title: Both plasma lysophosphatidic acid and serum autotaxin levels are increased in chronic hepatitis C.
abstract: OBJECTIVE
  Recent accumulating evidence indicates that lysophosphatidic acid (LPA) is a lipid mediator, abundantly present in blood, with a wide range of biologic actions including the regulation of proliferation and contraction in liver cells. Although it is speculated that LPA might play a role in pathophysiologic processes in vivo, not only its role but also even a possible alteration in its blood concentration under specific diseases is essentially unknown. Autotaxin (ATX), originally purified as an autocrine motility factor for melanoma cells, was revealed to be a key enzyme in LPA synthesis. We determined LPA and ATX levels in the blood of patients with liver disease.
  
  
  METHODS
  ATX activity was measured by determining choline with the substrate of lysophosphatidylcholine, and the LPA level by an enzymatic cycling method in 41 patients with chronic hepatitis C.
  
  
  RESULTS
  The serum ATX activity and plasma LPA level were significantly increased in patients, and were correlated positively with serum hyaluronic acid, and negatively with platelets, albumin, and prothrombin time. The plasma LPA level was strongly correlated with serum ATX activity. There were significant correlations between the histologic stage of fibrosis and both the serum ATX activity and plasma LPA level.
  
  
  CONCLUSIONS
  The serum ATX activity and plasma LPA level are increased in chronic hepatitis C in association with liver fibrosis. Our study may provide the first evidence showing a significant increase of both ATX and LPA in the blood under a specific disease.
authors.affiliation: Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
authors.forename: Naoko
authors.initials: N
authors.lastname: Watanabe
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ikeda
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Nakamura
authors.forename: Ryunosuke
authors.initials: R
authors.lastname: Ohkawa
authors.forename: Yukio
authors.initials: Y
authors.lastname: Kume
authors.forename: Junken
authors.initials: J
authors.lastname: Aoki
authors.forename: Kotaro
authors.initials: K
authors.lastname: Hama
authors.forename: Shinichi
authors.initials: S
authors.lastname: Okudaira
authors.forename: Masayuki
authors.initials: M
authors.lastname: Tanaka
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Tomiya
authors.forename: Mikio
authors.initials: M
authors.lastname: Yanase
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Tejima
authors.forename: Takako
authors.initials: T
authors.lastname: Nishikawa
authors.forename: Masahiro
authors.initials: M
authors.lastname: Arai
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Arai
authors.forename: Masao
authors.initials: M
authors.lastname: Omata
authors.forename: Kenji
authors.initials: K
authors.lastname: Fujiwara
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Yatomi
mesh_terms: D000368:Aged; D005260:Female; D019698:Hepatitis C, Chronic / Q000097:blood*; D006801:Humans; D006820:Hyaluronic Acid / Q000097:blood; D008103:Liver Cirrhosis / Q000097:blood; D008111:Liver Function Tests; D008246:Lysophospholipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009097:Multienzyme Complexes / Q000097:blood*; D043264:Phosphodiesterase I / Q000097:blood*; D010727:Phosphoric Diester Hydrolases; D010976:Platelet Count; D011755:Pyrophosphatases / Q000097:blood*; D015219:Substrate Cycling; D000099189:Lysophospholipase D
chemical_list: D006820:Hyaluronic Acid; D008246:Lysophospholipids; D009097:Multienzyme Complexes; D043264:Phosphodiesterase I; D010727:Phosphoric Diester Hydrolases; D011755:Pyrophosphatases; D000099189:Lysophospholipase D; C032881:lysophosphatidic acid