Systemic lupus erythematosus MRI

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

On gastrointerstinal 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 neurologic MRI, SLE may be characterized by white matter lesions, changes in brain vessel blood flow, 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 found with other more feasible imaging techniques. So MRI is not indicated primarily in the diagnosis of most complications of SLE, but if done, the following results can be found regarding the organ system involvement:

	Disease	MRI
Gastrointestinal system	Hepatitis	Hepatomegaly Nodules that ranging around 0.5-4.5 cm in diameter  T2: nonspecific, increased periportal edema
	Acute pancreatitis	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
	Mesenteric vasculitis	Comb sign Hypervascular appearance of the mesentery
Cardiac involvement	Mitral stenosis	Mitral leaflet thickening Reduced diastolic opening Abnormal valve motion toward the left ventricular outflow tract
	Acute pericarditis	The normal pericardial thickness is considered 2 mm while a thickness of over 4 mm suggests a pericarditis
	Pericardial effusion	Fluid density material surrounding the heart
	Myocarditis	Regional or global wall motion abnormalities Pericardial effusion Early postcontrast enhancement due to regional vasodilatation and increased blood volume, secondary to the inflammation
Neurological involvement	General	Focal neurological defects White matter lesions Periventricular hyperintensities Detects clinically silent lesions
	Stroke	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
	Neuropathies	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
	Autoimmune encephalitis	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
Musculoskeletal involvement	Raynaud phenomen	Contrast-enhanced MR angiograph Characteristic narrowing of digital vessels Tapering of digital vessels
	Myositis	Intramuscular edema (increased high T2 signal)
	Arthritis	Capsular swelling Proliferative tenosynovitis Synovial overgrowth
	Osteonecrosis (Avascular necrosis)	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