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Letters to the Editor |
Department of Radiology, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8575, Japan
Editor:
I read with great interest the article by Dr Vogl and colleagues (1) on a new magnetic resonance (MR) contrast agent for hepatocellular carcinoma (HCC) in the December 1997 issue of Radiology. Gadobenate dimeglumine is a unique and promising contrast agent for hepatic tumors since it has the dual characteristics of nonspecific and hepatobiliary agents. With 28 HCC nodules examined by using close time-interval, single-level dynamic MR imaging, Dr Vogl and colleagues described a double-ring sign noted at the arterial phase (unenhanced capsule, markedly enhanced peripheral part, and less enhanced central part of HCC nodule) as a characteristic finding of a large (>3-cm), well-differentiated HCC and devised a theory that explained how such findings were obtained (Figure). This theory also indicated that the HCC capsule remains hypointense up until the later perfusion phase and is surrounded by a markedly enhanced outer rim that histopathologically consists of veins and compressed surrounding tissue (another double-ring sign at the later perfusion phase).
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Dr Vogl and colleagues speculated in the Results that the hyperintense outer rim first noted at the venous perfusion phase was caused possibly by direct contact with the hepatic veins and the inferior vena cava. Unfortunately, I did not understand what they meant. Because the hepatic veins were used with the inferior vena cava, did they mean that the large hepatic veins were making contact with and surrounding the HCC nodule? This could not be the case since such enhancement occurs on the entire surface of the HCC nodule. Or, were there many hepatic venules or veins in the narrow zone outside of the capsule? In the Discussion, they also noted that enhancement seen during the venous perfusion phase was generally an indication of portal or hepatic venous vascularity, extent of the extracellular spaces, and possibly increased cellular uptake in peritumoral liver tissue. Extracellular space may play some role at the later perfusion phase; however, did cellular uptake occur so rapidly?
I guess this theory originated from imaging observation alone and not from imaging with histopathologic correlation by using their own resected specimen. Moreover, I wonder why Dr Vogl and colleagues did not cite any article on the use of dynamic CT or MR imaging for HCC and its capsule or any articles with regard to clinicopathology. They used a new MR contrast agent; however, at the perfusion phase, the pharmacokinetics of this new contrast agent is roughly the same as that of other gadolinium compounds and similar to that of iodinated contrast agents for CT.
There have been many dynamic CT and MR imaging studies on HCC and its capsule, especially from Japan (2–5). It has been clarified that (a) the pseudocapsule of HCC appears as a hypoattenuating or hypointense ring at unenhanced CT or MR imaging, respectively (in larger lesions, T2-weighted spin-echo MR imaging occasionally shows a double-layer rim [hypointense inner and hyperintense outer layers]), and this ring is scarcely noted in other hepatic tumors (2,4). (b) The capsule becomes hyperattenuating or hyperintense beginning at the portal-dominant phase ("delayed enhancement") and remains so for a long time ("prolonged enhancement") (2). (c) The pseudocapsule does not show enhancement at CT during arterial portography, but it represents marked enhancement at CT hepatic arteriography and dynamic CT and MR studies performed after intravenous administration of contrast material (5). (d) Histopathologically, the pseudocapsule is composed of two layers: an inner layer rich in collagen fiber (narrower in width and larger interstitial space for contrast enhancement with nonspecific agents) and an outer layer that contains various amounts of portal vein, bile duct, compressed artery, and collagen fiber (wider in width and large vascular and interstitial spaces) (4,5). (e) A recent article (5) on single-level dynamic CT hepatic arteriography clearly stated that the arterial blood flow in a liver tumor drains into the portal vein of the adjacent hepatic parenchyma through the portal venule in the HCC capsule, and this communication was proved histopathologically.
