Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and laboratory observations were made on 220 chronic alcoholics, regularly taking at least 150 g of alcohol daily. Haematological data concerning white blood cells, platelets and red cells counts, mean corpuscolar volume, hemoglobin and serum iron in these patients were compared with control values obtained from 150 healthy teetotal subjects. Hematological changes in chronic alcoholics were correlated with histological liver damages in transcutaneous needle-biopsies. No statistical differences were evident for white cells and platelets counts and for serum iron content; however, in chronic alcoholics, serum iron content showed a great dispersion around the mean. Mean corpuscolar volume (MCV) was significantly increased (P less than 0,001) in chronic alcoholics (even in those with a normal liver biopsy) but there was no significant difference in the degree and the incidence of macrocytosis between patients showing normal liver appearances or fatty changes only, and those showing more severe damage, i.e, acute alcoholic hepatitis (with or without steatosis), central hyaline-sclerosing necrosis and or hepatofibrosis, cirrhosis and hepatocarcinoma. No significant difference was seen between male and female alcoholics. Macrocytosis may be considered as an early marker for alcoholism but it does not correlate with the type of histological liver damage. Hemoglobin levels were significantly reduced in chronic alcoholics (P less than 0,01): the degree and incidence of anemia were more severe in those patients with advanced liver diseases and in female alcoholics. There is no statistically significant correlation between macrocytosis and anemia.
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PMID:[Macrocytosis and anemia in chronic alcoholism. Correlation with the results of hepatic needle biopsy]. 724 21

The cases of two patients with liver cirrhosis HCV-related, admitted in our Department in consequence of the development of ascites, anemia and clinical deterioration, are reported. Both patients had all major risk factors for hepatocellular carcinoma and anamnestic and physical findings suggesting this diagnosis; nevertheless, the alpha-1-fetoprotein serum levels and the ultrasonographic findings were not diagnostic for primary hepatic neoplasm. Explorative paracentesis was diagnostic, demonstrating the presence of hemoperitoneum (the hematocrit ratio in the ascitic fluid was 12 and 10, respectively). Magnetic resonance revealed extensive diffuse hepatocellular carcinoma on both cases. Hemoperitoneum, in patients with liver cirrhosis, in face of non diagnostic levels of alpha-1-fetoprotein and ultrasonographic findings, can be indicative of the spontaneous rupture of a diffuse type of hepatocellular carcinoma.
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PMID:[Hemoperitoneum supporting difficult diagnosis of diffuse hepatocarcinoma in liver cirrhosis]. 751 61

The precise cause of the anaemia that is commonly associated with severe pulmonary tuberculosis (PTB) has not been elucidated. The role of erythropoietin (Epo), the central hormone regulating red cell formation, still awaits clarification. We therefore determined serum Epo levels in patients with PTB; group 1, haemoglobin less than 110 g/L, group 2, haemoglobin greater than 110 g/L; group 3, controls, consisted of matched individuals with uncomplicated iron deficiency; group 4, healthy volunteers. Peripheral blood monocytes were obtained from patients with PTB and the controls, cultured, and the supernatant fluid (SNF) harvested. Tumour necrosis factor alpha (TNF alpha) levels were determined in the SNF, which were then added in various dilutions to a hepatocellular carcinoma cell line (HepG2) capable of regulated EPO synthesis in vitro. The influence of this cytokine was defined by the addition of specific neutralising anti-TNF alpha antibodies in this assay system. Patients in group 1 had significantly lower Epo levels (54 + 11 mU/mL) compared with those in group 3 (142 +/- 41 mU/mL) (p < 0.01). Monocyte supernatants from patients in the anaemic PTB group had markedly elevated TNF alpha levels and significantly suppressed Epo output by HepG2 cells in vitro (p < 0.01). This inhibition was consistently abrogated by anti-TNF alpha antibodies. Serum Epo levels were inappropriately low in untreated PTB patients when compared with corresponding haemoglobin levels in iron deficient controls. This blunted response could be ascribed to release of TNF alpha or other cytokines by activated monocytes.
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PMID:Blunted erythropoietin response to anaemia in tuberculosis. 758 43

