eMedicine Specialties > Pediatrics: General Medicine > Oncology

Hepatoblastoma: Differential Diagnoses & Workup

Author: Jennifer R Willert, MD, Assistant Clinical Professor of Pediatrics, University of California at San Diego; Consulting Staff, Department of Pediatrics, Division of Hematology, Oncology and Bone Marrow Transplant, San Diego Children's Hospital; Member, Rebecca Moore's Cancer Center, Translational Oncology, University of California San Diego Medical Center
Coauthor(s): Gary Dahl, MD, Professor, Department of Pediatrics, Division of Hematology/Oncology, Stanford University School of Medicine
Contributor Information and Disclosures

Updated: Jan 14, 2008

Differential Diagnoses

Hepatocellular Carcinoma

Other Problems to Be Considered

Malignant mesenchymal hepatic tumor (undifferentiated sarcoma, angiosarcoma, fibrosarcoma, leiomyosarcoma, rhabdoid tumor)
Hemangioma
Hemangioendothelioma
Mesenchymal hamartoma, often cystic
Embryonal sarcoma of the liver

Workup

Laboratory Studies

Diagnostic evaluation of a child in whom a liver tumor is suggested should include the following:

  • CBC count with differential should be obtained.
    • Normochromic normocytic anemia is often present.
    • Thrombocytosis may be present. In a study by Ortega et al, 60% of patients had platelet counts greater than 500 X 109/L, and 12% had platelet counts greater than 1000 X 109/L.17
  • Liver enzyme levels are moderately elevated in 15-30% of patients.
  • AFP is a major serum protein synthesized by fetal liver cells, yolk sacs, and the GI tract. AFP is found in high concentrations in fetal serum and in children with hepatoblastoma, hepatocellular carcinoma, germ cell tumors, or teratocarcinoma. The tumor's ability to synthesize AFP reflects its fetal origin. Embryonal tumors produce less AFP than fetal tumors.
    • Levels of AFP in hepatoblastoma are often as high as 100,000-300,000 mcg/mL. Ortega et al found AFP levels elevated for age in 97% of patients.17
    • The half-life of AFP is 4-9 days, and levels usually fall to within reference range within 4-6 weeks following resection.
    • Other causes of elevated AFP levels include viral hepatitis, cirrhosis, inflammatory bowel disease, and yolk sac tumors.
    • Although elevated AFP levels are not specific for hepatoblastoma, they provide an excellent marker for response to therapy, disease progression, and detection of recurrent disease.
    • Rarely, a hepatoblastoma can recur as a non–AFP-secreting tumor with metastases, even if the initial tumor was AFP secreting.
    • Interpretation of AFP levels can be difficult because hepatoblastoma tends to occur within the first 2 years of life. Reference range AFP levels are comparatively high at birth and even higher in premature infants, which can complicate interpretation of this value. By age 1 year, adult levels of 3-15 mcg/mL have been reached.
    • Data from the German Cooperative Pediatric Liver Tumor Study showed that both very low (<100 ng/L) and very high (>1,000,000 ng/L) AFP levels are associated with poorer prognosis than intermediate AFP levels.22  
    • Laboratory- and age-specific AFP values should be used.
    • Baseline testing of glomerular filtration rate (GFR) or creatinine clearance should be performed before cisplatin administration; follow-up studies are needed periodically to assess nephrotoxicity.

Imaging Studies

  • Abdominal radiography
    • Plain abdominal films reveal a right upper quadrant abdominal mass.
    • Calcification is seen in approximately 6% of hepatic masses and 12% of hemangiomas.
  • Ultrasonography
    • Abdominal ultrasonography allows assessment of tumor size and anatomy, which helps in surgical planning.
    • The mass usually appears hyperechoic on abdominal ultrasound images, which is particularly useful in determining vascular involvement (vessels have lower attenuation than surrounding parenchyma).
    • Baseline echocardiography is needed before anthracycline (doxorubicin) administration; follow-up studies are needed to assess cardiotoxicity.
  • CT scanning
    • CT scanning of the abdomen using contrast reveals patchy enhancement. 
    • CT scanning reveals involvement of nearby structures. Regional lymph nodes are almost never involved.
    • CT scanning of the chest is warranted to assess for pulmonary metastases.
  • MRI: This is believed to be superior to CT scanning but does not necessarily add to the anatomic detail seen on CT scans.
  • Radionuclide bone scanning: This is recommended to evaluate for bone metastases when a patient is symptomatic. 
  • Positron emission tomography (PET) scanning: Studies support a potential role for PET scanning at diagnosis and for follow-up evaluation in hepatoblastoma.23

