A Case of Hepatocellar Carcinoma in Egypt

Figs 1 and 2. Disease progression at the time of the last follow-up (March 2007).

Mr. E.S. is a 68-year-old male patient known to have had hepatitis B infection and liver cirrhosis since 1995. During regular follow-up in September 2004, abdominal sonography showed a right focal hepatic lesion. Spiral computerized tomography (CT) of the abdomen, performed on September 26, 2004, revealed the presence of liver cirrhosis as well as a focal hepatic lesion in the posterior segment of the right lobe of the liver, measuring 2.1 x 2.7cm. There was evidence of portal hypertension, although the portal vein was patent, and cholecystitis associated with gall-stones. Serum alpha-fetoprotein (AFP) was 110 ng/ml (normal is up to 13.6 ng/ml). The patient underwent laparotomy on October 31, 2004, at which time three lesions were identified in hepatic segments II, III, and VIII. The lesions in segments II and III were resected and that in segment VIII was destroyed by radiofrequency ablation. Pathological examination showed features of mixed cirrhosis and hyperplastic nodule formation as well as hepatocellular carcinoma. Spiral CT of the abdomen performed two months later, on December 12, 2004, revealed that the previously ablated segment VIII hepatic lesion had been adequately ablated and now showed central necrosis and no enhancing tissue. AFP on December 11, 2004 dropped to 20 ng/ml.

The patient was followed uneventfully until March 2005, when a routine abdominal sonography revealed two new focal lesions on the right side of the liver. A spiral CT of the abdomen and measurement of AFP (151 ng/ml) confirmed the relapse. Chemo-embolization with cisplatin was undertaken on August 28, 2005.

By October 10, 2005, AFP was elevated to 610 ng/ml. Magnetic resonance imaging (MRI) of the abdomen showed no evidence of residual activity within the lesion but the patient started to complain of bone pain, especially in the thoracic region. A bone scan, performed on December 3, 2005, showed uptake of isotope in multiple osseous lesions in the right occipito-parietal region, several ribs and the upper thoracic vertebrae. The patient was given three doses of systemic single-agent doxorubicin (50 mg/m2 every 3 weeks). CT of the abdomen and pelvis on February 15, 2006 showed no change in the right hepatic lesion. However, serial AFP measurements had shown a progressive increase in January and February, reaching 1540 ng/ml on February 13, 2006.

In view of this, a decision was made to stop doxorubicin. On July 18, 2006, the patient was started on Xeloda (an oral agent converted to 5-fluorouracil in the body) at a dose of 2 gm/m2 for 14 days every 3 weeks. The third cycle was completed in early September 2006. Re-evaluation showed a markedly elevated AFP and CT of the abdomen and pelvis on 18 September 2006 showed an increase in the size of the right hepatic lesion and new lesions in the left lobe of the liver. The physician-in-charge decided to stop further specific therapy and to give only best supportive care. Figures 1 and 2 show disease progression observed at the time of the last follow-up in March 2007 although the patient’s performance status was excellent.

Comment
Hepatocellular carcinoma accounts for over 650,000 deaths worldwide every year and nearly always arises in a setting of pre-existing liver damage, particularly cirrhosis, from viral hepatitis or alcohol. Only in rare patients, particularly in developing countries, is tumor sufficiently limited for complete surgical resection and a chance for cure. In appropriate settings liver transplantation may be performed. In spite of the poor prognosis in most patients, the disease can often be effectively controlled by a number of approaches, as illustrated by the present case.

Hussein Khaled
National Cancer Institute
Cairo, Egypt