[28, 29] A previous study showed that

the 3-year cumulati

[28, 29] A previous study showed that

the 3-year cumulative occurrence rate of liver cancer was 12.5% in cirrhotic patients and 3.8% in chronic hepatitis patients, suggesting that hepatitis B and C virus infection and high AFP values are risk factors.[30] Ascha and colleagues reported that HCC developed in 12.8% of cirrhotic patients with non-alcoholic steatohepatitis (NASH) and 20.3% of cirrhotic patients with hepatitis C virus (HCV) infection (P = 0.03) during a median follow-up period of 3.2 years; the cumulative incidence of HCC was 2.6% per year for NASH-cirrhosis and 4.0% in HCV-cirrhosis (P = 0.09).[31] As for the morphological aspects, a coarse parenchymal echo pattern in the liver is a risk factor for the development of HCC in patients with Nutlin-3a solubility dmso HCV-related cirrhosis.[32] The incidence of HCC differed depending JNK inhibitor library on the echo pattern of liver parenchyma; that is, HCC developed in 9 of 11 (82%) cases with a coarse-nodular pattern, 3 of 7 (43%) with a coarse pattern, and only 1 of 20 (5%) with a fine pattern. The study found that the incidence of a coarse-nodular pattern of liver parenchyma was significantly higher in the high DNA synthesizing group than in the low DNA synthesizing group; thus, increased DNA synthesis by hepatocytes may account for the increased risk of developing HCC. Additionally, hepatic lesions showing hypo-density in both the arterial and equilibrium

phases of contrast-enhanced CT were associated with an annual HCC incidence rate 上海皓元 of 15.8%.[33] This incidence rate was higher than in our study,

a discrepancy that may have been due to the marked differences with respect to lesion characteristics between the studies. The appearance of hepatic lesions in the so-called postvascular phase is based on microbubble accumulation using Sonazoid or Levovist.[10-15] Sonograms of this phase allow us to predict histological findings and to characterize focal hepatic lesions.[2, 6, 7] However, postvascular-phase findings are not specific because PIELs encompass a wide spectrum of hepatic lesions. In particular, PIELs may include well-differentiated HCC in cirrhotic patients, and may present an alternation from non-hypervascular lesion to hypervascular lesion. In our study, three PIELs had an arterial-phase hypervascular appearance, which is strongly suggestive of a malignant lesion. However, these lesions did not change the imaging findings during follow-up, indicating that arterial vascularity may not always be predictive for the development of HCC from a PIEL. The mean diameter of HCC lesions that occurred in our study was 15.1 mm, being sufficient to be cured by local treatment alone.[34] The time interval between HCC detection and the last imaging was 4.0 months, which is considered to be an acceptable duration. In fact, the American Association for the Study of Liver Diseases recommends a 6-month interval for HCC screening in cirrhotic patients.

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