This is the first reported case of primary lymphoma of the spleen coexisting with primary hepatocellular carcinoma. A 59-year-old woman was admitted to Ugo town hospital because of general malaise. Physical examination revealed no lymphadenopathy. Laboratory data showed mild anemia, thrombocytopenia, and slight elevation of alpha-fetoprotein (AFP). Ultrasonography of the abdomen revealed a mass in the left lobe of the liver and a mass in the splenic hilus. The liver tumor was presumed to be a primary liver cancer. Ultrasonically guided needle aspiration of the splenic mass was unsuccessful. Subsequently, the patient died of hepatic and renal failure. Autopsy revealed hepatocellular carcinoma and primary splenic non-Hodgkin's lymphoma of the diffuse large cell type.
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PMID:Primary lymphoma of the spleen with hepatocellular carcinoma. 760 94

Hepatocellular carcinomas may rupture in rare cases (5 to 15%) creating a serious short-term and mid-term situation. Over a period of 10 years, 20 patients (19 males, 1 female, mean age 68 years, range 38-82) were treated for ruptured hepatocellular carcinoma involving a cirrhotic (ethylic) liver in 12 cases, haemochromatosis in 2 and a normal liver in 6. Twelve patients underwent emergency surgery for acute haemoperitonium operation was delayed until after exploratory investigations (CT scan and arteriography +/- embolization) for pain in the right hypochondria associated with partitioned effusion and anaemia. The diagnosis of cancer had been known in 5 patients and rupture was the first manifestation in 15 others. Emergency procedures, 7 excisions, 3 sutures, were performed but 2 patients died during vascular clamping. Four deaths occurred within 8 days due to liver failure. There were no postoperative deaths after programmed procedures, 6 excisions, 1 ligature. One patient underwent embolization peroperatively and died 6 days later due to digestive haemorrhage and liver failure. Lesions were localized in the left liver (9), right liver (6) and in both with multiple nodules (5). Among the 13 survivors, 7 died within a delay of 2 to 30 months, 1 due to recurrent rupture (5%). Six patients are still living with a follow-up of 3 to 36 months (including 2 hepatocellular carcinomas on a healthy liver and 1 with haemochromatosis). A review of the literature confirms the severity of such events whatever the initial management. Acute rupture of hepatocellular carcinoma usually requires emergency procedures with a high risk of mortality (50%). Fissuration authorizes explorations and possibly peroperative embolization with better immediate results.
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PMID:[Ruptured hepatocarcinoma. Report of 20 cases and review of the literature]. 776 30

Sixteen patients with histologically confirmed inoperable hepatocellular carcinoma were treated with vindesine 3 mg/m2 i.v. weekly. Anemia, leukopenia and neuritis were documented but no severe or life-threatening toxicity was seen. There were no objective responses among the 14 evaluable patients. Eight had a no change status (median duration of 16 weeks, range 6-33), while the remaining 6 had progressive disease as their best evaluation. The median survival time was 20 weeks. Vindesine does not have a therapeutic effect in patients with advanced hepatocellular carcinoma.
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PMID:A phase II trial of vindesine in hepatocellular cancer. 780 Mar 50

Male and female F344 rats (30-33 rats/group) were administered piperonyl butoxide (alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylenedioxy-2-propylto luene) in the diet at levels of 0 (control), 0.6, 1.2, and 2.4% for nearly 2 years. Beginning at about 40 weeks, 10 rats in the 1.2% treated male group died due to cecal hemorrhages. Piperonyl butoxide induced hepatocellular carcinoma in both sexes in a dose-dependent manner. Hepatocellular carcinoma was found even in the 1.2% treated male group (incidence, 26.7%), and incidences in the 2.4% groups of males and females were 80.0 and 57.7% respectively of all those surviving. Piperonyl butoxide also caused essential thrombocythemia with a dose-response relationship. Hemorrhages in stomach and cecum, anemia, degenerative lesions of alveoli, and nephrotoxicity were also observed related to exposure. These results indicate that piperonyl butoxide is a hepatocarcinogen to the rat.
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PMID:Chronic toxicity studies of piperonyl butoxide in F344 rats: induction of hepatocellular carcinoma. 791 67

