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)

Abnormal coagulation studies indicative of a dysfibrinogen were found in the plasma of four of seven patients with malignant hepatoma. The abnormal fibrinogen was characterized by prolonged prothrombin, thrombin and reptilase times and inhibition of the coagulation of normal plasma. Purified fibrinogen revealed abnormalities similar to those in plasma. The functional defect was one of delayed polymerization of the fibrin monomer. The carbohydrate content of the abnormal fibrinogen was increased, and this change was related to the abnormal fibrinogen function. Enzymatic cleavage of sialic acid from the abnormal fibrinogen restored fibrinogen function to normal. This hepatoma-associated dysfibrinogen (acquired dysfibrinogenemia) is similar in many respects to fetal fibrinogen and may represent the presence of a fetal form of fibrinogen in hepatoma.
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PMID:Dysfibrinogenemia associated with hepatoma. Increased carbohydrate content of the fibrinogen molecule. 20 86

In the present study fibrinogen was assayed by the immunonephelometric method in 19 patients afflicted with hepatocarcinoma and 24 patients afflicted with cirrhosis. The two groups were similar in age, sex and presence of HbsAg. The incidence of values above the norm was significantly greater in patients with hepatocarcinoma (p less than 0.05). Then, the concentration of fibrinogen was measured in all using two other immunological methods (Laurell and Mancini) and two coagulative methods (Clauss and Ratnoff). A dysfibrinogenemia (an excess of fibrinogen assayed by immunological methods to be greater than 100 mg/dl with respect to biological methods). is more frequent using the Nephelometer-Clauss (p less than 0.01) and Mancini-Clauss (p less than 0.01) methods in patients with hepatocarcinoma with respect to those with cirrhosis. The study of the kinetics of antifibrinogen antigen-antibody reaction failed to show differences between patients with hepatocarcinoma or cirrhosis and normal subjects.
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PMID:The use of laser-nephelometry in evaluating fibrinogenaemia in patients with hepatocarcinoma and cirrhosis. 241 22

Dysfibrinogenemia in 36 patients with primary hepatocarcinoma and in 25 patients with cirrhosis of the liver was studied by means of reptilase time, thrombin coagulase time, fibrin polymerization and fibrinogen assays. Both groups of patients were similar in age, sex and incidence of HBs Ag. No electrolyte or fluid imbalances were present. Prolonged reptilase time and prolonged polymerization time were found in both groups; however, thrombin coagulase time was prolonged in 80% of the hepatocarcinoma group, but was normal in almost all patients with cirrhosis (p less than 0.001). In the hepatocarcinoma group, a difference of more than 100 mg per 100 ml was present between the immunologic and coagulative methods of fibrinogen determination in 36.1% of the cases, but in the cirrhotic group this difference was not present in any of the patients (p less than 0.01). We also found that by simply measuring fibrinogen levels by the Mancini method, we could distinguish hepatocarcinoma from cirrhosis in most cases.
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PMID:The importance of simple coagulation tests (fibrinogen assays and thrombin coagulase clotting time) in the diagnosis of liver cancer. 609 71

A 17-year-old male with previously undiagnosed congenital Factor IX deficiency (13%) presented with gastrointestinal bleeding and a hepatic mass. Prolonged thrombin and Reptilase times, which partially corrected with CaCl2 and a discrepancy between thrombin-clottable and immunoreactive plasma fibrinogen, suggested a dysfibrinogenemia. Laparotomy disclosed metastatic hepatoma. Adequate hemostasis was obtained with clotting factor replacement, but wound healing was delayed. Patient fibrinogen purified with 2.1 M glycine migrated normally on immunoelectrophoresis and 7.5% polyacrylamide-SDS gel electrophoresis. However, fibrin monomers prepared from purified patient fibrinogen displayed impaired aggregation at high and low ionic strengths when compared with fibrin monomers from normal and control Factor IX deficient subjects. Aggregation of normal monomers was delayed when mixed 1:1 with patient monomers. Fibrinopeptide release was normal, and total sialic acid content was similar to that of normal and control fibrinogens. Chemotherapy, consisting of 5-FU given via intra-arterial hepatic infusion, was accompanied by significant transient clinical improvement which coincided with correction of thrombin clotting times and fibrin monomer aggregation. Reappearance of fibrinogen dysfunction occurred with clinical deterioration prior to death from metastatic hepatoma and sepsis. This case is the first to corroborate the postulated tumor marker role of dysfibrinogenemia in a patient with hepatoma by documenting a direct relationship with response to chemotherapy.
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PMID:Acquired dysfibrinogenemia in a hemophiliac with hepatoma: resolution of fibrinogen dysfunction following chemotherapy. 626 56