Our observation and theoretic explanation for enhancement of the HCC capsule are as follows (Figure): The HCC capsule receives the contrast agent from the hepatic tumor via the hepatic artery and starts to show enhancement about 10 seconds after tumor enhancement (5). Because of different vascular structures of the inner and outer layers of the capsule, the outer part shows more marked enhancement than that of the inner part at the intermediate perfusion phase (thin double-ring sign; however, we encounter it at dynamic CT and MR imaging, and at angiography at times, partly because hypervascular HCC drains enough contrast agent to enhance both the outer and inner parts of the capsule and partly because a wide inner collagen rim is noted mainly in huge HCC nodules alone).
The contrast agent then moves into the portal vein in the adjacent liver parenchyma through the portal venules in the capsule. Thus, the enhanced rim becomes wider and ill defined irrespective of the state of enhancement of the inner part of the capsule. Thereafter, the degree of enhancement depends mainly on the extent of the interstitial space of the capsule and the surrounding liver parenchyma (2). Generally, the degree and progression of contrast enhancement are determined by many factors such as flow speed in the vascular space, diffusion speed into and out of the interstitial space, and the extent of both spaces (6).
In conclusion, the authors were unclear as to the correctness of their theory of delayed enhancement of the outer cross-hatched areas of the upper right scheme (Figure) in encapsulated HCC, and other imaging, histopathologic, and theoretic evidence is necessary to support their theory.
References
Department of Radiology, University Hospital, Johann Wolfgang Goethe University of Frankfurt, Theodor Stern Kai 7, 60590 Frankfurt, Germany
Department of Radiology, Charite Humboldt University of Berlin, Germany
We thank Dr Itai for his comments regarding our article (1). We hypothesized in our study that different dynamic contrast enhancement characteristics of HCC are shown when the hepatobiliary contrast medium gadobenate dimeglumine is used. Dr Itai posed some questions that need to be commented on. First, the histopathologic correlation in our study regarded solely the tissue of the HCC and the degree of differentiation. We focused especially on the characteristics of dynamic gadobenate dimeglumine–enhanced MR imaging. However, it was not possible for us to correlate the MR morphology of the capsule or pseudocapsule directly with ex vivo histopathologic findings.
Analyzing our data, we speculated that the hyperintense outer rim first noted at the venous perfusion phase possibly was caused by direct contact of the HCC with hepatic veins near the inferior vena cava. Dr Itai asserted that this could not be the case since such enhancement occurs on the entire surface of the HCC nodule. However, we believe that there is a narrow outer part of the capsule with many postcapillary venous vessels. Our theory is based on the fact that the observed increase in signal intensity is measured simultaneously with an increase in signal intensity in the hepatic veins. So far, we have not been able to obtain histopathologic proof for our theory in ex vivo specimens. Current studies are aimed at improving this knowledge.
Second, it is well known that the extracellular spaces are enlarged in the peritumoral tissue, resulting in increased permeability. Thus, the compressed hepatocytes do show a changed pattern of enhancement with the use of hepatobiliary contrast agents. This is considered a valid explanation for our early and late venous rim phenomena in well-differentiated HCC.
We fully agree with Dr Itai that the inner zone of the capsule is composed of hypovascularized soft-tissue structures, which serve as an explanation for our rim phenomenon. However, there are certain aspects that should be discussed, including the characteristics of gadobenate dimeglumine in contrast to the extracellular contrast agent gadopentetate dimeglumine mentioned in our article. Also, we found interesting data on the enhancement patterns of well-differentiated HCC versus undifferentiated HCC.
In conclusion, we consider that our observed effects are influenced mainly by the histopathologic characteristics of the tumors and those of the new hepatobiliary contrast agent gadobenate dimeglumine.
References
This article has been cited by other articles:
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  R. F. Hanna, D. A. Aguirre, N. Kased, S. C. Emery, M. R. Peterson, and C. B. Sirlin Cirrhosis-associated Hepatocellular Nodules: Correlation of Histopathologic and MR Imaging Features RadioGraphics, May 1, 2008; 28(3): 747 - 769. [Abstract] [Full Text] [PDF]
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