AJR 2003; 181:889-890
© American Roentgen Ray Society
Hepatocellular Carcinoma Supplied by Portal Flow After Repeated Transcatheter Arterial Chemoembolization
Seung Hong Choi,
Jin Wook Chung and
Hye Seung Lee colleagues
Seoul National University College of Medicine Seoul National
University Hospital Seoul 110-744, Korea
A 76-year-old man was admitted to our hospital for transcatheter arterial
chemoembolization for recurrent hepatocellular carcinoma. Ten years earlier,
he had undergone a wedge resection to treat hepatocellular carcinoma in the
left lobe of the liver. At that time, preoperative hepatic angiography had
shown a hypervascular nodule that at the subsequent pathologic examination was
found to be a 2-cm hepatocellular carcinoma. Two years after the tumorectomy,
angiography revealed a focal hypervascular nodule indicative of recurrent
hepatocellular carcinoma supplied by the right hepatic artery. Since that
time, the patient had undergone repeated transcatheter arterial
chemoembolization (19 sessions, including the initial session after the
tumorectomy) through the hepatic and right inferior phrenic arteries and had
received chemotherapy (5-fluorouracil, mitomycin, and leucovorin).
CT performed 1 year before the patient's recent admission revealed
persistent enhancing lesions in hepatic segment VIII. These nodules displayed
isoattenuation during the hepatic arterial phase and hyperattenuation during
the portal venous phase (Figs.
2A and
2B). On celiac angiography
performed at the patient's admission to the hospital, no corresponding
hypervascular lesions and no parasitic blood supply could be found
(Fig. 2C). CT arterial
portography confirmed that these nodules were being supplied by the portal
vein (Fig. 2D). Percutaneous
needle biopsy was performed on one of these nodules. The pathologic diagnosis
was well-differentiated hepatocellular carcinoma.
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Fig. 2A. —76-year-old man with recurrent hepatocellular carcinoma.
Contrast-enhanced CT scan obtained during hepatic arterial phase 1 year before
hospital admission shows hyperattenuating nodules, indicating compact iodized
oil retention (arrowheads), but no evidence of enhancing lesions is
visible.
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Fig. 2B. —76-year-old man with recurrent hepatocellular carcinoma. On
contrast-enhanced transverse CT scan obtained during portal venous phase on
same day as A, several enhancing nodules (arrows) are visible
that were not depicted on hepatic arterial phase scan (A). Arrowheads
indicate nodules with compact iodized oil retention.
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Fig. 2C. —76-year-old man with recurrent hepatocellular carcinoma.
Celiac angiogram obtained in posteroanterior projection at hospital admission
shows no focal nodules. Segmental branches of right hepatic artery cannot be
identified.
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Fig. 2D. —76-year-old man with recurrent hepatocellular carcinoma. CT
arterial portogram obtained on same day as C shows that these nodules
(arrows) are supplied by portal vein. Iodized oil-retaining lesions
observed 1 year earlier (arrowheads in A and B) have
disappeared, probably because iodized oil had been washed out.
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This patient represents a case of an unusual vascular supply pattern in
hepatocellular carcinoma in which the tumor was supplied by portal blood flow.
Although untreated hepatocellular carcinomas have been reported as displaying
hypoattenuation on CT hepatic arteriography and hyperattenuation on CT
arterial portography in their initial manifestation
[1], to our knowledge, the
transition in the pattern of blood supply (i.e., from the hepatic artery to
the portal vein) in hepatocellular carcinoma that we observed in our patient
has not previously been reported. Considering the change in the enhancement
pattern, the transition in the vascular supply in the hepatocellular carcinoma
nodules from the hepatic artery to the portal vein may be associated with the
gradual destruction of the hepatic arteriole by repeated transcatheter
arterial chemoembolization. The stenosis and occlusion of the arterial
branches as a consequence of arteritis are well-documented adverse effects of
repeated chemoembolization. We are not certain whether the vessels supplying
the tumor in our patient developed from the destroyed arteries and then
communicated with the adjacent portal venules or directly sprouted from the
portal system.
Researchers have hypothesized that after chemoembolization, a small number
of hepatocellular carcinoma cells can be nourished directly by the portal
blood flow and may then act as foci of tumor recurrence
[2]. However, all the tumor
nodules in our patient had been supplied exclusively by the portal vein for
years. It is thought that the source of vascular supply in a nodule switches
from the portal vein to the hepatic artery during a multistep process of
hepatocarcinogenesis and that these changes can be detected on dynamic
contrast-enhanced imaging [3].
This intranodular hemodynamic change can be explained by the increased number
of neovascularized arteries and the loss of preexisting hepatic arteries and
portal veins [4]. Our patient
is an exception to the theory, and this case suggests that portal venous
supply of hepatocellular carcinoma nodules may be restored as a result of the
arterial damage from repeated transcatheter arterial chemoembolization.
References
- Hirano K, Kondo Y, Teratani T, et al. Hepatocellular carcinoma
depicted as hypoattenuation on CT hepatic arteriography and hyperattenuation
on CT during arterial portography. J Gastroenterol2001; 36:346
-349[Medline]
- Goseki N, Nosaka T, Endo M, Koike M. Nourishment of hepatocellular
carcinoma cells through the portal blood flow with and without transcatheter
arterial embolization. Cancer1995; 76:736
-742[Medline]
- Honda H, Tajima T, Kajiyama K, et al. Vascular changes in
hepatocellular carcinoma: correlation of radiologic and pathologic findings.
AJR 1999;173:1213
-1217[Abstract/Free Full Text]
- Tajima T, Honda H, Taguchi K, et al. Sequential hemodynamic change
in hepatocellular carcinoma and dysplastic nodules: CT angiography and
pathologic correlation. AJR2002; 178:885
-897[Abstract/Free Full Text]
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