:859–862.
5. Carassou P, Aletti M, Cinquetti G, Banal F, Landais C, Graffin B, Carli P. Respiratory manifestations of giant cell arteritis: 8 cases and review of the literature. Presse Med. 2010;39:e188–e196.
6. Manganelli P, Fietta P, Carotti M, Pesci A, Salaffi F. Respiratory system involvement in systemic vasculitides. Clin Exp Rheumatol. 2006;24(2 suppl 41):S48–S59.
7. Edrees A. Ortner’s syndrome as a presenting feature of giant cell arteritis. Reumatol Int. [published online ahead of print May 29, 2010] doi: 10.1007/s00296-010-1533-z.
8. Pfeiffer J, Ridders GJ. An old woman with a severe sore throat. J Am Geriatrics Soc. 2009;57:1118–1119.
9. Lemos J, Vaz A, Mós M, Ribeiro P, Monteiro A, Henriques P. Temporal arteritis: a confounding diagnosis. Acta Med Port. 2011;24:355–360.
© 2012 Lippincott Williams & Wilkins, Inc.