title: Levels of plasma thrombomodulin are increased in atheromatous arterial disease.
abstract: The plasma thrombomodulin (TM) level depends on the integrity of the endothelium and the clearance of the molecule. In several different pathological conditions, plasma TM levels increase with damage to the endothelium. We studied plasma TM levels in patients with various localizations of atheromatous arterial disease who had normal serum creatinine levels. Two groups of patients had a single symptomatic localization, which was either peripheral occlusive arterial disease (POAD) or ischemic heart disease (IHD) and a third group of patients had multiple symptomatic localizations (polyvascular). We compared the plasma TM levels with the plasma levels of other specific markers of endothelial cell activation such as: prostacyclin (PGI2), tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1). Plasma TM levels were significantly increased in all three individual groups and when all patients were considered (total patients), as compared with normal controls. When all patients were considered, there was a significant positive correlation between plasma TM levels and t-PA and between plasma TM levels and PGI2. A significant positive correlation was also found between the plasma TM levels and PAI-1 for patients with POAD. Thus, our findings suggest that an increased influx of TM into the plasma may be caused by endothelial cell damage in patients with atheromatous arterial disease. However in our study, the plasma TM levels obtained were similar for all three types of atheromatous arterial disease. Though plasma thrombomodulin is a marker of endothelial cell injury, it cannot be of a clinical interest until its levels are related to the extend of the atheromatous lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Hematology Laboratory, University of Bordeaux II, France.
authors.forename: M
authors.initials: M
authors.lastname: Seigneur
authors.forename: P
authors.initials: P
authors.lastname: Dufourcq
authors.forename: C
authors.initials: C
authors.lastname: Conri
authors.forename: J
authors.initials: J
authors.lastname: Constans
authors.forename: P
authors.initials: P
authors.lastname: Mercié
authors.forename: A
authors.initials: A
authors.lastname: Pruvost
authors.forename: J
authors.initials: J
authors.lastname: Amiral
authors.forename: D
authors.initials: D
authors.lastname: Midy
authors.forename: J C
authors.initials: JC
authors.lastname: Baste
authors.forename: M R
authors.initials: MR
authors.lastname: Boisseau
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001161:Arteriosclerosis / Q000097:blood*; D015415:Biomarkers; D003404:Creatinine / Q000097:blood; D004730:Endothelium, Vascular / Q000378:metabolism; D011464:Epoprostenol / Q000097:blood; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D018180:Thrombomodulin / Q000032:analysis*; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D018180:Thrombomodulin; D005340:Fibrinogen; D003404:Creatinine; D011464:Epoprostenol; D010959:Tissue Plasminogen Activator