Abstract

A 70-year-old man originally from Poland was referred to the hepatoma service for investigation of two liver lesions found during routine hepatocellular carcinoma (HCC) screening. Active medical history included both castrate sensitive metastatic prostate cancer and Child–Pugh A cirrhosis secondary to type 2 diabetes mellitus and previous heavy alcohol use. For his prostate cancer, he was treated with androgen deprivation therapy (ADT) with goserelin and received upfront docetaxel chemotherapy with prednisolone, before being enrolled on a clinical trial of enzalutamide. Prostate specific antigen (PSA) level remained suppressed at <0.01 μg/L on therapy. The patient was asymptomatic with no features of hepatic decompensation. His Child–Pugh status was A6. Biochemistry revealed preserved synthetic liver function; alpha fetoprotein (AFP) level was 5 μg/L. Computed tomography (CT) chest, abdomen, and pelvis demonstrated two 10-mm arterially enhancing hepatic nodules in segments 7/8 and 4a (Fig. 1a) with no portal venous washout (Fig. 1b). On magnetic resonance imaging (MRI) with Primovist, both lesions retained Primovist and hence both were indeterminate (Liver Imaging Reporting and Data System [LI-RADS]-3). Differentials at discussion at the Hepatoma Multidisciplinary meeting included regenerative or dysplastic nodules, given metastatic prostate cancer typically shows hypodensity on contrast-enhanced imaging. The nodules were followed up in tandem with the patient's prostate cancer at 6 monthly intervals and were stable on contrast-enhanced CT (LI-RADS 3) at 12 and 18 months (Fig. 1c) (LI-RADS 3) and therefore did not meet criteria for biopsy. In addition, there were numerous new pulmonary nodules. At 24 months however, CT revealed new lesions concerning for multifocal HCC (Fig. 1d), increase in the size of the segment 7 and 8 lesions with a new 1.5-cm lesion in segment 2 with washout (LI-RADS 5). The patient remained clinically stable and had a suppressed PSA level. He underwent an ultrasound guided biopsy of the segment 2 lesion. Histopathology was consistent with a diagnosis of metastatic small cell neuroendocrine carcinoma. The patient was commenced on single agent Carboplatin to treat his now de-differentiated small cell prostate cancer, to which he has responded well with interval response demonstrated on serial CT of pulmonary and liver lesions in addition to the bony disease on CT SPECT. The diagnosis of HCC is typically made on cross-sectional radiological findings without the need for confirmatory tissue in cirrhotics. LI-RADS scoring system has high sensitivity and specificity in diagnosing HCC in cirrhotic patients and is applicable to lesions ≥ 1 cm. Thus, biopsy is rarely required to diagnose HCC. Current guidelines support the use of the LI-RADS as a classification system for reporting liver lesions. The decision to biopsy is a contentious clinical question that is not definitively answered by current guidelines. Biopsy carries known risks of bleeding, tumor seeding, and failure to obtain adequate tissue for sampling. There are several mimics of HCC on imaging. Intrahepatic cholangiocarcinomas are known to mimic HCC. Tumors such as neuroendocrine tumors, squamous cell carcinoma metastases, and lung cancer metastases require pathological differentiation from HCC. Prostate cancer metastasis to the liver is heralded by hypoenhancement on contrast-enhanced imaging, whereas small cell prostate cancer itself is ill defined in imaging and there is currently a paucity of literature describing its imaging characteristics. It is aggressive in nature and 40–50% of cases are reported to occur in men with pre-existing prostate adenocarcinoma. The PSA is highly sensitive to progression of metastatic prostate adenocarcinoma but not to de-differentiated carcinoma, and it can therefore be difficult to differentiate de-differentiated prostate cancer from HCC in the cirrhotic patient. This case demonstrates that although current clinical practice guidelines deliver a safe approach to the diagnosis of HCC, alternative diagnoses can be missed if they carry similar characteristics on cross-sectional imaging, especially in cirrhotic patients and particularly in those with a cancer history. The role of biopsy in indeterminate liver lesions is often a discussion point and requires multidisciplinary team discussion, and the LI-RADS criteria should always be interpreted in the clinical context.

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