eMedicine Specialties > Oncology > Carcinomas of the Gastrointestinal Tract

Hepatic Carcinoma, Primary: Treatment & Medication

Author: Keith E Stuart, MD, Chairman, Department of Hematology and Oncology, Lahey Clinic
Coauthor(s): Zsofia K Stadler, MD, Clinical Fellow, Department of Hematology and Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School
Contributor Information and Disclosures

Updated: Jan 12, 2009

Treatment

Medical Care

Available treatment options depend on the size, number, and location of tumors; presence or absence of cirrhosis; operative risk based on extent of cirrhosis and comorbid diseases; overall performance status; patency of portal vein; and presence of metastatic disease.17,18,19

Before instituting definitive therapy, it is best to treat the complications of cirrhosis with diuretics, paracentesis for ascites, lactulose for encephalopathy, ursodiol for pruritus, sclerosis or banding for variceal bleeding, and antibiotics for spontaneous bacterial peritonitis.

Surgical resection and liver transplantation are the only chances of cure but have limited applicability. The main prognostic factors for resectability are tumor size and liver function. Only about 5% of hepatocellular carcinoma patients are suitable for transplantation; these patients may have a 5-year survival of greater than 75% with tumor recurrence rates as low as 15% at 5 years.20 Other local therapies are chemoembolization, ethanol ablation, radiofrequency ablation, cryoablation, and radiotherapy. Patients whose disease is downstaged following chemoembolization may be eligible for transplantation. Systemic treatment with chemotherapy may be used for advanced disease.

  • Systemic chemotherapy
    • For patients with advanced hepatocellular carcinoma who are not candidates for surgical resection, liver transplantation, or localized tumor ablation, systemic chemotherapy remains the mainstay of therapy. Unfortunately, hepatocellular carcinoma is a relatively chemotherapy-resistant tumor; therefore, outcomes using this mode of treatment are unsatisfactory. Resistance to chemotherapy may be caused by the universal expression of the multidrug resistance gene protein on the surface of the malignant cells, leading to active efflux of chemotherapeutic agents. Chemotherapy is usually not well tolerated and seems to be less efficacious in patients with hepatocellular carcinoma with underlying hepatic dysfunction. Younger patients with well-compensated cirrhosis due to chronic hepatitis B or C infections have better outcomes with chemotherapy than older patients with alcoholic cirrhosis and other comorbid diseases.
    • The most active single agent drugs tested have been doxorubicin, cisplatin, and fluorouracil. Response rates are about 10%, and treatment shows no clear impact on overall survival.21,18 More recently, gemcitabine and capecitabine have been evaluated in clinical trials; response rates have been low and short term.
    • Various combination chemotherapy regimens have also been studied. Recently, cisplatin-based combination regimens, such as gemcitabine and oxaliplatin, have shown improved response rates around 20%, but to date, no survival advantage as compared to supportive care alone has been shown. No difference seems to exist in response rates between 2- or 3-drug regimens. Moreover, some of these combination regimens cause considerable toxicity.
    • Chemoimmunotherapy uses a combination of chemotherapy and immunomodulatory agents, such as interferon-alpha, to try to achieve better tumor response rates. Immunotherapy has had encouraging results in patients with certain types of cancers such as renal cell carcinoma and melanoma. PIAF is a combination of cisplatin, interferon-alpha, doxorubicin, and infusional 5-fluorouracil that is associated with a response rate of 26%, which is higher than the response rates with single chemotherapy agents. Although overall median survival is longer with PIAF than single-agent doxorubicin, treatment-related toxicity is significant. The best candidates for this therapy are young patients without liver cirrhosis and normal bilirubin levels.22
    • Antiangiogenesis agents (ie, bevacizumab), which work by disrupting the formation of blood vessels that feed tumors, are a new class of drugs that may prove to be of benefit in the treatment of hepatocellular carcinoma. The highly vascular nature of hepatocellular carcinoma tumors suggested that therapy with an antiangiogenesis agent might be effective. Bevacizumab by itself, however, is of limited clinical use. The combination of bevacizumab with gemcitabine and oxaliplatin, though, produced a 20% response rate with an additional 27% of patients who had stable disease.23
    • [#Sorafenib]Sorafenib, a multitargeted oral kinase inhibitor, has recently been shown in a phase III trial to prolong survival in patients with hepatocellular carcinoma.24 This agent, which targets various pathways, including VEGFR, PDGFR, KIT, FLT-3, and RET, was compared to placebo in a trial of 602 patients. Median survival was prolonged significantly to 10.7 from 7.9 months, and time to progression was 5.5 months, compared with 2.8 in the placebo group. Currently, this is the only FDA-approved antineoplastic for hepatocellular carcinoma. The recently revised National Comprehensive Cancer Network (NCCN) guidelines for hepatocellular carcinoma recommend sorafenib as a treatment option at several points in the treatment algorithm.17 Sunitinib is another multitargeted tyrosine kinase inhibitor with reported activity in hepatocellular carcinoma,25 Erlotinib, an oral epidermal growth factor (EGF) receptor tyrosine kinase inhibitor, has also shown some activityagainsthepatocellular carcinoma when used alone or in combination with bevacizumab.26,27 A recent report has suggested that the mTOR inhibitor sirolimus may have benefit in the treatment of both cholangiocellular carcinoma and hepatocellular carcinoma.27
    • Chemoembolization is the delivery of high concentrations of chemotherapeutic agents directly to the hepatocellular carcinoma tumor via the hepatic artery, which provides the tumor with most of its blood supply. The remainder of the liver may be spared because it can rely on the portal vein for its blood supply.28
    • Embolizing agents such as cellulose, microspheres, lipoidal, and gelatin foam particles are used to deliver intra-arterial chemotherapy (mitomycin, doxorubicin, cisplatin) to the tumor via the hepatic artery.
    • Morbidity from this procedure is greatly dependent on the extent of cirrhosis. In general, patients with portal vein thrombosis, encephalopathy, or biliary obstruction are not candidates for chemoembolization.29
    • Response rates of 60-80% are seen. In addition, 2 recent clinical trials from Spain and Hong Kong showed a modest survival benefit with the use of doxorubicin (Adriamycin) or cisplatin with embolization as compared to supportive care only in patients with unresectable tumors.30,31,32
  • See related CME at Diagnosis and Management of Hepatocellular Carcinoma.

