Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
On abdominal MRI, systemic lupus erythematosus (SLE) may be characterized by hepatomegaly, pancreatic parenchymal enlargement, and hypervascularity of mesentery. On cardiac MRI, SLE may be characterized by mitral leaflet thickening, pericardial thickness, and pericardial effusions. On brain MRI, SLE may be characterized by white matter lesions, changes in blood circulation of the brain, and patchy areas of enhancement. On musculoskeletal MRI, SLE may be characterized by intramuscular edema, proliferative tenosynovitis, and bone marrow edema.
Key MRI findings in systemic lupus erythematosus
Most of the SLE complications can be visualized with other more feasible imaging techniques. So, MRI is not the imaging modality of choice for the diagnosis of most complications of SLE, but if done, the following changes can be found in different organ systems of the body:
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Disease
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MRI
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| Gastrointestinal system
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Hepatitis
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- Hepatomegaly
- Nodules that ranging around 0.5-4.5 cm in diameter
- T2: nonspecific, increased periportal edema
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| Acute pancreatitis
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- Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis
- Abnormalities that may be seen in the pancreas include:
- Parenchymal enlargement
- Surrounding retroperitoneal fat stranding
- Abscess formation
- Circumscribed fluid collection
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| Mesenteric vasculitis
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- Comb sign
- Hypervascular appearance of the mesentery
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| Cardiac involvement
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Mitral stenosis
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- Mitral leaflet thickening
- Reduced diastolic opening
- Abnormal valve motion toward the left ventricular outflow tract
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| Acute pericarditis
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- The normal pericardial thickness is considered 2 mm while a thickness of over 4 mm suggests a pericarditis
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| Pericardial effusion
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- Fluid density material surrounding the heart
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| Myocarditis
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- Regional or global wall motion abnormalities
- Pericardial effusion
- Early postcontrast enhancement due to regional vasodilatation and increased blood volume, secondary to the inflammation
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| Neurological involvement
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General
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- Focal neurological defects
- White matter lesions
- Periventricular hyperintensities
- Detects clinically silent lesions
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| Stroke
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- Changes in brain vessel blood flow (occlusion on MRA)
- No parenchymal changes
- Slow or stagnant flow in vessels as a loss of normal flow void
- High T2 signal after 6 hours of stoke
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| Neuropathies
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- Optic neuritis
- Retrobulbar intra-orbital segment of the optic nerve appears swollen
- High T2 signal that may persists and be permanent
- Chronic involvement of optic nerve
- Atrophied nerve
- Contrast enhancement of the nerve, best seen with fat-suppressed T1 coronal images
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| Autoimmune encephalitis
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- Mostly in temporal lobes and limbic systems
- Bilateral involvement is most common (60%), although often asymmetric
- Cortical thickening
- Increased T2/FLAIR signal intensity of affected regions
- Patchy areas of enhancement
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| Musculoskeletal involvement
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Raynaud phenomen
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- Contrast-enhanced MR angiograph
- Characteristic narrowing of digital vessels
- Tapering of digital vessels
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| Myositis
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- Intramuscular edema (increased high T2 signal)
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| Arthritis
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| Osteonecrosis (Avascular necrosis)
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- Lack of enhancement and devascularized areas on gadolinium-enhanced MR imaging
- Bone marrow edema on MRI
- Low-signal-intensity marginal areas on standard spin-echo T1- and T2-weighted images
- Intermediate to high signal intensity inside bone tissue on T2-weighted images, producing a line of low signal intensity with an adjacent high-signal-intensity line
- High signal intensity on T2-weighted images due to subchondral fractures that may be accompanied by fluid signal intensity or edema
- Low signal intensity on T2-weighted images due to collapse of the articular surface
- Early or subtle insufficiency fractures especially on T2-weighted MR imaging
- In characteristic stress locations insufficiency fractures may appear as areas of high signal intensity due to bone marrow edema
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References
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