Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To establish useful predictors of the intrahepatic recurrence of hepatocellular carcinoma (HCC) after partial hepatectomy, retrospective analyses of clinical and pathologic factors were done in 112 of 206 patients treated by partial hepatectomy. The absence or presence of intrahepatic recurrence was confirmed by a follow-up study. Cancer-free survival rates after 1, 2, 3, and 5 years were 54.8%, 36.7%, 32.5%, and 25.6%, respectively. The significant factors affecting recurrence were tumor size, number of tumors, cancer cell infiltration of the fibrous capsule of the tumor, portal involvement, and stage of the tumor, but the grade of anaplasia according to Edmondson-Steiner's classification and the severity of associated liver cirrhosis did not show a correlation with the incidence of recurrence. According to Akaike's Information Criteria (AIC), tumor number is useful for predicting early prognosis, and capsular infiltration is a good indicator of long-term survival. However, portal involvement gives much prognostic information throughout the entire postoperative period.
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PMID:Predictive factors for intrahepatic recurrence of hepatocellular carcinoma after partial hepatectomy. 131 Apr 34

Hepatic resection can be performed safely in carefully selected patients with cirrhosis. To minimize morbidity and mortality, it is essential to reliably estimate functional hepatic reserve and the extent of tumor before resection is performed. Child's classification is a reliable predictor of long term survival, but a more sensitive measure of hepatic function is needed to predict early morbidity and mortality. Child's classification can also be used to stratify patients and exclude those at high risk from hepatic resection. Promising predictors of operative mortality focus on the mitochondrial function of hepatocytes and include cytochrome a (+a3) contents and the redox tolerance index. Patients with advanced cirrhosis are not candidates for extensive hepatic resection and require careful evaluation before consideration for any hepatic resection. In patients with well-compensated cirrhosis and unifocal tumors, the procedure of choice is an anatomic resection of the tumor. If tumor size and location allows, a segmentectomy offers the best outcome, minimizing postoperative liver dysfunction while offering a long term outcome not dissimilar to a major liver resection. In highly selected patients with incidental tumors, a central tumor and perhaps in patients with multifocal hepatocellular carcinoma, hepatic transplantation may be of benefit. By using the appropriate predictors of hepatic function, refined surgical techniques and optimal postoperative care, a mortality rate of less than 10 per cent is achievable in cirrhotic patients with hepatocellular carcinoma who require resection.
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PMID:Hepatic resection in patients with cirrhosis and hepatocellular carcinoma. 131 68

Between April 1986 and August 1990, 151 liver transplantations were performed at our institution, 16 (11%) of them in 14 patients with primary hepatic tumors. There were 12 hepatocellular carcinomas, 1 angiosarcoma, and 1 Klatskin tumor. None of the tumors was resectable, and there was no preoperative evidence of extrahepatic tumoral extension. Exploratory laparotomy was performed prior to transplantation in three patients and selective embolization of the tumor in six patients. There was no difference in the intraoperative requirements for blood or plasma in the patients with hepatic tumors when compared with other transplant recipients (28.6 +/- 23.6 units packed red blood cells [PRBC] versus 20.1 +/- 17.8 units PRBC, and 17.9 +/- 12.2 units plasma versus 17.1 +/- 10.5 units plasma, respectively). Extracorporeal venovenous bypass was used in all but one patient. There was no significant differences in the incidence of acute rejection or in the length of hospitalization in these patients when compared with other transplant recipients. All patients received triple immunosuppressive therapy (corticosteroids, azathioprine, and cyclosporin A). Intraoperative mortality was zero. At a mean of 13.3 months' follow-up (range: 1 to 47 months), 2 of 14 patients had died of sepsis and 1 of terminal cirrhosis (autopsies revealed no evidence of tumor recurrence); 3 patients (21%) had recurrences of the tumor (1 in the central nervous system and liver, and the other 2 in the lung). One of the three patients with a recurrent tumor is still alive after 16 months. The remaining nine patients (64%) are still alive.
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PMID:Liver transplantation in malignant primary hepatic neoplasms. 131 58

Hepatocellular carcinoma is endemic in Africa, where in the incidence of the disease in males ranges from 20-100,000 per annum. The tumor tends to occur at a younger age compared to the age of presentation in Europeans or Chinese. The majority of African patients with HCC are HBsAg positive, but HBsAg is more commonly detected in younger vs older patients. Approximately 30% of patients are anti-HCV positive. Both these chronic virus infections may induce disease via the development of cirrhosis. Other environmental factors including carcinogens such as aflatoxin may act as co-factors. Resection rates for hepatocellular carcinoma are low in this population group, and screening for small tumours is not generally undertaken in Africa.
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PMID:Hepatocellular carcinoma in Africans. 131 16

One hundred eighty-nine surgically resected hepatocellular carcinomas (HCC) were analyzed to study tumor encapsulation and the pathologic features that might account for the better prognosis in relation to it, and to examine the prognostic and pathobiologic significance of capsular thickness. Tumor encapsulation was found in 72 (46.8%) of the 154 cases with adequate histologic sections of the tumor-nontumor junctions. Encapsulated tumors showed a much lower incidence of direct liver invasion (P less than 0.0001), tumor microsatellites (P less than 0.0001), and venous permeation (P = 0.02) when compared with nonencapsulated ones. Significantly better disease-free and actuarial survival times were observed in patients with encapsulated tumors (medians, 9.9 and 18.3 months, respectively), compared with those with nonencapsulated ones (medians, 4.0 and 5.9 months, respectively; P = 0.0001 and 0.001, respectively). The incidence of tumor encapsulation did not increase or decrease with tumor size. Tumor encapsulation did not correlate with the presence of cirrhosis or the abundance of tumor stroma, suggesting that formation of the tumor capsule was independent of the degree of fibrosis within and outside the tumor. Among the 72 cases of encapsulated HCC, the capsular thickness ranged from 0.13 to 3.09 mm (mean +/- standard deviation = 0.87 +/- 0.59 mm), and it was unrelated to tumor size or presence of cirrhosis. Although it was apparent that a lower extensive tumor invasiveness contributed significantly to the better prognosis in encapsulated HCC, there was no correlation between capsular thickness and liver invasion, microsatellites, venous permeation, or survivals. Therefore, the thickness of tumor capsules was not helpful in prognostication.
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PMID:Tumor encapsulation in hepatocellular carcinoma. A pathologic study of 189 cases. 131 78