Surgical Care

  • Partial hepatectomy
    • In the United States, resection is possible in only 5% of patients. In general, solitary hepatocellular carcinoma lesions confined to the liver without vascular invasion with well-preserved hepatic function have the best outcomes. Although there are no strict criteria in terms of tumor size, many surgeons use less than 5 cm as their cutoff.
    • Five-year survival rates for resectable lesions vary widely from 30% to as high as 90% for very early stage hepatocellular carcinoma lesions.33,34 Fibrolamellar hepatocellular carcinoma may have a better prognosis for survival after surgical resection because of a more favorable size, predominantly left lobe location, and the absence of cirrhosis in the unaffected portion of the liver.
    • Appropriate evaluation of patients prior to resection is crucial since intraoperative mortality is doubled in cirrhotic versus noncirrhotic patients. Preoperative laparoscopic inspection aids in diagnosing both the tumor and extent of cirrhosis.
  • Transplantation
    • Many patients are not candidates for partial hepatectomy due to extent of underlying liver disease. Some of these patients are good candidates for liver transplantation since it has the potential for eliminating the cancer as well as curing the underlying liver disease.
    • Orthotopic liver transplantation can be considered for patients who meet the Milan criteria—one tumor less than 5 cm or up to 3 tumors all less than 3 cm. These highly selected patients have excellent survival rates, similar to those of patients who undergo liver transplantation for end-stage liver disease without hepatocellular carcinoma.35,36,37,38
    • Although availability of donor organs is still limited, the Organ Procurement and Transplantation Network (OPTN) and the United Network for Organ Sharing (UNOS) have recognized the urgency of proceeding to transplantation in patients with limited stage hepatocellular carcinoma. Over the past 5 years, revision of the UNOS policy has established medical criteria by which a patient with early/small hepatocellular carcinoma can be assigned additional priority for liver allocation so as to increase the likelihood of a favorable transplant outcome. This has resulted in shorter wait times to transplantation and better overall outcomes. Bridging therapy with local therapies, such as chemoembolization or radiofrequency ablation (RFA), is sometimes considered for patients on the transplant waiting list.
  • Local tumor ablation
    • Intratumoral injections of ethanol or acetic acid, heat (via radiofrequency, microwave, or laser ablation), or cold (cryoablation with liquid nitrogen) may be used to locally control tumors smaller than 4-5 cm. These techniques are frequently performed percutaneously as outpatient procedures. In general, these procedures are reserved for patients who do not meet criteria for surgical resection yet are candidates for a liver-directed procedure based on the presence of limited liver-only disease.
    • Radiofrequency ablation (RFA) is the delivery of radiofrequency thermal energy to the hepatocellular carcinoma lesion causing necrosis of the tumor. During RFA, a high frequency alternating current is delivered from the tip of an electrode into the surrounding tissue. The ions within the tissue attempt to follow the direction of the alternating current resulting in friction and eventual heating of the tissue. As tissue temperature elevates above 60°C, tumor cells begin to die resulting in an area of tumor necrosis. The needle electrode is advanced into the hepatocellular carcinoma lesion usually via a percutaneous route with the guidance of ultrasonography. The procedure can also be performed surgically via laparoscopy or laparotomy.
    • RFA is usually used for treatment of tumors less than 4 cm in size. For small tumors, studies show good initial local tumor control with an average local recurrence rate of 5-6% within the first 20 months. The treatment of larger tumors results in much higher rates of local recurrence. Unfortunately, a significant proportion of patients eventually develop clinically detectable hepatic or extrahepatic disease from their preexisting micrometastatic lesions. RFA is usually well-tolerated, but complications including fever, pain, bleeding, pleural effusion, hematoma, and intermittent transaminitis among others have been reported.39
    • Percutaneous ethanol or acetic acid ablation is reserved for patients with small tumors; however, in many areas, the ease and efficacy of RFA has now replaced these older techniques. Radiation therapy is limited by dose-related radiation hepatitis, which precludes the administration of external beam radiation in doses effective for tumor eradication. Doses of 2500 cGy may be used for palliative measures.
    • CyberKnife system is a new technology that uses a combination of robotics and image guidance to deliver concentrated and highly focused beams of radiation to the tumor while minimizing radiation exposure to the surrounding healthy liver tissue. CyberKnife stereotactic radiosurgery is a promising new treatment tool for localized hepatocellular carcinoma lesions. Currently, its availability is limited to a few medical centers, and long-term efficacy for hepatocellular carcinoma lesions is yet to be determined.

