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Br J Ophthalmol 2004;88:298-301 doi:10.1136/bjo.2003.021592
  • Letter

Heparin therapy in giant cell arteritis

  1. L M Buono1,
  2. R Foroozan2,
  3. M de Virgiliis3,
  4. P J Savino4
  1. 1Neuro-Ophthalmology Service, Duke University Eye Center, Erwin Road, Box 3802, Durham, NC 27710, USA
  2. 2The Cullen Eye Institute, Baylor College of Medicine, Department of Ophthalmology, 6565 Fannin Street, NC-205, Houston, TX 77030, USA
  3. 3Department of Ophthalmology, Hospital Pedro Lagleyze, Buenos Aires, Argentina
  4. 4Neuro-Ophthalmology Service, Wills Eye Hospital, Thomas Jefferson Medical College, 840 Walnut Street, Philadelphia, PA 19107, USA
  1. Correspondence to: Dr Lawrence M Buono Duke University Eye Center, Erwin Road, Box 3802, Durham, NC 27710, USA; buono001mc.duke.edu
  • Accepted 19 March 2003

Giant cell arteritis (GCA) is a systemic vasculitis that affects large and medium sized arteries. Visual loss is one of the most devastating complications of GCA and usually occurs from occlusion of the posterior ciliary arteries (PCA) leading to anterior ischaemic optic neuropathy (AION). Visual loss can also occur from occlusion of other arteries that supply the visual pathway, such as the central retinal and ophthalmic arteries.

Corticosteroid therapy, given orally or intravenously, is the standard treatment for GCA associated visual loss.1 The optimal route of administration and dosage to prevent further visual loss are not known; however, most clinicians advocate higher doses in patients who already have experienced visual loss. Treatment with corticosteroids usually results in stabilisation of visual loss and some patients may have some degree of visual recovery.2,3 However, despite treatment with high dose intravenous corticosteroids, visual loss may progress.1 The reported use of adjunctive agents under these circumstances has been limited. We report a patient who had progressive visual loss while on high dose intravenous corticosteroids and who markedly improved after treatment with heparin.

Case report

An 85 year old man presented to his optometrist for a routine eye examination. His visual acuity was 20/40 both eyes and his optic discs were normal. Three weeks later (day 1), he lost vision in his right eye. His visual acuity was now 20/100 right eye and 20/40 left eye. On visual field testing with static perimetry he had an inferior altitudinal defect in the right eye and his visual field was normal in the left. His right optic disc was pale and oedematous and his left optic disc was normal. He was suspected of having GCA and was admitted for treatment with intravenous methylprednisolone (IVMP) 250 mg every 6 hours. On day 2, the visual field …

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