Other Tests

  • A baseline audiology evaluation is needed before cisplatin or carboplatin administration; follow-up studies are needed to assess ototoxicity.

Procedures

  • Pathologic diagnosis: Before commencing therapy, surgical diagnosis must be made. Surgical resection is the usual manner in which material for pathologic assessment is obtained. Open biopsy is performed when complete surgical resection is not possible. Needle biopsy is not recommended because these lesions usually are highly vascular.

Histologic Findings

Standardizing criteria for histologic classification of hepatoblastoma has been suggested because of the significant variation in the current medical literature. Particular attention to the subtypes of this tumor and direct correlation with clinical outcomes is increasingly being incorporated into all major protocols internationally.24

Six histologic variants of hepatoblastoma have been described, as follows:

  • Epithelial type
    • Fetal pattern
    • Embryonal and fetal pattern
    • Macrotrabecular pattern
    • Small cell undifferentiated pattern
  • Mixed epithelial and mesenchymal type
    • With teratoid features
    • Without teratoid features

Pure epithelial tumors account for approximately 56% of cases; they contain varying amounts of fetal cells, embryonal cells, or both. Within this group, purely fetal tumors account for 31% of hepatoblastomas; embryonal tumors account for 19% of hepatoblastomas; and macrotrabecular tumors and small cell undifferentiated types each account for 3% of hepatoblastomas. The remaining 44% of hepatoblastomas are mixed tumors containing primitive mesenchymal tissue and specialized derived components, such as myofibroblastic, chondroid, and osteoid tissues in addition to epithelial elements. Mixed tumors may express teratoid features. Teratoid hepatoblastomas are admixed with various heterologous structures of epithelial or mesenchymal origin.

Fetal cells are smaller than normal hepatocytes and have low nuclear-to-cytoplasmic (N/C) ratios and infrequent mitoses; cells form slender cords. Embryonal cells have a higher N/C ratio and more mitoses; they resemble early ducts of embryonal liver. Extramedullary hematopoiesis can be associated with mixed tumors. In tumors that have been completely resected, pure fetal histologic (PFH) results (with a 92% rate of disease-free survival) are associated with better prognosis than other histologic types, which have an overall disease-free survival rate of 57%. The absence of mitoses is a good prognostic sign. In advanced disease in which tumors cannot be completely resected, PFH results do not predict a better outcome.

Staging

Staging of hepatoblastoma is based on degree of surgical resection, histologic evaluation, and presence of metastatic disease. The system cited here is based on the work of von Schweinitz et al.25

  • Stage I
    • The tumor is completely resectable via wedge resection or lobectomy.
    • The tumor has PFH results.
    • The AFP level is within reference range within 4 weeks of surgery.
  • Stage IIA
    • The tumor is completely resectable.
    • The tumor has histologic results other than PFH (UH).
  • Stage IIB
    • The tumor is completely resectable.
    • AFP findings are negative at time of diagnosis (ie, no marker to follow).
  • Stage IIC
    • The tumor is completely resected or rendered completely resectable by initial radiotherapy or chemotherapy or microscopic residual disease is present. 
    • The AFP level is elevated 4 weeks after resection.
  • Stage III (any of the following)
    • The tumor is initially unresectable but is confined to one lobe of liver.
    • Gross residual disease is present after surgery.
    • Tumor ruptures or spills preoperatively or intraoperatively.
    • Regional lymph nodes are involved.
  • Stage IV: Distant bone or lung metastasis is present.

