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Castán et al.                                                                                                                                           Radiology of hepatocarcinoma in non-cirrhotic patients

           in underdeveloped countries. In developed countries,   later stages. Sometimes, the edges are imprecise,
           most HCC originate in a setting of alcoholic cirrhosis   which also determines more aggressive tumors.
           or non-alcoholic steatosis related to obesity. However,   Growth is usually expansive although there may
           there is an incidence of 0.5-1% per year in patients   be transcapsular infiltration into the surrounding
                                 [2]
           with non-cirrhotic livers.  Usually, such patients are   parenchyma.
           not subject to monitoring prevention programs and
           so HCC detection is usually late and secondary to   However,  a  high  percentage  of  patients  do  not
           symptoms produced by the tumor. Less frequent      demonstrate pathognomonic HCC criteria, showing
           risk  factors  are  type  II  diabetes  and  metabolic   atypical features. Thus, in a retrospective study
                                                                                                        [5]
           syndrome, congenital diseases such as hereditary   of  243  patients  conducted  by  Lee  et al.,  the
           hemochromatosis, tobacco, parasitic infections or   most typical behavior of tumors corresponded to
           genotoxin intake. The average age at diagnosis of   moderately differentiated HCC. A high percentage
           HCC is 63 years old, with an incidence three times   of cases showed atypical behavior (43.6%). Most
           higher in men than in women. [2]                   of these tumors corresponded histologically to well

           Clinically, it is a silent disease in early stages. When   A
           symptoms appear, the most common is abdominal pain
                 [3]
           (52%).  Less common symptoms are chronic diarrhea,
           jaundice, fever, or paraneoplastic syndromes such
           as hypercalcemia or hypoglycemia. It may occur with
           increased serum levels of alpha-fetoprotein, considered
                                            [4]
           indicative of HCC above 400 ng/dL.  However, this
           determination has low sensitivity and specificity for
           diagnosis and for monitoring.

           RADIOLOGICAL DIAGNOSIS OF HCC

           There are three basic diagnostic tests: computed         B
           tomography (CT), magnetic resonance imaging (MRI)
           and ultrasound (US).

           Computed tomography
           Proper  technique  is  essential  for  the  accurate
           assessment of HCC: a baseline study, an arterial
           phase after administration of intravenous contrast
           (30-35 s), a portal phase (75-90 s) and a late phase
           (after 3 min). HCC presents as a single nodular
           lesion in most cases. Around 20% are multinodular.
           Without contrast, its density is similar to normal or
           slightly lower than liver parenchyma. Contrast series    C
           shows a typical dynamic behavior. It is a tumor
           with neoangiogenesis of arterial origin; therefore, it
           enhances intensely in arterial phase. In portal phase
           (venous) and late phase, the tumor washes the
           contrast and becomes hypodense relative to normal
           parenchyma [Figure 1].

           This  behavior  of  early  enhancement  and  late
           washing (wash in - wash out) is part of the main
           diagnostic criteria for HCC. Its mosaic appearance
           is also characteristic with areas of different density   Figure 1: Computed tomography axial planes obtained in arterial
           within the liver, visible especially in post-contrast   phase (A), portal phase (B), and late phase (C). Lesion located in
           phases. The tumor is often encapsulated, identifying   the segment III of left hepatic lobe, heterogeneous enhancement
           one hypodense halo. The capsule enhances more      of the lesion is observed in the arterial phase (arrow in A) with
                                                              washout in the portal and late phases. Mosaic pattern is shown in
           slowly and gradually and uptake usually persists in   the arterial and portal phases (yellow arrow)
             2                                                                                                      Hepatoma Research ¦ Volume 3 ¦ January 12, 2017
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