In patients with the anemia of chronic diseases, the plasma level of EPO is often low in relation to the blood hemoglobin concentration. Because infectious and inflammatory processes cause activation of cytokine-producing macrophages and lymphocytes, we investigated whether isolated inflammatory cytokines influence the synthesis of EPO in vitro. IL-1 and TNF-alpha were shown to inhibit EPO mRNA levels and EPO formation in the human hepatoma cell cultures HepG2 and Hep3B, and to lower EPO formation in isolated perfused rat kidneys. IFN-alpha and IFN-beta also induced some inhibition of EPO production in HepG2 cultures. IL-3, TGF-beta 2, and IFN-gamma did not inhibit. IL-6 stimulated the production of EPO in Hep3B cells but was ineffective in HepG2 cells and lowered EPO production in isolated perfused rat kidneys. IL-1, TNF-alpha, and possibly other cytokines could contribute to defective EPO production in renal and nonrenal immune responses.
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PMID:Inhibition of erythropoietin production by cytokines. Implications for the anemia involved in inflammatory states. 818 37

We measured serum erythropoietin (EPO) immunoenzymatically in 245 subjects (151 male, 94 female) to investigate the pathophysiology of its liberation in patients with liver disease. Twelve patients had acute hepatitis, 60 mild chronic liver disease (CLD), 50 cirrhosis (CIR), 43 hepatocellular carcinoma (HCC), 16 malignant extrahepatic disease, 32 benign extrahepatic disease (BEN); 32 subjects served as healthy controls. Higher EPO levels were found in all groups of patients as compared with controls (Bonferroni's test, P < 0.01); CIR and HCC had higher values than CLD and BEN (P < 0.01). By multiple regression analysis, EPO correlated with haematocrit, cholinesterase and C-reactive protein (F = 18.63, P < 0.0001). Thus, circulating EPO increases in patients with liver disease, particularly in its more advanced forms. Besides anaemia, both impairment of liver function (possibly via decreased EPO metabolism) and inflammation seem to play contributory roles in elevating serum EPO.
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PMID:Evidence for a multifactorial control of serum erythropoietin concentration in liver disease. 755 88

The regulation of erythropoietin (Epo) production was investigated by competitive polymerase chain reaction, a highly sensitive and accurate means of measuring Epo mRNA levels. Co-amplification of the test sample with added mutant Epo cDNA template corrects for variability in the efficiency of amplification. Epo mRNA levels were determined in tissues of normal rats and in animals with varying degrees of anemia. Reduction of the hematocrit level from 0.40 to 0.15-0.20 resulted in a 300-fold increase in kidney Epo mRNA, which comprised 80% of the total Epo mRNA versus 20% from the liver. In contrast, very low levels detected in lung and spleen were not significantly increased by anemia. The human hepatoma cell line, Hep3B, secretes high levels of Epo in response to hypoxia. This regulation is, to a large extent, transcriptional. When Hep3B cells were incubated in the presence of decreasing O2 tension from 160 to 7 mm Hg, there was a monotonic increase in Epo mRNA to 50 to 100 times the normoxic level. Hyperoxia did not suppress basal expression. When cells were incubated at a PO2 of 7 mm Hg, induction of Epo mRNA was first noted at 30 minutes and was maximal at 5 to 6 hours. After Epo mRNA was boosted by a 4-hour hypoxic incubation, cells were then exposed to normoxia, which shut off further transcription of the Epo gene. The decay of Epo mRNA levels closely followed first order kinetics with a half-life of 2 hours, an effective measurement of message stability.
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PMID:In vivo and in vitro regulation of erythropoietin mRNA: measurement by competitive polymerase chain reaction. 838 7


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