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Rheumatology Advance Access originally published online on February 19, 2008
Rheumatology 2008 47(4):488-490; doi:10.1093/rheumatology/ken012
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Is intimal hyperplasia a marker of neuro-ophthalmic complications of giant cell arteritis?

D. Makkuni1, A. Bharadwaj1, K. Wolfe2, S. Payne2, A. Hutchings3 and B. Dasgupta1

1Department of Rheumatology, 2Department of Pathology, Southend University Hospital, Westcliff on Sea, Essex and 3Health Services Research Unit, London School of Hygiene & Tropical Medicine, London, UK.

Correspondence to: B. Dasgupta, Department of Rheumatology, Southend University Hospital, Prittlewell Chase, Westcliff on Sea, Essex SS0 0RY, UK. E-mail: bhaskar.dasgupta{at}southend.nhs.uk


   Abstract

Objective. The ischaemic complications of giant cell arteritis (GCA) such as blindness and stroke may result from luminal narrowing of the affected arteries. This study focuses on the association between the severity of intimal proliferation on temporal artery biopsy (TAB) histology and neuro-ophthalmic complications (NOCs) of GCA.

Method. We identified 30 cases of biopsy-proven temporal arteritis. One histopathologist (blinded to the clinical details) evaluated the TAB specimens and categorized the degree of maximum stenosis due to intimal hyperplasia into four grades: grade 1 is <50% luminal occlusion due to intimal hyperplasia, grade 2 is 50–75%, grade 3 is >75% and grade 4 is complete luminal occlusion. A second histopathologist (also blinded to the clinical details) independently evaluated the TAB specimens using the same grading system. The NOCs in these patients were noted after a case record review.

Results. Of the 30 patients, 12 had NOC-10 with eye complications (complete visual loss, anterior ischaemic neuropathy, visual field defects), one patient had cerebral infarcts and one had both cerebral infarcts and vision loss. There was evidence for a statistically significant trend of NOC associated with higher intimal hyperplasia scores (P = 0.001). The scores of the histopathologists agreed for 23 (77%) patients and differed by 1 category for the remaining 7 ({kappa}-statistic 0.88).

Conclusions. Our study suggests that the degree of intimal hyperplasia on TAB histology (routinely available to all hospital units) seems to be closely associated with NOCs of GCA. The study highlights the possible prognostic as well as diagnostic role of the biopsy. We feel that intimal hyperplasia noted in biopsy specimens may help us in the risk stratification of GCA patients and targeting of appropriate and novel therapies.

KEY WORDS: Intimal hyperplasia, Giant cell arteritis, Neuro-ophthalmic complications

Submitted 1 June 2007; revised version accepted 7 January 2008.
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