Diagnosing HCC in Chronic Liver Disease


Richard Finn, MD: The case we are discussing now is of a 62-year-old lady who has a history of tobacco use and heavy alcohol use—though she has not drunk for period of time—diabetes, and hypertension. She presents to her primary care doctor complaining of fatigue. On evaluation, the doctor orders blood tests, serum chemistries, and identifies some abnormalities in her liver function test. Her bilirubin is slightly elevated at 1.4 mg/dL; her albumin is fairly normal at 3.8 g/dL; her INR is normal; her platelet count is 90,000; and her kidney function is normal as well. Her performance status is ECOG 1, so she is fairly functional. On the exam, she has some stigmata of chronic liver disease, such as spider angioma on her chest, but no ascites and no history of encephalopathy.

Given the complaint of fatigue in the setting of chronic liver disease, the patient also has some weight loss. She’s referred for imaging. Imaging of the chest and the pelvis looking for a malignancy identifies a 6-cm hypervascular mass in the liver. This mass is invading into the right portal lane, and there’s evidence of enlarged lymph nodes in the abdomen and multiple small lesions in the chest, which are concerning for metastases.

So, the question for us initially is, what’s the diagnosis? This is a patient who has evidence of chronic liver disease. The CT scan shows a hypervascular mass. There’s some evidence of portal hypertension both on imaging with small varices as well as on the lab tests, indicating thrombocytopenia. In the setting of chronic liver disease, this patient can be diagnosed with hepatocellular carcinoma. They have a hypervascular tumor in the setting of chronic liver disease. As far as the stage of this tumor, we start to get concerned because there are some findings that are consistent with an advanced tumor. In liver cancer, we don’t use the known tumor metastases staging system or the PNM system so much as other staging systems, but take into account not only the tumor extent but also the underlying liver function.

We know that the risk factor for liver cancer includes anything that leads to chronic liver disease. Therefore, a patient should generally be screened for liver cancer. Unfortunately, this patient, who has a long history of alcohol abuse, was not identified as having liver disease and was not screened to find this tumor earlier. This patient presented fairly late with evidence of advance disease. Still, her liver function is fairly well preserved. Regardless of the etiology of liver cancer—such as hepatitis B, hepatitis C, or alcohol or metabolic causes—there are always a subset of patients who present with well-preserved liver function. Those are the patients we want to find. Hepatitis B patients, because of the mechanism of the viral infection, are more commonly less cerotic at presentation—that’s in contrast to hepatitis C.

Patients with alcohol liver disease do have some ability to recover liver function if they stop drinking. So, it is not necessarily uncommon for someone who has stopped drinking, or has a history of alcoholism in the past, to still present with well-preserved liver function as this patient did.

Transcript edited for clarity.

June 2015

  • A 62-year old female smoker with a history of alcoholism and type 2 diabetes, HTN is experiencing fatigue
  • ECOG=1
  • Child-Pugh A
  • T bilirubin 1.4; albumin 3.8; INR 1.1; no ascites, no encephalopathy; platelets 94
  • CT scan reveals one 6-cm liver mass with invasion into the right branch of the portal vein, metastatic disease involving the abdominal lymph nodes and lung
  • Biopsy confirmed HCC diagnosis; poorly differentiated
  • Patient admitted nonadherence to anti-hypertensive medications
  • Therapy was initiated with sorafenib at 400 mg BID
  • Patient experienced grade 1 HTN, fatigue, dyspepsia, grade 3 diarrhea
  • Dose was reduced to 400 mg QD, antimotility agents were given
  • Patient was counselled regarding diet

July 2016

  • Follow-up imaging has shown stable disease
  • ECOG=1
  • Patient is now Child-Pugh B
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