AJR 2000; 174:965-971
© American Roentgen Ray Society
MR Imaging of Diffuse Liver Disease
Ichiro Tani1,
Yasuyuki Kurihara1,
Atsua Kawaguchi1,
Yasuo Nakajima1,
Tohru Ishikawa1,
Shiro Maeyama2 and
Ryoichi Tanaka3
1
Department of Radiology, St. Marianna University School of Medicine, 2-16-1
Sugao, Miyamae-ku, Kawasaki City, Kanagawa, 216-0015 Japan.
2
Department of Pathology, St. Marianna University School of Medicine, Kawasaki
City, Kanagawa, 216-0015 Japan.
3
Philips Medical Systems Corporation, Philips Bldg., 13-37 Kohnan 2 chome,
Minato-ku, Tokyo, 108-0075 Japan.
Received April 1, 1999;
accepted after revision September 10, 1999.
Address correspondence to I. Tani.
Introduction
Recent advances in the development of MR systems and IV contrast media have
strengthened the role of MR imaging in the evaluation of focal lesions of the
liver. Such lesions include hepatocellular carcinoma, hemangioma, and
metastasis. MR imaging also provides information on diffuse parenchymal
abnormalities and multifocal involvement in multiorgan and systemic diseases.
We present a diagnostic approach to diffuse liver disease using MR imaging.
Additionally, we discuss the distribution, signal intensities, and appearances
of each hepatic disorder.
For practical analysis, we divided diffuse liver disease into four
categories on the basis of patterns of distribution and abnormal signal
intensity: diffuse homogeneous distribution, segmental distribution, nodular
distribution, and perivascular distribution. Homogeneous distribution involves
disorders of hepatocytes and reticuloendothelial cells. Parenchymal signal
intensity in the liver may appear as homogeneous high or low signal intensity
on T1- or T2-weighted MR images (Fig.
1A). Segmental distribution of abnormal signal intensity (hepatic
perfusion) involves disorders such as segmental fatty liver and focal
confluent segmental fibrosis resulting from subacute hepatitis
(Fig. 1B). Nodular distribution
is characterized by multiple abnormal nodular intensities and includes
disorders (e.g., cirrhosis, Wilson's disease, and sarcoidosis) that cause
numerous nodular lesions corresponding to iron deposits in regenerative
nodules or granulomas (Fig.
1C). Disorders of perivascular distribution involve the periportal
lymphatic channel and Glisson's capsules
(Fig. 1D). Congestive liver and
Budd-Chiari syndrome are usually associated with periportal high signal
intensity of the liver, and schistosomiasis japonica can affect Glisson's
capsules, resulting in septal or capsular high intensity on T2-weighted MR
images.
Diseases of Diffuse Homogeneous Distribution
Hemochromatosis
Hemochromatosis is an iron overload disorder resulting in hepatic
parenchymal or reticuloendothelial deposition of iron. On T2-weighted MR
images, the superparamagnetic effect of iron causes decreased signal intensity
of liver parenchyma in comparison with that of the paraspinal muscle
[1]
(Fig. 2A). Gradient-echo
T2*-weighted MR images are more sensitive to magnetic
susceptibility effects without the 180° refocusing pulse. T1-weighted MR
images also show decreased signal intensity of liver parenchyma resulting from
a T2 shortening effect (Fig.
2B).
Steatohepatitis
Nonalcoholic steatohepatitis is fatty liver caused by inflammatory response
without alcohol abuse or an underlying clinical condition such as obesity,
diabetes, hyperlipidemia, or anorexia nervosa. Nonalcoholic steatohepatitis is
sometimes associated with acute hepatic failure, and in a minority of
patients, the disease progresses to cirrhosis
[2]. Liver histology of
patients with steatohepatitis shows diffuse steatosis and parenchymal
inflammation with concomitant fibrosis and Mallory's bodies
(Fig. 3A). To our knowledge, no
reports discuss the MR imaging features of nonalcoholic steatohepatitis. We
reviewed MR images and noted diffuse homogeneous increased signal intensity on
in-phase T1-weighted MR images (Fig.
3B) and diffuse homogeneous low signal intensities on
opposed-phase T1-weighted MR images (Fig.
3C). Inflammatory pathologic changes do not affect MR
images.
Glycogen Storage Disease
Patients with glycogen storage disease type I are characterized by an
inability to convert glucose-6-phosphate dehydrogenase to glucose; however,
they can produce glucose endogenously. The accumulation of glycogen in the
hepatocytes causes increased echogenicity on sonographic images
(Fig. 4A), abnormally dense
liver on CT images (Fig. 4B),
and increased signal intensity on T1-weighted MR images
(Fig. 4C) when compared with
bone marrow. Patients with this disease may also have hepatocellular adenoma,
manifesting as a low-attenuation tumor on conventional CT images
(Fig. 4B) and as
hyperintensity on T1- and T2-weighted MR images (Figs.
4C and
4D).
