eMedicine Specialties > Radiology > Gastrointestinal

Hepatocellular Carcinoma

Daniel R Jacobson, MD, MS, Clinical Instructor, Department of Radiology, University of Rochester School of Medicine, Radiology Residency Program Director, Rochester General Hospital

Updated: Feb 20, 2009

Introduction

Background

Hepatocellular carcinoma (HCC) is the most common primary hepatic tumor and one of the most common cancers worldwide. HCC is a primary malignancy of hepatocellular origin.¹

CT scan in the hepatic arterial phase of contrast enhancement showing neovascularity in a low-density hepatic mass.

Ultrasound shows hyperechoic mass representing hepatocellular carcinoma.

Pathophysiology

Hepatocellular carcinoma (HCC) is a malignant tumor of hepatocellular origin that develops in patients with risk factors such as alcohol abuse, viral hepatitis, and metabolic liver disease. It can also occur, rarely, in patients with normal liver parenchyma.²  

Grossly, HCC can undergo hemorrhage and necrosis because of a lack of fibrous stroma. Vascular invasion, particularly of the portal system, is common. Invasion of the biliary system is less common. Aggressive HCC can cause hepatic rupture and hemoperitoneum.

There are 3 growth patterns exhibited by HCC:  

• Solitary mass - Often large
• Multifocal or nodular pattern - Multiple nodules
• Diffuse - Multiple, small foci scattered diffusely throughout the liver

Microscopically, HCC cells resemble normal hepatocytes and can be confused with cells of hepatic adenoma. Tumors that are more differentiated can produce bile.

HCC can produce alpha-fetoprotein (AFP) as well as other serum proteins.

Frequency

United States

Hepatocellular carcinoma (HCC) is rare in the Western Hemisphere. The prevalence is 4 cases per 100,000 population, or 2% of all malignancies. Approximately 5,000-10,000 cases per year are seen. Prevalence rates in the United States vary among ethnic groups, with the highest rate being in men of Chinese descent. In the United States, the most common causes of HCC are alcoholic cirrhosis, steroid use, and hemochromatosis.

International

Hepatocellular carcinoma (HCC) is more common in Asia and Africa than in the United States. The highest incidence of HCC is in Japan (4-5%). Other high-incidence regions include sub-Saharan Africa. Internationally, the common causes of HCC are hepatitis B, hepatitis C, and aflatoxin exposure.

Mortality/Morbidity

• Most patients with hepatocellular carcinoma (HCC) die within 1 year after diagnosis. Survival is dependent on tumor size and on associated diseases at the time of diagnosis. Patients with cirrhosis have a shorter survival. Surgical cure is possible in less than 5% of patients.
• The causes of death include bleeding (variceal, intraperitoneal) and cachexia.

Race

• A high incidence is seen in Japan and Africa.
• In the United States, hepatocellular carcinoma (HCC) is most common in men of Chinese descent, probably because of the high incidence of viral hepatitis in this subgroup.

Sex

• In high-incidence regions of the world (ie, Asia, Africa), the male-to-female ratio is approximately 8:1.
• In low-incidence regions (ie, Western Hemisphere), the male-to-female ratio is approximately 2:1.

Age

• In high-incidence regions of the world (ie, Asia, Africa), patients present at age 30-50 years.
• In low-incidence regions (ie, Western Hemisphere), patients present at age 70-80 years. Patients with cirrhosis may present earlier.

Presentation

Clinical presentations vary among high-incidence and low-incidence regions.

In high-incidence regions (ie, Asia, Africa), the clinical presentation of hepatocellular carcinoma (HCC) tends to be aggressive and includes bleeding, hepatic rupture, and hemoperitoneum.

In low-incidence regions (ie, Western Hemisphere), the clinical presentation of HCC tends to be less aggressive and includes symptoms such as fever of unknown origin, abdominal pain, malaise, weight loss, and hepatomegaly. Jaundice is rare.

Liver function tests can be normal. Alpha-fetoprotein (AFP) levels may be elevated because this protein is commonly produced by HCC; however, this is an insensitive parameter because AFP levels may be normal in more than one third of patients.

