Histologically, he had a poorly-differentiated hepatocellular carcinoma with multinucleated giant cells, numerous mitoses and a Ki-67 labeling index of 15%. Hyaline inclusions were noted in the cytoplasm of malignant cells. Pedunculated hepatocellular carcinoma is defined as a carcinoma protruding from

the liver with or without a pedicle. These carcinomas are unusual and only account for a small minority of all hepatocellular carcinoma cases (0.2–3%). Histologically, most of these carcinomas are poorly differentiated and show features of rapid growth including numerous mitoses and a high Ki-67 labeling index. Although peritoneal metastases are common, vascular invasion is not a prominent feature and most of these patients do not have early distant metastases. However, LDE225 datasheet as in the above case, tumor rupture can occur with either major or minor bleeding into the peritoneal cavity. Occasionally, surgical resection of these tumors is curative and

this may include resection of small peritoneal metastases. Contributed by “
“We read with great interest the article by Mannaerts et al.,1 who demonstrated the inhibitory effect of valproic acid (VPA) on hepatic stellate cell activation and consequent liver fibrosis in a chronically injured mouse liver. The authors’ initial concept is rather surprising because VPA, one of the most widely prescribed anticonvulsants, has been considered a hepatotoxic agent.2 The successful results of this study may make

clinicians expect implications for therapeutic options for liver fibrosis. Although NVP-BGJ398 in vitro they have presented hopeful information, we as pathologists insist that one must carefully ponder the risk-benefit balance. There medchemexpress have been many reports warning of the hepatotoxicity of VPA, including microvesicular steatosis, steatohepatitis, hepatocellular carcinomas, and even fulminant hepatitis.3, 4 We have also experienced an autopsy case of severe steatohepatitis related to chronic VPA administration. The patient, a 22-year-old man with an approximately 14-year medical history of VPA administration under a diagnosis of Lennox-Gastaut syndrome, died of fatal aspiration pneumonia. Most autopsy findings were concordant with clinical diagnoses, except for a markedly fatty liver. The liver was tender and yellowish and weighed 955 g. A cut surface of the liver showed a peculiar nodular appearance (Fig. 1A). Histological examination revealed a hallmark of incomplete septal cirrhosis associated with steatohepatitis (Fig. 1B). Because he was a nonobese nondrinker and was negative for any hepatitis viruses, it was concluded that VPA was the most likely cause of steatohepatitis in this case. The liver disorder had been subclinical (serum aminotransferases had been almost normal until just before death); therefore, an accurate diagnosis could not have been made while he was alive.