View larger version (116K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 4C. —36-year-old man with glycogen storage disease. T1-weighted spin-echo
MR image reveals homogeneously increased signal intensity of hepatic
parenchyma compared with that of bone marrow. Note round high-signal-intensity
tumor (arrow) in lateral segment.
|
|
Diseases of Segmental Distribution
Fatty Liver
Fatty change in hepatocytes occurs in patients with diabetes mellitus,
obesity, hyperalimentation, transplanted liver, alcohol abuse, and chemical
toxicity. Segmental fatty liver is characterized by segmental distribution of
fatty infiltration, depending on regional differences in perfusion.
T1-weighted spin-echo MR images show slightly increased signal intensity
resulting from fatty infiltration. In-phase MR images show similar intensity
for normal liver parenchyma and fatty changes
(Fig. 5A). Opposed-phase
T1-weighted MR images are the most useful for detecting
[3] low signal intensity caused
by fatty change (Fig. 5B).
View larger version (130K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 5A. —55-year-old-man with fatty liver. In-phase T1-weighted gradient-echo
MR image shows increased signal intensity of liver. Note similar intensity of
normal hepatic parenchyma and fatty change.
|
|
Subacute Hepatitis
Subacute hepatitis is caused primarily by viral infection, such as
hepatitis B or C, or by drug use. The disease has a poor prognosis and is
associated with a high mortality rate. When the liver is severely damaged,
parenchymal intensity is reduced on T1-weighted MR images
(Fig. 6A) and increased on
T2-weighted MR images (Fig.
6B). Additionally, segmental atrophy may manifest as abnormal
signal intensity (i.e., areas of focal confluent fibrosis with abnormal signal
intensity and abnormal enhancement)
[4]
(Fig. 6C).
Diseases of Diffuse Nodular Distribution
Liver Cirrhosis Caused by Viral Infection
Cirrhosis, the chronic response to repeated episodes of hepatocellular
injury, is characterized by regeneration and fibrosis. Common causes of
cirrhosis include alcoholism and viral infections such as hepatitis B and C.
Regenerative changes caused by cirrhosis appear throughout the liver as small
round masslike structures. These lesions appear as hypointense nodules on
T2-weighted MR images (Fig.
7A), are most apparent on gradient-echo images, and are believed
to be caused by deposition of hemosiderin in the regenerative nodules. CT
scans obtained during arterial portography show enhanced nodules resulting
from portal flow (Fig. 7B) and
hepatocellular carcinoma that appears as an area of defect.
View larger version (98K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 7A. —53-year-old woman with liver cirrhosis. T2-weighted MR image reveals
multiple regenerative nodules with low signal intensity (arrows).
Nodules resemble small round masslike structures.
|
|
Wilson's Disease
In patients with Wilson's disease the biliary excretion of copper is
impaired, resulting in the accumulation of toxic levels of copper in the
liver, brain, and cornea. Copper deposition resulting from Wilson's disease
occurs in the periportal regions and along the hepatic sinusoids and incites
an inflammatory reaction that can lead to cirrhosis. Copper has no
ferromagnetic effect on MR imaging
[5] because copper in
hepatocytes may combine with proteins. The most common finding of Wilson's
disease is cirrhotic change. Iron in regenerative nodules causes numerous
small nodular intensities scattered throughout the liver on T2-weighted MR
images. The nodular intensities are similar to those of deposits seen in
patients with cirrhosis resulting from viral infection (Fig.
8A,8B).
View larger version (86K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 8A. —16-year-old girl with Wilson's disease. T2-weighted spin-echo MR
image shows numerous small low-signal-intensity nodules scattered throughout
liver, probably corresponding to iron in regenerative nodules
(arrow).
|
|
Sarcoidosis
Sarcoidosis, a common systemic granulomatous disease, occasionally involves
the liver, spleen, and subdiaphragmatic lymph nodes. Noncaseating epithelioid
granulomas with surrounding fibrosis are present in the periportal region and
portal tracts (Fig. 9A). Previously reported CT findings in hepatic and splenic sarcoidosis include
hepatosplenomegaly with or without innumerable tiny hypoattenuating nodules.
These nodules are hypointense to surrounding parenchyma on T2-weighted MR
images and are enhanced on gadolinium-enhanced T1-weighted MR images
[6]. In the 53-year-old woman
with sarcoidosis in Figure
9A,9B,9C,
T2-weighted MR imaging revealed splenomegaly with numerous small
hypointensities that were not detected on CT. T2-weighted MR images revealed
liver lesions as numerous areas of low signal intensity and faint patchy
high-signal-intensity structures (Fig.
9B) that corresponded to the enhanced areas seen on
contrast-enhanced T1-weighted MR images
(Fig. 9C). Such intensities
may correspond histologically to granulomas with surrounding fibrosis.