Other proteins can be produced by HCC and cause paraneoplastic syndromes, such as erythrocytosis, hypercalcemia, hypoglycemia, and hirsutism.³

Preferred Examination

Cross-sectional imaging with computed tomography (CT) and magnetic resonance imaging (MRI) is most commonly used to detect hepatocellular carcinoma (HCC). CT is frequently the first examination; however, MRI has superior contrast resolution and may better detect lesions less than 1 cm in diameter.

Ultrasound (US) can be sensitive in detecting HCC and, depending on the operator, can detect small lesions. US can evaluate for vascular invasion of the portal and hepatic veins through color Doppler imaging.

Nuclear medicine imaging, angiography, and plain films are less useful.

Limitations of Techniques

Plain films are nonspecific but may show a mass in the upper abdomen if the hepatocellular carcinoma (HCC) is large.

Nuclear medicine provides relatively nonspecific findings. The HCC may present as a "cold" defect on a sulfur-colloid study or may demonstrate uptake of radiopharmaceuticals if the mass produces bile. Gallium uptake is seen in 90% of HCCs.

The US appearance of HCC varies; it may be hyperechoic or hypoechoic. A small hyperechoic HCC may be confused with hemangioma.

Perform CT in hepatic arterial, portal venous, and delayed phases. Similarly, if MRI is used, precontrast, arterial, venous, and delayed phases are essential. Enhancement patterns of regenerative, dysplastic, and HCC nodules overlap; therefore, nodules of cirrhosis may not be differentiated from small HCCs.

Angiography study may show increased vascularity of other hepatic tumors, including benign masses.

Differential Diagnoses

Other Problems to Be Considered

Metastatic disease
Angiosarcoma
Regenerative nodules
Dysplastic nodules
Hemangioma

Radiography

Findings

Nonspecific findings on plain film are standard. An abdominal mass may be visible. Calcification is rare in hepatocellular carcinoma (HCC) but more frequent in other hepatic masses such as fibrolamellar HCC.

Patients with hemochromatosis as a predisposing factor in the development of HCC may show deposition of calcium pyrophosphate in the cartilage of joints.

Patients with prior exposure to Thorotrast may be identified by noting contrast material deposition in the liver and lymph nodes.

Degree of Confidence

Plain films are completely nonspecific.

False Positives/Negatives

Many other causes of chondrocalcinosis exist, such as gout, hyperparathyroidism, Wilson disease, and degenerative joint disease.

Computed Tomography

Findings

Proper technical performance of CT with imaging in the hepatic arterial and portal venous phases, as well as delayed contrast images, is important in detecting hepatocellular carcinoma (HCC). Lesions may be missed if early vascular imaging is not performed. It is important to use high injection rates and appropriate bolus timing. Sensitivity of good-quality dual- or triple-phase CT for the detection of patients with tumors is 60-70%.⁴  

The CT appearance of HCC varies depending on tumor size and the imaging phase. The most common attenuation pattern is iso-hyper-isoattenuation on prephase, arterial phase, and venous phase, respectively; however, this pattern is shared by other hepatocellular nodules, including regenerative and dysplastic nodules.

• Unenhanced CT typically reveals an iso-hypodense mass. If the mass is large, central areas of necrosis may be seen. Look for signs of cirrhosis or hemochromatosis.
• In the hepatic arterial phase, lesions typically are hyperdense (relative to hepatic parenchyma) as a result of hepatic arterial supply. Larger tumors may have necrotic central regions that are typically hypodense during this imaging phase. Look for neovascularity to indicate the presence of inconspicuous lesions.
• In the portal venous phase, small lesions may be isodense or hypodense and difficult to see, since the remainder of the liver increases in attenuation. Larger lesions with necrotic regions remain hypodense.
• In the delayed-postcontrast phase, small lesions may be inconspicuous on late phases. Delayed phase scans may show a tumor capsule, one of the more specific signs indicating HCC.

CT can also evaluate complications of HCC such as portal venous or hepatic venous invasion. In addition, be alert and evaluate for other complications such as bleeding within the tumor and hemoperitoneum.

Evaluate underlying disease on CT, which can indicate the etiology of a hepatic mass. Look for signs of cirrhosis and hemochromatosis.

