vitamin-k-semiquinone-radical and Liver-Cirrhosis--Alcoholic

Topics: Blood Transfusion; Central Venous Pressure; Cimetidine; Emergencies; Esophageal and Gastric Varices; Esophagoscopy; Esophagus; Fluid Therapy; Gastrointestinal Hemorrhage; Hemostasis, Surgical; Humans; Hypertension, Portal; Liver Cirrhosis, Alcoholic; Prognosis; Sclerosing Solutions; Vasopressins; Vitamin K

Topics: Aminocaproic Acid; Blood Transfusion; Deamino Arginine Vasopressin; Edema; Factor VII Deficiency; Factor VIIa; Hemostatics; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Postoperative Hemorrhage; Recombinant Proteins; Shock; Tooth Extraction; Vitamin K

We measured serum PIVKA-II concentrations in 18 patients with alcoholic liver cirrhosis. Alcoholic liver disease was diagnosed by the history of ethanol intake of more than 900 ml/day for over 10 years. Liver cirrhosis was diagnosed histologically. Infections with hepatitis B and C viruses were ruled out by assaying serum virus markers. No tumor was detected in liver by ultrasonography and computed tomography during observation period. None of the patients studied were positive for alpafetoprotein (AFP). Eight out of 18 (44.4%) patients with alcoholic liver cirrhosis showed elevated serum PIVKA-II levels. In contrast, only eight out of 93 (8.6%) patients with nonalcholic liver cirrhosis had elevated serum PIVKA-II levels. PIVKA-II is well known as a tumor marker of hepatocellular carcinoma (HCC). The rates of positive PIVKA-II found in alcoholic liver cirrhosis approached its rates in HCC. However, the time course for the elevation of serum PIVKA-II levels was different each other in alcoholic liver cirrhosis and HCC. In HCC, serum PIVKA-II "levels" continued to elevate until therapy. In contrast, its elevation was transient and its levels returned to baseline in alcoholic liver cirrhosis. The values of ALT (GPT), gamma-GTP, and ALP correlated poorly with serum PIVKA-II levels in patients with alcoholic liver cirrhosis. To investigate the mechanism by which elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis occurred, we studied the effect of vitamin K on production of PIVKA-II and AFP by hepatocytes. Hepatocytes(Alexander PLC/PRF/F cell line) were cultured in the presence of various concentrations of vitamin K (Kaytwo, Eisai, Tokyo). Vitamin K had no effect on AFP production. In contrast, PIVKA-II production was inhibited by addition of vitamin K in a dose dependent manner. Moreover, elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis was suppressed by administration of vitamin K (Kaytwo) to these patients. Taken together, these results suggest that vitamin K may have a role in the mechanism of PIVKA-II elevation in sera of these patients. Then, we measured serum concentrations of vitamin K(PK, MK-4, MK-7) in these patients. There was no correlation observed between vitamin K and PIVKA-II in these patients. This result suggests that elevation of serum PIVKA-II in these patients may not be due to vitamin K deficiency. One question not answered here is how serum PIVKA-II levels in these patients are suppr

Topics: alpha-Fetoproteins; Biomarkers; Humans; Liver Cirrhosis, Alcoholic; Protein Precursors; Prothrombin; Vitamin K

The purpose of this study is to determine serum des-gamma-carboxy prothrombin (DCP) levels in benign liver diseases by a new sensitive method, and to demonstrate the elevation of serum DCP in alcoholic liver disease (ALD) without hepatocellular carcinoma (HCC). Median values of serum DCP were 16.2 mAU/ml (range: 3.2 to 1570 mAU/ml) in ALD and 16.7 mAU/ml (1.2 to 75.4 mAU/ml) in viral liver disease (VLD). Using the cut-off value of 40 mAU/ml as a tumor marker for HCC, 21% (11/52) was positive in ALD and 2% (1/57) was positive in VLD (p = 0.0014, Fisher's exact probability test), and 27% (9/33) was positive in alcoholic liver cirrhosis and 3% (1/39) was positive in viral liver cirrhosis (p = 0.0042, Fisher's exact probability test). The positive rate of DCP was significantly (p < 0.001, Spearman's rank correlation test) correlated with the severity of liver disease in ALD. Serum vitamin K level was not decreased in cases with ALD. In a demonstrable case, serum DCP was decreased after abstinence and was increased again after the beginning of ethanol intake, suggesting the involvement of ethanol to the elevation of serum DCP in ALD. In conclusion, serum DCP was significantly elevated in ALD, compared with VLD, although the mechanism of the elevation of DCP was not clarified. Ethanol intake may act, in part, on the increase of serum DCP in ALD.

Topics: Aged; Biomarkers; Biomarkers, Tumor; Carcinoma, Hepatocellular; Ethanol; Female; Hepatitis, Viral, Human; Humans; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Liver Diseases, Alcoholic; Liver Neoplasms; Male; Middle Aged; Protein Precursors; Prothrombin; Reference Values; Vitamin K

Having briefly analyzed the metabolism of ethanol in man, the author describes hepatocellular damage induced by alcohol abuse and histological, clinical and biohumoral features of steatosis and fibrosis. One hundred clinical cases of hepatic steatosis and fibrosis are also illustrated, studied and observed during five years.

Topics: Colchicine; Drug Combinations; Fatty Liver, Alcoholic; Female; Humans; Liver; Liver Cirrhosis, Alcoholic; Male; Prognosis; Pyridoxine; Pyrrolidonecarboxylic Acid; Tiopronin; Vitamin K

Topics: Alcoholism; Antifibrinolytic Agents; Bilirubin; Blood; Drug Therapy; Hematologic Tests; Humans; Infusions, Parenteral; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Liver Function Tests; Prothrombin; Serum Albumin; Vitamin K; Vitamin K 1; Vitamins

Topics: Adrenal Cortex Hormones; Alcoholism; Arginine; Diet; Diet Therapy; Diuretics; Folic Acid; Glutamates; Humans; Lipotropic Agents; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Liver Extracts; Malates; Pterins; RNA; Spironolactone; Sulfonamides; Vitamin B Complex; Vitamin K