Recently the authors proposed a new staging and grading system for primary biliary cirrhosis (PBC) that takes into account necroinflammatory activity and histological heterogeneity. Herein is proposed a convenient version of this system. Scores for fibrosis, bile duct loss, and chronic cholestasis were combined for staging: stage 1, total score of 0; stage 2, score 1-3; stage 3, score 4-6; and stage 4, score 7-9. Cholangitis activity (CA) and hepatitis activity (HA) were graded as CA0-3, and HA0-3, respectively. Analysis of interobserver agreement was then conducted. Digital images of 62 needle liver biopsy specimens of PBC were recorded as virtual slides on DVDs that were sent to 28 pathologists, including five located overseas. All participants were able to apply this version in all 62 cases. For staging, kappa was 0.385 (fair agreement) and the concordance rate was 63.9%. For necroinflammatory activity, the kappa and concordance rate were 0.110 (slight agreement) and 36.9% for CA, and 0.197 (slight agreement) and 47% for HA, respectively. In conclusion, this new staging and grading system for PBC seems to be more convenient and practical than those used at present, but more instruction and guidance are recommended for the grading of necroinflammatory activity in practice.
BACKGROUNDThe therapeutic results of nonsurgical treatment for patients with hepatocellular carcinoma (HCC) have been poor, and improved treatments are needed. The authors recently developed a new technique called angiographic subsegmentectomy for the treatment of patients with small HCC.METHODSThe technique includes confirming the diagnosis of small HCC using a helical computed tomography (CT) scan combined with an angiography system for identifying the tumor‐feeding subsegmental hepatic artery, injecting lipiodol containing farmorubicin until it enters the portal vein in sufficient amounts, and injecting sponge particles into the hepatic artery for embolization. Occlusion of the hepatic artery with gel particles and occlusion of the portal vein by lipiodol induce infarction necrosis, which encompasses the entire tumor and the surrounding liver parenchyma.RESULTSThe treatment was given to 23 patients with 30 HCC tumors that measured < 20 mm in greatest dimension. It was successful in all 23 patients. Serum alanine aminotransferase levels were elevated to a significant level in the majority of patients after treatment, mild ascites developed in three patients, and the patients complained of pain and fever posttreatment that were controlled readily. No patients developed hepatic failure. Only one patient developed recurrent disease posttreatment at 1.5 years, for a recurrence rate of 5% at 1 year and 6.6% at 1.5 years, a rate that has never been achieved with other treatment modalities.CONCLUSIONSAngiographic subsegmentectomy is a novel treatment for patients with small HCC. The results indicated that it is equivalent to undergoing small resection and is superior to conventional arterial chemoembolization. Cancer 2003;97:1051–6. © 2003 American Cancer Society.DOI 10.1002/cncr.11106
BACKGROUND:The authors successfully adopted an interesting and effective treatment for hepatocellular carcinoma (HCC) referred to as angiographic subsegmentectomy (AS). This treatment involved simultaneous embolization of the peripheral feeding artery and the portal vein. The result was that almost all of the HCC and peripheral liver parenchyma developed complete anatomic necrosis. METHODS: To determine the effectiveness of this method, the authors retrospectively studied the local recurrence rates of 49 solitary HCCs and the long-term survival rates of 120 patients with HCC between 2000 and 2008. RESULTS: The results indicated that, in 31 small, solitary HCCs (<2.0 cm), the local recurrence rate was only 9.6%; and, in 10 slightly larger HCCs (<3.0 cm), the local recurrence rate was only 10%. The 5-year, 8-year, and 10-year survival rates for patients with stage I and stage I/Child-Pugh grade A HCC were 74.27% and 77.65%, 53.05% and 51.76%, and 53% and 51.76%, respectively; and the 5-year, 8-year, and 10-year survival rates for patients with stage II and stage II/Child-Pugh grade A HCC were 66.21% and 71.41%, 39.9% and 39.60%, and 29.92% and 25%), respectively. There were no severe complications. CONCLUSIONS: AS should be investigated further as potential first-line therapy for the treatment of patients with stage I and II HCC. Cancer 2010;116:393-9.
Pedunculated hepatocellular carcinoma (HCC) or extrahepatic growth of HCC is an uncommon but not rare pathological form, but its genesis is unknown. Right-sided adrenal metastases of HCC that were abutting on or about to fuse with the right hepatic lobe were resected in three patients. The masses seemed to have originated in the para-adrenal tissue, leaving the adrenal gland intact. They were partially supplied by the hepatic artery as well as by the suprarenal artery. Four cases of autopsied pedunculated HCC of the right lobe were also studied. The mass was protruding caudad from the noncancerous parenchyma of the right lobe. Postmortem angiography carried out on one liver showed that only a small portion of the mass toward the liver was supplied from the hepatic artery. These observations suggest that some, perhaps most, of the right-sided pedunculated HCCs represent fusion of the right lobe and para-adrenal or adrenal metastatic HCC. This phenomenon may be explained by possible transport of cancer cells toward the right adrenal gland through the so-called adrenohepatic fusion, a relatively common anatomical change in advanced age. (HEPATOLOGY 1998;27:81-85.)
Humoral hypercalcemia caused by parathyroid hormone-related peptide (PTHrP), associated with cholangiocellular carcinoma (CCC), has rarely been documented. There have been no reports of CCC associated with extensive calcification of the tumor with psammoma body formation. A 66-year-old man was admitted with a large calcified tumor in the liver detected on an abdominal X-ray. An ultrasound-guided fine needle biopsy specimen of the liver tumor showed evidence of adenocarcinoma. He had hypercalcemia with an elevated PTHrP level. The patient died because of disseminated intravascular coagulation and progressive hepatic failure. A postmortem examination revealed a large poorly differentiated CCC in the liver. Immunohistochemical examination showed the presence of PTHrP-positive tumor cells. The calcified lesion consisted of a number of accumulated psammoma bodies. We present a case of PTHrP producing CCC with a marked psammoma formation.
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