Degree of Confidence

In the setting of an abnormal liver with elevated alpha-fetoprotein (AFP), a vascular mass or a large necrotic mass strongly suggests HCC; however, other hepatic lesions both benign and malignant can mimic hepatocellular carcinoma (HCC) on CT. MRI or nuclear imaging can assist in this differentiation.

In addition, cirrhotic nodules cannot be reliably differentiated from small HCCs. Since success of therapy depends on early HCC detection, the distinction is important; MRI can assist with nodule differentiation.

False Positives/Negatives

False-negative CT imaging can occur. Even the best CT scanner may have difficulty detecting small lesions, especially if good-quality, triphasic scanning is not performed. Prospective detection rates of patients with tumors and of tumor nodules were reported as 59% and 37%, respectively, in a large series with pathologic correlation.⁵

Magnetic Resonance Imaging

Findings

Hepatocellular carcinoma (HCC) appearance varies on MRI depending on multiple factors, such as hemorrhage, degree of fibrosis, histologic pattern, degree of necrosis, and the amount of fatty change.

• HCC on T1-weighted images may be isointense, hypointense, or hyperintense relative to the liver.
• On T2-weighted images, HCC is usually hyperintense.
• Precontrast and postcontrast MRI has a 70-85% chance of detecting a solitary mass of HCC.
• MRI can help differentiate cirrhotic nodules from HCC:
  
  
  • If the mass is bright on T2-weighted images, it is HCC until proven otherwise.
  • If the mass is dark on T1- and T2-weighted images, it is a siderotic regenerative nodule or siderotic dysplastic nodule.
  • If the mass is bright on T1-weighted images and dark or isointense on T2-weighted images, it is a dysplastic nodule or low-grade HCC.
• Gadolinium-enhanced MRI typically demonstrates that HCCs densely enhance, usually in the arterial phase, particularly if they are small. A lesion showing arterial enhancement is most likely HCC; however, dysplastic nodules and, less likely, regenerative nodules can show similar enhancement. The degree of enhancement varies, particularly with the degree of necrosis in larger tumors. Look carefully for enhancement in small portions of tumor. (In addition, a "flash filling" hemangioma can have rapid arterial enhancement but could be differentiated by lack of washout on delayed images.)
• Administration of superparamagnetic iron oxide may demonstrate HCC because most HCCs contain fewer or no Kupffer cells.
• The contrast agent mangafodipir trisodium can evaluate questionable lesions in the liver. Mangafodipir trisodium is taken up by normal hepatocytes and masses that contain hepatocytes, causing increased signal intensity on T1-weighted images. This agent may help differentiate a tumor of hepatocellular origin, such as HCC, from secondary hepatic masses.
• Complications (eg, vascular invasion) are evaluated well by MRI.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. 

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble  moving  or  straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

Some well-differentiated HCCs can mimic cirrhotic nodules on MRI.

Some HCCs can contain Kupffer cells, thus having signal characteristics similar to normal liver on images contrasted with superparamagnetic iron oxide.

Ultrasonography

Findings

US appearance of hepatocellular carcinoma (HCC) is variable. Note that the quality of a US examination is operator dependent. Take care to evaluate the entire liver completely because it is not difficult to overlook a small hepatic mass.^6,7,8

Small HCCs can be homogeneously hyperechoic and can mimic hemangioma. This can result from a large proportion of fat being present in the tumor.

Small HCCs also can appear hypoechoic, with larger HCCs frequently mixed in echogenicity.

Good-qualityUS with careful evaluation of the entire liver can be a screening examination for HCC in patients at risk, in combination with serum alpha-fetoprotein (AFP) evaluation; however, sensitivity of US for the detection of lesions in a cirrhotic liver is limited.

Vascular invasion can be adequately evaluated using color Doppler imaging with conventional gray-scale US. Look for tumor thrombus in hepatic and portal veins as well as in the inferior vena cava. Portal venous invasion is more common in HCC, but hepatic vein invasion is more specific for HCC.

Degree of Confidence

In particular, small hyperechoic masses seen on US require further evaluation because they can represent hemangioma (most commonly), metastatic disease, or, less likely, HCC. Further imaging with CT or MRI during dynamic contrast enhancement shows the typical peripheral, nodular contrast enhancement pattern of hemangioma. MRI or CT can further characterize many nonspecific hepatic masses seen on US (described in MRI).

