Volume 63, Issue 10 pp. 3048-3057
Systemic Lupus Erythematosus

Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus

Amy E. Ramage

Corresponding Author

Amy E. Ramage

University of Texas Health Science Center at San Antonio and Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio

UTHSCSA, Research Imaging Institute, 7703 Floyd Curl Drive, MSC 6240, San Antonio, TX 78229Search for more papers by this author
Peter T. Fox

Peter T. Fox

University of Texas Health Science Center at San Antonio and Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio

Search for more papers by this author
Robin L. Brey

Robin L. Brey

Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio

Search for more papers by this author
Shalini Narayana

Shalini Narayana

University of Texas Health Science Center at San Antonio and Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio

Search for more papers by this author
Matthew D. Cykowski

Matthew D. Cykowski

University of Texas Health Science Center at San Antonio and University of Oklahoma Health Sciences Center, Oklahoma City

Search for more papers by this author
Mohammad Naqibuddin

Mohammad Naqibuddin

Johns Hopkins University School of Medicine, Baltimore, Maryland

Search for more papers by this author
Margaret Sampedro

Margaret Sampedro

Johns Hopkins University School of Medicine, Baltimore, Maryland

Search for more papers by this author
Stephen L. Holliday

Stephen L. Holliday

Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio

Search for more papers by this author
Crystal Franklin

Crystal Franklin

University of Texas Health Science Center at San Antonio

Search for more papers by this author
Daniel J. Wallace

Daniel J. Wallace

Cedars-Sinai Medical Center/David Geffen School of Medicine, University of California, Los Angeles

Search for more papers by this author
Michael H. Weisman

Michael H. Weisman

Cedars-Sinai Medical Center/David Geffen School of Medicine, University of California, Los Angeles

Search for more papers by this author
Michelle Petri

Michelle Petri

Johns Hopkins University School of Medicine, Baltimore, Maryland

Search for more papers by this author
First published: 26 May 2011
Citations: 52

Abstract

Objective

Central nervous system (CNS) involvement occurs frequently in systemic lupus erythematosus (SLE) and frequently results in morbidity. The primary pathophysiology of CNS involvement in SLE is thought to be inflammation secondary to autoantibody-mediated vasculitis. Neuroimaging studies have shown hypometabolism (representing impending cell failure) and atrophy (representing late-stage pathology), but not inflammation. The purpose of this study was to detect the presence and regional distribution of inflammation (hypermetabolism) and tissue failure, apoptosis, or atrophy (hypometabolism).

Methods

Eighty-five patients with newly diagnosed SLE, who had no focal neurologic symptoms, were studied. Disease activity was quantified using the Safety of Estrogens in Lupus Erythematosus: National Assessment version of the SLE Disease Activity Index (SELENA–SLEDAI), a validated index of SLE-related disease activity. 18Fluorodeoxyglucose (FDG) positron emission tomography (PET) images of glucose uptake were analyzed by visual inspection and as group statistical parametric images, using the SELENA–SLEDAI score as the analysis regressor.

Results

SELENA–SLEDAI–correlated increases in glucose uptake were found throughout the white matter, most markedly in heavily myelinated tracts. SELENA–SLEDAI–correlated decreases were found in the frontal and parietal cortex, in a pattern similar to that seen during visual inspection and presented in previous reports of hypometabolism.

Conclusion

The SELENA–SLEDAI–correlated increases in glucose consumption are potential evidence of inflammation, consistent with prior reports of hypermetabolism in inflammatory disorders. To our knowledge, this is the first imaging-based evidence of SLE-induced CNS inflammation in an SLE inception cohort. The dissociation among 18FDG uptake characteristics, spatial distribution, and disease activity correlation is in accordance with the notion that glucose hypermetabolism and hypometabolism reflect fundamentally different aspects of the pathophysiology of SLE with CNS involvement.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.

click me