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Rheumatology Advance Access originally published online on September 6, 2009
Rheumatology 2009 48(11):1460-1461; doi:10.1093/rheumatology/kep271
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Letters to the Editor

MMP-12, a novel matrix metalloproteinase associated with giant cell arteritis

Alicia Rodríguez-Pla1, Francisco Martínez-Murillo2, Peter J. Savino3, Ralph C. Eagle, Jr4, Philip Seo5 and Mark J. Soloski1

1Division of Rheumatology, 2Johns Hopkins Microarray Core Facility, The Johns Hopkins University School of Medicine, Baltimore, MD, 3Neuro-Ophthalmology Service, 4Ocular-Pathology Service, Wills Eye Institute, Thomas Jefferson University, Philadelphia, PA and 5The Johns Hopkins Vasculitis Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA

Correspondence to: Alicia Rodríguez-Pla, Baylor Institute for Immunology Research, 3434 Live Oak Street, Dallas, TX 75204, USA. E-mail: Alicia.Pla@Baylorhealth.edu

The first 10% of the full text of this article appears below.


   Introduction
 
SIR, Identification of specific mediators of arterial damage in GCA is crucial to understand its pathogenesis, and may have important clinical implications both for diagnosis and treatment. Thirty-two non-consecutive patients who underwent a temporal artery biopsy for evaluation of GCA were included in this study. Nineteen of the 32 biopsies had histological evidence of GCA. Detailed pathological findings were recorded on every biopsy and assessed using semi-quantitative scales [1]. Patients’ demographic and clinical information was collected. All subjects gave written informed consent. The study . . . [Full Text of this Article]


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