Nuclear Imaging

Findings

On a gallium scan, up to 90% of hepatocellular carcinomas (HCCs) demonstrate uptake of the radiopharmaceutical. Gallium may help distinguish regenerating nodules of cirrhosis from HCC, as regenerating nodules typically do not label with gallium.

On a liver-spleen scan, a sulfur-colloid study typically demonstrates an area of decreased labeling in HCC. Look for signs of cirrhosis, such as heterogeneous labeling of the liver with a large spleen and colloid shift to the bone marrow. Prominent left and caudate lobes of the liver are also signs of cirrhosis. A "cold" defect in the liver with signs of cirrhosis strongly suggests HCC.

Hepatobiliary scans can show labeling of HCC due to the presence of hepatocytes. HCC may have no uptake initially but may show delayed uptake as the rest of the normal liver clears. This is related to malignant hepatocytes, which are hypofunctional relative to normal hepatocytes.

Positron emission tomography with fluorodeoxyglucose (FDG-PET) is primarily useful in assessing the degree of differentiation and in staging moderately and poorly differentiated tumors, rather than in primary lesion detection. Sensitivity of FDG-PET for the detection of HCC is 50-70%. This limited sensitivity is due to the low level of FDG uptake in well-differentiated tumors; however, FDG-PET may be superior to CT in detecting extrahepatic spread.

Degree of Confidence

On a gallium scan, the liver normally labels early and may obscure HCC labeling. Differential diagnoses of a mass that shows labeling in the liver include other types of malignancy and infection.

Angiography

Findings

Angiography for the diagnosis of hepatocellular carcinoma (HCC) has been replaced largely by cross-sectional imaging. Normal vasculature is typically displaced by a large mass. HCC is characteristically hypervascular with bizarre neovascularity and arteriovenous shunting. An enlarged hepatic artery may be present. Look for vascular invasion (portal veins, hepatic veins).

Intervention

Percutaneous ethanol injection has been widely used for the treatment of focal, small hepatocellular carcinoma (HCC) in cirrhotic livers. In addition to ethanol injection, acetic acid injection, interstitial laser hyperthermia, and microwave therapy have been used to treat HCC. Percutaneous radiofrequency ablation has also been advocated for treatment of small HCCs. Percutaneous radiofrequency ablation appears to be effective in achieving tumor necrosis in HCC.^9,10,11

Embolization of particles such as Gelfoam into the hepatic artery can be performed to affect blood supply to the tumor. Response rates of 60-80% have been reported, but there has been no demonstration of increased survival.

The prognosis of radiologic interventions is generally poor. Long-term survival does not appear to significantly differ from survival of those who undergo surgical treatment.

Long-term survival rates for transplantation are 20-30%, while the rate for resection (possible in only about 15% of patients) is 30-40%.

Multimedia

Media file 1: CT scan in the hepatic arterial phase of contrast enhancement showing neovascularity in a low-density hepatic mass.

Media file 2: Ultrasound shows hyperechoic mass representing hepatocellular carcinoma.

References

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Keywords

hepatocellular carcinoma, hepatoma, typical hepatocellular carcinoma, primary liver carcinoma, clear cell carcinoma of the liver, HCC

Contributor Information and Disclosures

Author

Daniel R Jacobson, MD, MS, Clinical Instructor, Department of Radiology, University of Rochester School of Medicine, Radiology Residency Program Director, Rochester General Hospital
Daniel R Jacobson, MD, MS is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

Medical Editor

John L Haddad, MD, Clinical Associate Professor, Department of Radiology, Weill Medical College of Cornell University; Director of Body MRI, Department of Radiology, Methodist Hospital in Houston
John L Haddad, MD is a member of the following medical societies: American College of Radiology, American Medical Association, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Udo P Schmiedl, MD, PhD, Clinical Professor, Department of Radiology, University of Washington; Consulting Staff, Swedish Medical Center, University of Washington Medical Center, Seattle Radiologists
Udo P Schmiedl, MD, PhD is a member of the following medical societies: American College of Radiology and Radiological Society of North America
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

John Karani, MBBS, FRCR, Consulting Staff, Department of Radiology, King's College Hospital, London
Disclosure: Nothing to disclose.

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