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

Amy E. Ramage, Peter T. Fox, Robin L. Brey, Shalini Narayana, Matthew D. Cykowski, Mohammad Naqibuddin, Margaret Sampedro, Stephen L. Holliday, Crystal Franklin, Daniel J. Wallace, Michael H. Weisman, Michelle Petri

Research output: Contribution to journalArticle

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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.

Original languageEnglish (US)
Pages (from-to)3048-3057
Number of pages10
JournalArthritis and rheumatism
Volume63
Issue number10
DOIs
StatePublished - Oct 1 2011

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Neuroimaging
Systemic Lupus Erythematosus
Inflammation
Estrogens
Safety
Central Nervous System
Glucose
Atrophy
Parietal Lobe
White Matter
Fluorodeoxyglucose F18
Frontal Lobe
Vasculitis
Neurologic Manifestations
Positron-Emission Tomography
Autoantibodies
Apoptosis
Pathology
Morbidity

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Rheumatology
  • Immunology
  • Pharmacology (medical)

Cite this

Ramage, A. E., Fox, P. T., Brey, R. L., Narayana, S., Cykowski, M. D., Naqibuddin, M., ... Petri, M. (2011). Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus. Arthritis and rheumatism, 63(10), 3048-3057. https://doi.org/10.1002/art.30458

Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus. / Ramage, Amy E.; Fox, Peter T.; Brey, Robin L.; Narayana, Shalini; Cykowski, Matthew D.; Naqibuddin, Mohammad; Sampedro, Margaret; Holliday, Stephen L.; Franklin, Crystal; Wallace, Daniel J.; Weisman, Michael H.; Petri, Michelle.

In: Arthritis and rheumatism, Vol. 63, No. 10, 01.10.2011, p. 3048-3057.

Research output: Contribution to journalArticle

Ramage, AE, Fox, PT, Brey, RL, Narayana, S, Cykowski, MD, Naqibuddin, M, Sampedro, M, Holliday, SL, Franklin, C, Wallace, DJ, Weisman, MH & Petri, M 2011, 'Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus', Arthritis and rheumatism, vol. 63, no. 10, pp. 3048-3057. https://doi.org/10.1002/art.30458
Ramage, Amy E. ; Fox, Peter T. ; Brey, Robin L. ; Narayana, Shalini ; Cykowski, Matthew D. ; Naqibuddin, Mohammad ; Sampedro, Margaret ; Holliday, Stephen L. ; Franklin, Crystal ; Wallace, Daniel J. ; Weisman, Michael H. ; Petri, Michelle. / Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus. In: Arthritis and rheumatism. 2011 ; Vol. 63, No. 10. pp. 3048-3057.
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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.",
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