Consultations

  • Hepatobiliary surgeon
  • Oncologist
  • Interventional radiologist
  • Interventional gastroenterologist

Medication

Antineoplastic agents

Few options are available for the systemic therapy of hepatocellular carcinoma (see Treatment).


Sorafenib (Nexavar)

First oral multikinase inhibitor that targets serine/threonine and tyrosine receptor kinases in both the tumor cell and the tumor vasculature. Targets kinases involved in tumor cell proliferation and angiogenesis, thereby decreasing tumor cell proliferation. These kinases included RAF kinase, VEGFR-2, VEGFR-3, PDGFR-beta, KIT, and FLT-3. Indicated for unresectable hepatocellular carcinoma.

Adult

400 mg PO bid 1 h ac or 2 h pc; continue until benefit no longer observed or unacceptable toxicity occurs; may decrease dose to 400 mg qd or 400 mg qod if skin toxicity occurs

Pediatric

Not established

CYP450 2B6 and 2C8 inhibitor; predominantly eliminated by UGT1A1 pathway (caution when coadministered with other drugs eliminated by UGT1A1 [eg, irinotecan]); coadministration with warfarin may increase INR or bleeding; increases AUC for docetaxel and doxorubicin

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Common adverse reactions include hand or foot skin reaction and rash (modify dose); may increase risk of hemorrhage, cardiac ischemia and/or infarction, alopecia, pruritus, or diarrhea; caution with severe hepatic impairment (ie, Child-Pugh C)


Sunitinib (Sutent)

Mulitkinase inhibitor that targets several tyrosine kinase inhibitors implicated in tumor growth, pathologic angiogenesis, and metastatic progression. Inhibits platelet-derived growth factor receptors (ie, PDGFR-alpha, PDGFR-beta), vascular endothelial growth factor receptors (ie, VEGFR1, VEGFR2, VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony-stimulating factor receptor type 1 (CSF-1R), and the glial cell-line–derived neurotrophic factor receptor (RET).

Adult

Standard dose: 50 mg PO qd on a schedule of 4 wk on treatment followed by 2 wk off treatment, then repeat cycle
Dose modification: Increase or reduce dose in 12.5-mg increments based on individual safety and tolerability
Coadministration with potent CYP4503A4 inhibitors: Minimum dose of 37.5 mg PO qd during treatment phase of cycle
Coadministration with CYP4503A4 inducers: Maximum dose of 87.5 mg PO qd during treatment phase of cycle

Pediatric

Not established

Potent CYP4503A4 inhibitors (eg, ketoconazole, itraconazole, clarithromycin, atazanavir, indinavir, nefazodone, nelfinavir, ritonavir, saquinavir, telithromycin, voriconazole) may increase plasma concentrations; CYP4503A4 inducers (eg, dexamethasone, phenytoin, carbamazepine, rifampin, rifabutin, phenobarbital) may decrease plasma concentrations; St John's wort induces metabolism and decreases plasma concentrations unpredictably (do not take concurrently)

Documented hypersensitivity; concurrent administration with St John's wort

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Common adverse effects include diarrhea, skin discoloration, mouth irritation, weakness, and altered taste; may cause fatigue, hypertension, bleeding, swelling, and hypothyroidism; in clinical trials, decreased left ventricular ejection fraction to below lower limits of normal in 15% of patients (monitor for CHF and discontinue if clinical manifestations of CHF develop); may prolong QT interval, which may lead to Torsade de Pointes; may cause hemorrhagic events that may include epistaxis or rectal, gingival, GI, genital, or wound bleeding


Erlotinib (Tarceva)

Pharmacologically classified as a human epidermal growth factor receptor type 1/epidermal growth factor receptor (HER1/EGFR) tyrosine kinase inhibitor. EGFR is expressed on the cell surface of normal cells and cancer cells.