View larger version (151K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 9A. —53-year-old woman with sarcoidosis. Photomicrograph of histology
specimen shows epithelioid granulomas (arrows) in portal area with
fibrous expansion (arrowheads). (Masson's trichrome, x10)
|
|
View larger version (90K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 9B. —53-year-old woman with sarcoidosis. T2-weighted MR image shows faint
patchy or geographic high-signal-intensity lesions (large arrows) in
liver. Numerous small low-signal-intensity nodules (small arrows) are
also seen. Note splenomegaly with numerous small low-signal-intensity nodules
(arrowheads).
|
|
View larger version (96K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 9C. —53-year-old woman with sarcoidosis. Gadolinium-enhanced
gradient-echo T1-weighted MR image reveals patchy or geographically enhanced
area (long arrow) in liver and numerous small low-signal-intensity
nodules (short arrows) in liver and spleen.
|
|
Diseases of Perivascular Distribution
Congested Liver
Passive hepatic congestion is caused by venous stasis in the liver
parenchyma resulting from compromised hepatic venous drainage. Congested liver
is a common complication of congestive heart failure, constrictive
pericarditis, and right-sided heart failure resulting from pulmonary artery
obstruction caused by lung cancer. Inhomogeneous mottled reticulated mosaic
parenchyma and periportal low attenuation may appear on contrast-enhanced CT
images [7]
(Fig. 10A). T2-weighted MR
images of patients with congested liver show periportal hyperintensity and
prominent perivascular zones of diminished attenuation resulting from presumed
perivascular lymphedema (Fig.
10B).
Schistosomiasis Japonica
Infection with Schistosoma japonicum results in a significant
hepatic disorder. Schistosomes live in the bowel lumen and lay eggs in the
mesenteric veins. The eggs are carried into portal veins and embolize to
terminal branches of the portal veins, where they cause presinusoidal
hypertension and incite granulomatous reactions. The inflammatory response
results in extensive fibrosis, with the formation of broad fibrous septa
throughout the liver. The eggs do not survive but undergo dystrophic
calcification resulting in characteristic periportal and pericapsular septate
calcification, the so-called tortoise-shell appearance
(Fig. 11A). Enhancement
appears at septal calcification and noncalcification sites on
contrast-enhanced CT (Fig.
11B). MR imaging shows the calcified septa observed on CT scans as
linear abnormalities that are frequently seen in the subdiaphragmatic portion
of the right lobe of the liver. The septa have low signal intensity on
T1-weighted MR images and high signal intensity on T2-weighted MR images
[8]. MR imaging with
superparamagnetic iron oxide reveals high-signal-intensity fibrous septa on
T1- and T2-weighted MR images (Fig.
11C).
View larger version (80K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 11C. —64-year-old woman with schistosomiasis japonica. T2-weighted
spin-echo MR image after injection of superparamagnetic iron oxide shows
high-signal-intensity lesions (arrows) corresponding to enhancement
area on CT scan (B).
|
|
References
-
Stark DD, Mosely ME, Bacon BR, et al. Magnetic resonance imaging of
hepatic iron overload. Radiology
1985; 154: 137
-142[Abstract/Free Full Text]
-
Powell EE, Cooksley WGE, Hanson R, Searle J, Halliday JW, Powell
LW. The natural history of nonalcoholic steatohepatitis: a follow-up study of
forty-two patients for up to 21 years. Hepatology
1990; 11: 74
-80[Medline]
-
Mitchell DG, Kim I, Chang TS, et al. Fatty liver: chemical shift
saturation and phase-difference MR imaging techniques in animal, phantoms and
humans. Invest Radiol
1991;26: 1041
-1052[Medline]
-
Ohtomo K, Baron RL, Dodd GD III, Federle MP, Ohtomo Y, Confer SR.
Confluent hepatic fibrosis in advanced cirrhosis: evaluation with MR imaging.
Radiology 1993; 189
: 871-874[Abstract/Free Full Text]
-
Mergo PJ, Ros PR. Imaging of diffuse liver disease.
Radiol Clin North Am
1998;36: 365
-375[Medline]
-
Warshauer DM, Semelka RC, Ascher SM. Nodular sarcoidosis of the
liver and spleen: appearance on MR images. J Magn Reson
Imaging 1994;4: 553
-557[Medline]
-
Gore RM, Mathieu DG, White EM, Ghahremani GG, Panella JS, Rochester
D. Passive hepatic congestion: cross-sectional imaging features.
AJR 1994; 162
: 71-75[Abstract/Free Full Text]
-
Monzawa S, Ohtomo K, Oba H, Nogata Y, Kachi K, Uchiyama G. Septa in
the liver of patients with chronic hepatic schistosomiasis japonica: MR
appearance. AJR 1994; 162
: 1347-1351[Abstract/Free Full Text]
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
S. Sartori, R. Galeotti, N. Calia, M. Gualandi, I. Nielsen, L. Trevisani, P. Ceccotti, and V. Abbasciano
Sonographically Guided Biopsy and Sonographic Monitoring in the Diagnosis and Follow-up of 2 Cases of Sarcoidosis With Hepatic Nodules and Inconclusive Thoracic Findings
J. Ultrasound Med.,
September 1, 2002;
21(9):
1035 - 1039.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Introduction
Diseases of Diffuse Homogeneous...