We report a 65-yr-old man with hepatitis B virus-related liver cirrhosis and biopsy-proven hepatocellular carcinoma who has undergone spontaneous regression. The tumor became impalpable, and was no longer detectable by ultrasonography and computed axial tomography, 5 and 30 months later. The alpha-fetoprotein level also decreased to normal range. The clinical course is silent, and the patient is alive and well 37 months after the initial diagnosis.
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PMID:Spontaneous regression of hepatocellular carcinoma. 131 72

Fifty-four patients with cirrhosis, found to have a space-occupying lesion in the liver by ultrasound (US), underwent US-assisted biopsy of the lesion and were then followed prospectively to define outcome and survival. Histologic examination revealed hepatocellular carcinoma in 26 patients, while five had liver cell dysplasia without hepatocellular carcinoma and 23 had no evidence of tumor or of dysplasia. All five patients with an initial diagnosis of dysplasia developed hepatocellular carcinoma during follow-up and their survival curve was similar to that of patients with liver cancer and significantly worse than that of patients without dysplasia or tumor. There were five false-negative cases of hepatocellular carcinoma among the patients with negative histology. Overall, US-assisted liver biopsy diagnosed malignancy with a sensitivity of 72%, which increased to 86% when dysplasia was considered a pre-neoplastic lesion.
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PMID:Space-occupying lesions of the liver detected by ultrasonography and their relation to hepatocellular carcinoma in cirrhosis. 132 Jan 76

We report a case of severe hypoglycemia and hepatic masses suspected to be an insulin-like growth factor-II (IGF-II)-producing hepatocellular carcinoma. A 62-year-old man presented with mental disorder in the night and early morning associated with extremely low blood sugar levels (less than 21 mg/dl). Computerized axial tomography and ultrasonography revealed a massive tumor in the right lobe of the liver with multiple secondary nodules, and a tumor thrombus in the portal vein. At autopsy 107 days after admission, the liver weighed 3070 g, histologically showing an Edmondson type II tumor with liver cirrhosis. IGF-II in plasma (899 ng/ml) and tumor tissue (2.4 micrograms/g) was higher than that in normal plasma (374-804 ng/ml) and non-tumor liver tissue (0.2 micrograms/ml), while IGF-I (14 ng/ml) was significantly reduced. IGF-II, probably produced by the liver tumor, appeared to be involved in the mechanism of hypoglycemia.
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PMID:Primary hepatocellular carcinoma with severe hypoglycemia: involvement of insulin-like growth factors. 132 Jan 77

Computed tomography (CT) during arterial portography (CTAP) is an important technique for evaluating the liver before hepatic tumor resection. With this technique, most tumors are of low attenuation compared with that of enhancing parenchyma. At times, low-attenuation lesions are encountered that represent perfusion abnormalities rather than tumor deposits. These perfusion abnormalities can be categorized as (a) those resulting from improper technique; (b) those extending from hilum to capsule (straight-line sign), with or without an obstructing mass; (c) perihilar and periligamentous abnormalities; (d) subcapsular defects (linear or wedge shaped); and (e) those seen with cirrhosis or regenerating nodules. Adjuvant use of delayed CT, magnetic resonance imaging, and intraoperative ultrasound aids in characterization of these nontumorous defects, thereby improving specificity. The authors conclude that when potential candidates are evaluated for hepatic tumor resection, knowledge of the existence of the various diagnostic pitfalls of CTAP and their imaging characteristics is imperative to avoid inadvertent false results.
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PMID:CT during arterial portography: diagnostic pitfalls. 132 80

We examined loss of heterozygosity at 13 loci on 5 chromosomes in hepatocellular carcinomas (HCCs) from 56 patients. In 42 of these cases, regenerative nodules of liver cirrhosis were also analyzed. High frequencies of allelic losses were detected on chromosomes 13q (47%), 16q (40%) and 17p (64%), whereas losses on chromosome 4p and 11p were observed in less than 22% of cases in HCCs. In contrast, LOH was not detected on any loci in cirrhotic nodules. On chromosome 13q, the common region of allelic loss was mapped to the region including the retinoblastoma (RB) locus, by using 8 polymorphic probes. Furthermore, one case with 13q loss had an interstitial deletion of the RB gene, indicating the involvement of inactivation of the RB gene in hepatotumorigenesis. Losses were associated with portal-vein thrombosis or intrahepatic metastasis, increased tumor size, a poorly differentiated phenotype and clinical stage. Losses occurring together on 13q, 16q and 17p were significantly higher in patients in clinical stage IV or histologically poorly differentiated tumors, suggesting that the accumulation of allelic loss occurs in advanced tumors and that patients with multiple allelic losses may have a worse prognosis than those with a single loss.
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PMID:Accumulation of allelic loss on arms of chromosomes 13q, 16q and 17p in the advanced stages of human hepatocellular carcinoma. 132 76


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