European groups have also developed a staging system through SIOPEL-1; the system uses the predictive value of pretreatment extent of disease (PRETEXT) in order to stage patients and determine which therapy is most appropriate.18 Using this system, physicians are able to refer higher risk patients for evaluation by liver transplant teams earlier with improved outcomes. These groups also advocate for chemotherapy treatment of lung metastases followed by surgical resection, with attempts for negative surgical margins providing optimal outcomes.

Which staging regimen is preferred among the Children’s Cancer Group (CCG) staging, Pediatric Oncology Group (POG) staging, and the European group staging is still actively discussed. However, for comparability reasons, following one staging regimen has been suggested, and international collaboration with consistency is ideal for this rare tumor.

More on Hepatoblastoma

Overview: Hepatoblastoma
Differential Diagnoses & Workup: Hepatoblastoma
Treatment & Medication: Hepatoblastoma
Follow-up: Hepatoblastoma
Multimedia: Hepatoblastoma
References
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Further Reading

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Keywords

hepatoblastoma, embryonal hepatic tumor, hepatic neoplasms in children, liver tumor, liver cancer, pediatric cancer, pediatric neoplasm, childhood hepatic tumor, Beckwith-Wiedemann syndrome, BWS, pulmonary metastases, hemihypertrophy, trisomy 20, epithelial hepatoblastoma, familial adenomatous polyposis, FAP, colonic polyps, adenocarcinoma, Wnt pathway, low birth weight infants, very low birth weight infants, anorexia, osteopenia, acute abdomen, chronic hepatitis B infection, isosexual precocity, talipes equinovarus, persistent ductus arteriosus, tetralogy of Fallot, extrahepatic biliary atresia, dysplastic kidney, horseshoe kidney, cleft palate, Goldenhar syndrome, Prader-Willi syndrome, Meckel diverticulum, Simpson-Golabi-Behmel syndrome, fetal alcohol syndrome, neurofibromatosis type 1, NF1, Li-Fraumeni syndrome

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Contributor Information and Disclosures

Author

Jennifer R Willert, MD, Assistant Clinical Professor of Pediatrics, University of California at San Diego; Consulting Staff, Department of Pediatrics, Division of Hematology, Oncology and Bone Marrow Transplant, San Diego Children's Hospital; Member, Rebecca Moore's Cancer Center, Translational Oncology, University of California San Diego Medical Center
Jennifer R Willert, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Blood and Marrow Transplantation, American Society of Hematology, American Society of Pediatric Hematology/Oncology, and Children's Oncology Group
Disclosure: Nothing to disclose.

Coauthor(s)

Gary Dahl, MD, Professor, Department of Pediatrics, Division of Hematology/Oncology, Stanford University School of Medicine
Gary Dahl, MD is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and American Society of Pediatric Hematology/Oncology
Disclosure: Nothing to disclose.

Medical Editor

Stephan A Grupp, MD, PhD, Director, Stem Cell Biology Program, Department of Pediatrics, Division of Oncology, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania
Stephan A Grupp, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society for Blood and Marrow Transplantation, American Society of Hematology, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Steven K Bergstrom, MD, Assistant to the Chairman, Department of Pediatrics, Division of Hematology-Oncology, Kaiser Permanente Medical Center of Oakland
Steven K Bergstrom, MD is a member of the following medical societies: Alpha Omega Alpha, American Society of Clinical Oncology, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Children's Oncology Group, and International Society for Experimental Hematology
Disclosure: Nothing to disclose.

CME Editor

Helen SL Chan, MBBS, FRCP(C), FAAP, Senior Scientist, Research Institute; Professor, Division of Hematology/Oncology, Department of Pediatrics, The Hospital for Sick Children, University of Toronto, Canada
Helen SL Chan, MBBS, FRCP(C), FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Cancer Research, American Society of Clinical Oncology, American Society of Hematology, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Chief Editor

Max J Coppes, MD, PhD, MBA, Executive Director, Center for Cancer and Blood Disorders, Children's National Medical Center, Washington, DC; Professor of Medicine, Oncology, and Pediatrics, Georgetown University
Max J Coppes, MD, PhD, MBA is a member of the following medical societies: American Association for Cancer Research, American Society of Clinical Oncology, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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