title: Evaluation of nontumorous tissue damage by transcatheter arterial embolization for hepatocellular carcinoma.
abstract: The serial changes in serum hepatic enzyme activities by transcatheter arterial embolization (TAE) were analyzed in 17 patients with hepatocellular carcinoma to estimate the contribution to the value by the damage of tumor or nontumorous hepatic cells. The serum levels of relatively tumor-specific fructose 1,6-diphosphate (FDP) aldolase were elevated after TAE in the cases of both superselective and nonsuperselective TAE that were performed from the segmental and the nonsegmental hepatic artery, respectively, but we found the marked elevation of FDP aldolase in the cases of the superselective TAE. In contrast, the non-tumor-specific fructose 1-phosphate (F1P) aldolase was markedly elevated only in the cases of nonsuperselective TAE. The total amount of FDP aldolase released by TAE correlated significantly with the integrated tumor tissue volume (P less than 0.005), whereas the total amount of F1P aldolase output correlated significantly with the integrated nontumorous tissue volume (P less than 0.005) as defined by lipiodol accumulation on computerized tomography scan. The consequent changes in the total nontumorous liver volumes after TAE were also analyzed by the follow-up computerized tomography scan. The nonsuperselective TAE caused the significant total nontumorous liver atrophy when compared with the superselective TAE. The progression of the total nontumorous liver atrophy correlated significantly with F1P aldolase output by TAE (P less than 0.001) but not with FDP aldolase output. These results suggest that the outputs of FDP and F1P aldolase are useful to estimate the degree of the tumorous and nontumorous tissue damage by TAE, respectively, and F1P aldolase output can be used to predict the progression of liver atrophy caused by TAE.
authors.affiliation: First Department of Internal Medicine, School of Medicine, Nagasaki University, Japan.
authors.forename: K N
authors.initials: KN
authors.lastname: Khan
authors.forename: K
authors.initials: K
authors.lastname: Nakata
authors.forename: Y
authors.initials: Y
authors.lastname: Kusumoto
authors.forename: M
authors.initials: M
authors.lastname: Shima
authors.forename: N
authors.initials: N
authors.lastname: Ishii
authors.forename: T
authors.initials: T
authors.lastname: Koji
authors.forename: S
authors.initials: S
authors.lastname: Nagataki
mesh_terms: D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D001284:Atrophy; D006528:Carcinoma, Hepatocellular / Q000201:enzymology / Q000628:therapy*; D004621:Embolization, Therapeutic; D005260:Female; D005635:Fructosediphosphates / Q000097:blood; D005636:Fructosephosphates / Q000097:blood; D006801:Humans; D008099:Liver / Q000473:pathology; D008113:Liver Neoplasms / Q000201:enzymology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D000509:alpha-Fetoproteins / Q000032:analysis
chemical_list: D005635:Fructosediphosphates; D005636:Fructosephosphates; D000509:alpha-Fetoproteins; C032284:fructose-1-phosphate; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; C029063:fructose-1,6-diphosphate