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Uveitis as a Presenting Sign of Giant Cell Arteritis

Bandini, Fabio MD; Benedetti, Luana MD; Ceppa, Paola MD; Corallo, Guido MD

Journal of Neuro-Ophthalmology: September 2005 - Volume 25 - Issue 3 - p 247-248
doi: 10.1097/01.wno.0000177306.13458.56
Letters to the Editor

Laboratory of Neuro-ophthalmology Department of Neurosciences, Ophthalmology, and Genetics Department of Pathology University of Genoa Genoa, Italy

The relevance of uveitis as an ocular manifestation of giant cell arteritis (GCA) is controversial. Védrine et al (1) emphasized its occurrence as a presenting feature of GCA. In contrast, Salvarani et al (2) argued that the reported cases of uveitis and GCA could merely represent a chance association. We present a patient with biopsy-proven GCA who had developed an acute uveitis some weeks previously, for which the GCA can be considered the cause.

A 69-year-old hypertensive man complained of anorexia and a dull widespread headache. One week later he noted blurred vision, conjunctival hyperemia, and photophobia in the left eye. Examination elsewhere disclosed a visual acuity of 20/20 OD and 20/40 OS. Thin folds of Descemet's membrane were noted OS, together with keratic precipitates and flare in the anterior chamber. Intraocular pressures were 14 mm Hg OD and 13 mm Hg OS. There was no relative afferent pupillary defect. The fundus examination was unrevealing. The erythrocyte sedimentation rate (ESR) was not measured at that time. Acute anterior uveitis in the left eye was diagnosed.

The patient was treated with topical corticosteroids to which his ocular symptoms initially responded. Anorexia and headache, however, persisted. Three weeks later, the visual acuity in his OS suddenly dropped to no light perception, preceded by one week of fatigue, jaw claudication, and scalp tenderness. Physical and neurological examinations were normal but for tenderness of both temporal arteries. Neuro-ophthalmological examination did not reveal any abnormality OD. There was a left relative afferent pupillary defect. No signs of anterior uveitis were seen. The optic disc OS showed pallid swelling with a few peripapillary hemorrhages. Ocular motility was normal. Fluorescein angiography demonstrated diffuse hyperfluorescence of the left optic disc.

Laboratory tests revealed a hypochromic microcytic anemia, an erythrocyte sedimentation rate (ESR) of 90 mm/hr and a C-reactive protein of 28.1 mg/l (normal 0-5 mg/l). The angiotensin converting enzyme level, VDRL, thyroid function studies, autoantibody profile (including anticardiolipin antibodies), and computed tomography scan of head and orbits were all normal. Doppler imaging showed mild stenosis of the right internal carotid artery.

The patient was treated with intravenous methylprednisolone 250 mg every six hours for three days followed by oral prednisone 75 mg/day, with a dramatic and complete relief of the constitutional symptoms but no improvement in vision. The ESR decreased to 20 mm/hr after three days. A left temporal artery biopsy showed evidence of giant cell arteritis (Figure 1).

FIG. 1

FIG. 1

When last examined six months later, there was no recovery of vision in the OS, whose optic disc appeared pale. There were no keratic precipitates in the anterior chamber. Intraocular pressures were 15 mm Hg OD and 14 mm Hg OS.

Uveitis as a presenting feature of GCA is uncommon. To the best of our knowledge, there are only two reported patients (3,4). Unlike the patient of Rajesh and Cole (3), who suffered from a subacute bilateral panuveitis, our patient had a unilateral anterior uveitis, occurring only three weeks before GCA diagnosis was made. The patient of Dasgupta et al (4) had an acute anterior and posterior uveitis OS which preceded by two months the diagnosis of GCA. However, although their patient fulfilled the clinical criteria for GCA, her temporal artery biopsy was not indicative of arterial inflammation.

In order to avoid delays in treatment and devastating visual consequences, clinicians should be reminded that, although unusual, uveitis in elderly patients can be a presenting feature of GCA.

Fabio Bandini, MD

Luana Benedetti, MD

Paola Ceppa, MD

Guido Corallo, MD

Laboratory of Neuro-ophthalmology, Department of Neurosciences, Ophthalmology, and Genetics, Department of Pathology, University of Genoa Genoa, Italy

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1. Salvarani C, Cantini F, Boiardi L, Hunder GG. Polymyalgia reumatica and giant-cell arteritis. N Engl J Med 2002;347:261-71.
2. Védrine L, Algayres JP, Coutant G. Giant-cell arteritis. N Engl J Med 2003;348:1497-8.
3. Rajesh CV, Cole M. Panuveitis as a presenting feature of giant cell arteritis. Br J Ophthalmol 2000;84:340.
4. Dasgupta B, Pitzalis C, Panayi GS. Inflammation of the uveal tract as a presenting feature of temporal arteritis. Ann Rheum Dis 1989;48:964-5.
© 2005 Lippincott Williams & Wilkins, Inc.