Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus
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 authorPeter 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 authorRobin L. Brey
Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio
Search for more papers by this authorShalini 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 authorMatthew 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 authorMohammad Naqibuddin
Johns Hopkins University School of Medicine, Baltimore, Maryland
Search for more papers by this authorMargaret Sampedro
Johns Hopkins University School of Medicine, Baltimore, Maryland
Search for more papers by this authorStephen L. Holliday
Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio
Search for more papers by this authorCrystal Franklin
University of Texas Health Science Center at San Antonio
Search for more papers by this authorDaniel J. Wallace
Cedars-Sinai Medical Center/David Geffen School of Medicine, University of California, Los Angeles
Search for more papers by this authorMichael H. Weisman
Cedars-Sinai Medical Center/David Geffen School of Medicine, University of California, Los Angeles
Search for more papers by this authorMichelle Petri
Johns Hopkins University School of Medicine, Baltimore, Maryland
Search for more papers by this authorCorresponding 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 authorPeter 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 authorRobin L. Brey
Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio
Search for more papers by this authorShalini 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 authorMatthew 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 authorMohammad Naqibuddin
Johns Hopkins University School of Medicine, Baltimore, Maryland
Search for more papers by this authorMargaret Sampedro
Johns Hopkins University School of Medicine, Baltimore, Maryland
Search for more papers by this authorStephen L. Holliday
Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio
Search for more papers by this authorCrystal Franklin
University of Texas Health Science Center at San Antonio
Search for more papers by this authorDaniel J. Wallace
Cedars-Sinai Medical Center/David Geffen School of Medicine, University of California, Los Angeles
Search for more papers by this authorMichael H. Weisman
Cedars-Sinai Medical Center/David Geffen School of Medicine, University of California, Los Angeles
Search for more papers by this authorMichelle Petri
Johns Hopkins University School of Medicine, Baltimore, Maryland
Search for more papers by this authorAbstract
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.
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