Adult

100 mg PO qd 1 h ac or 2 h pc

Pediatric

Not established

Predominantly metabolized by CYP3A4; potent CYP3A4 inhibitors may decrease clearance (eg, ketoconazole increased AUC by two-thirds), caution with other strong CYP3A4 inhibitors (eg, atazanavir, clarithromycin, indinavir, itraconazole, nefazodone, nelfinavir, ritonavir, saquinavir, telithromycin, troleandomycin [TAO], voriconazole); CYP3A4 inducers may decrease AUC (ie, rifampin decreased AUC by two-thirds)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with hepatic impairment; may cause interstitial lung disease (including fatalities), elevated INR and bleeding; instruct patient to immediately seek medical attention for severe or persistent diarrhea, nausea, anorexia, vomiting, onset or worsening of unexplained shortness of breath or cough, or eye irritation; commonly causes rash and diarrhea (diarrhea unresponsive to loperamide may require dose reduction or temporary therapy interruption)

Immunosuppressant agents

Agents that inhibit signal transduction pathways may be of benefit.


Sirolimus (Rapamune)

Interferes with signal transduction pathways.

Adult

6 mg PO loading dose, then 2-5 mg PO qd

Pediatric

Not established

Drug levels and toxicity may increase with diltiazem, nicardipine, clotrimazole, verapamil, erythromycin, ketoconazole, itraconazole, fluconazole, bromocriptine, grapefruit juice, metoclopramide, methylprednisolone, danazol, cyclosporine, cimetidine, and clarithromycin; levels may decrease with rifabutin, rifampin, phenobarbital, phenytoin, and carbamazepine; administer sirolimus 4 h after cyclosporine

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate hyperlipidemia and thrombocytopenia; caution with hepatic impairment (decrease maintenance dose by one third); monitor blood sirolimus blood levels in pediatric patients, in patients with hepatic impairment, during coadministration of strong CYP450-3A4 inducers or inhibitors, or if cyclosporine dosing is markedly reduced or discontinued
Not recommended for use in de novo liver or lung transplantation; coadministration with cyclosporine or tacrolimus in liver transplant patients recipients increases hepatic artery thrombosis risk; bronchial anastomotic dehiscence (fatal in most cases) has been reported in de novo lung transplantation when sirolimus has been part of immunosuppressive regimen; increased susceptibility to infection and possible lymphoma development may result from immunosuppression; risk for renal impairment increased when sirolimus and cyclosporine used concomitantly, compared to cyclosporine alone

More on Hepatic Carcinoma, Primary

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Differential Diagnoses & Workup: Hepatic Carcinoma, Primary
Treatment & Medication: Hepatic Carcinoma, Primary
Follow-up: Hepatic Carcinoma, Primary
Multimedia: Hepatic Carcinoma, Primary
References
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Further Reading

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Keywords

primary hepatocellular carcinoma, HCC, liver cancer, primary liver cancer, liver carcinoma, primary liver carcinoma, cirrhosis, liver failure, hepatoma, liver dysfunction, hepatic dysfunction, liver tumor, hepatic tumor, liver disease, jaundice, hepatitis B virus, HBV, hepatitis C virus, HCV, hepatitis virus, alcoholism, alcoholic liver disease, hemochromatosis, aflatoxin, liver function test, liver function testing, LFTs, OLT, orthotopic liver transplantation, liver transplantation, liver transplant

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Contributor Information and Disclosures

Author

Keith E Stuart, MD, Chairman, Department of Hematology and Oncology, Lahey Clinic
Disclosure: Nothing to disclose.

Coauthor(s)

Zsofia K Stadler, MD, Clinical Fellow, Department of Hematology and Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School
Disclosure: Nothing to disclose.

Medical Editor

Antoni Ribas, MD, Department of Medicine, Division of Hematology-Oncology, Assistant Professor of Medicine, University of California at Los Angeles Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

Rajalaxmi McKenna, MD, FACP, Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD, Clinical Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine at Tucson; Consulting Staff, Arizona Cancer Center
Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research
Disclosure: GlobeImmune Salary Consulting; Amplimed Consulting fee Consulting; FibroGen Consulting fee Consulting

 
 
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