2.1. Case 1 Description
This case refers to a 53-year old woman with HCV-related cirrhosis and portal hypertension, not included in any surveillance program. In October 2011, due to abdominal pain she underwent abdominal ultrasound (US) and contrast-enhanced computed tomography (CT), both showing six focal liver lesions suspicious for HCC, the largest in the right lobe and measuring 70 mm × 87 mm. In November 2011 she was admitted to her local hospital because of hepatic decompensation with ascites and endoscopic finding of grade III esophageal varices at high risk of bleeding. She was referred to our Unit in order to confirm the suspicion of HCC. Contrast-enhanced ultrasound (CEUS) of focal liver lesions was consistent with the diagnosis of multifocal HCC. A biopsy specimen obtained from the major nodule showed HCC (Edmondson grade II). Due to the detection on Doppler US of a high flow arteroportal fistula within the major HCC lesion, she underwent percutaneous transcatheter endovascular embolization. Control endoscopy showed grade I-II esophageal varices. Since the patient was considered not eligible for endovascular treatment of HCC, but had a good liver function (Child-Pugh class A), treatment with sorafenib was started in December 2011. Alpha-fetoprotein (AFP) serum levels were 19 ng/ml (< 7 ng/ml).
Three months later, treatment was stopped due to CT evidence of disease progression. The major lesion had increased to 90 mm × 87 mm, with persistent high vascularization, and involved the corresponding segmentary portal vessel (Figure 1, A and B). There was also an increase in size and in number of the other lesions from 5 to 7. AFP serum levels were 17 ng/ml. Given the absence of second-line therapy and the unmodified liver function, we proposed treatment with capecitabine. The patient gave her informed consent and in March 2012 she started therapy at a dosage of 500 mg twice/daily. Since one month later she developed a grade 3 hand-foot syndrome (HFS), treatment was temporarily stopped and she was treated with emollient and urea-based creams until complete resolution of the HFS. Capecitabine was re-started at a reduced dose of 750 mg per day but, in June 2012, grade 2 HFS and anemia (hemoglobin dropped from 12 to 9 g/dl) occurred. Capecitabine was again interrupted, until resolution of HFS and anaemia, and then re-started at a dosage of 150 mg thrice daily. At the end of June, contrast-enhanced CT scan showed size reduction of the major lesion to 75 mm × 72 mm with hypodense necrotic areas (Figure 1, C and D), the persistence of three subcentimetric lesions, and the complete disappearance of the other four lesions. Capecitabine was continued and, after a further dose reduction to 150 mg twice daily due to a transient reappareance of grade 2 HFS which required one week interruption, was well tollerated. The last contrast-enhanced CT assessments showed further decrease of the tumor, with the major lesion decreased to 43 mm × 39 mm in October 2012, and to 39 mm × 39 mm in January 2013 (Figure 1, E and F). AFP serum levels remained stable over the treatment period. The patient is still in good clinical condition (ECOG performance status 0) with a preserved liver function.
Figure 1.
Contrast-enhanced CT scan of the liver performed as baseline assessment in March 2012 (A and B), at the end of June 2012 (C and D), and in January 2013, showing a progressive shrinkage of the the large HCC lesion of the right lobe. A, C, and E panels: arterial phase. B, D, and F panels: equilibium phase
Note that the HCC lesion detected in the segment II (arrows in panels A and B) was also markedly reduced at the first CT control (C and D), and was no longer clearly distinguishable from the surrounding tissue at the last radiologic control (C and D).
2.2. Case 2 Description
This is the case of an 80-year old male without history of liver disease. His past medical history included hypertensive heart disease and chronic atrial fibrillation with cardioembolic cerebellar stroke in June 2009 for which he was assuming warfarin. In May 2010 the patient was admitted for severe anemia due to acute bleeding of a voluminous mass of the right liver lobe. Anticoagulant therapy was stopped and he underwent a contrast-enhanced liver CT that showed a radiologic pattern consistent with a malignant lesion. A percutaneous biopsy of the liver lesion revealed grade 2 HCC. AFP serum levels were normal. In December 2011 the patient was referred to our Unit and was staged with a contrast-enhanced CT scan that showed a lesion in segment VI of 111 mm x 95 mm with a small adjacent satellite lesion, and other three lesions with a maximum diameter of 22 mm (segment I), 25 mm (segment VIII), and 24 mm (segment IV) (Figure 2, A, B, E, F). Due to the multifocal HCC with a high risk of bleeding and spontaneous rupture of the major lesion, we judged the patient not eligible for endovascular or sorafenib treatment ( 5 ). Considering the absence of chronic liver disease, and the good clinical conditions (ECOG Performance status 0), we proposed an off label treatment with metronomic capecitabine at the dose of 500 mg thrice daily. The patient gave the informed consent and started treatment in January 2012. The contrast-enhanced CT scan, scheduled every three months, showed a progressive reduction in vascularity of all nodules with a global dimensional stability of the major lesion. The last control CT scan of January 2013 showed an increase of necrotic area within the largest lesion (Figure 2, C and D). The lesion of the segment VIII (Figure 2, G and H), after a reduction in size over the time, was no longer distinguishable from the surrounding tissue. The patient is still in treatment with a good quality of life, without side effects or laboratoristic alterations.
Figure 2.
Contrast-enhanced CT scan of the liver performed in December 2011, as baseline assessment, showing the large HCC lesion of the right lobe including a necrotic component (A and B), a small satellite lesion (arrow in panel A), and the lesion in segment VIII (arrow in panel E). A, C, E, and G panels: arterial phase. B, D, F, and H panels: equilibrium phase.
The last contrast-enhanced CT scan performed in January 2013 showed a reduction in vascularity of the large lesion with an increase of tumor necrosis, and a significant shrinkage of the satellite lesion (C and D). The lesion in segment VIII was no longer clearly distinguishable from the surrounding tissue (G and H).
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