title: Plasma levels of tumor necrosis factor and endothelial response in patients with chronic arterial obstructive disease or Raynaud's phenomenon.
abstract: Tumor necrosis factor alpha (TNF-alpha) is a cytokine that affects endothelial cells' function by changing their antithrombotic potential to a net procoagulant effect. Only a few data have so far been reported for the pathophysiologic role of TNF in vascular diseases in the involvement of microvessels and/or macrovessels and a prothrombotic state. In the present study the authors evaluated plasma TNF (and interleukin-1) levels in 20 patients with chronic arterial obstructive disease (CAOD) with intermittent claudication and 10 CAOD patients with more severe disease (pain at rest/skin ulcers). In addition, they studied 10 patients with Raynaud's phenomenon (RP), suspected to be secondary to a collagen disease. The control group consisted of 20 subjects matched for sex and age with the three groups of patients. TNF levels were assayed by enzyme-linked immunosorbent assay. The antigen levels of von Willebrand factor (vWF), tissue plasminogen activator (t-PA), and its inhibitor (PAI) were also determined as markers of release from the endothelium, while the fragment 1 + 2 of prothrombin (F1 + 2) and thrombin-antithrombin III (TAT) complexes were assessed as indexes of systemic thrombin generation. TNF levels were significantly higher in both groups of CAOD patients than in controls or RP patients, and the same was true for vWF. t-PA was significantly higher only in the CAOD subjects with more severe disease. No differences among groups were seen in PAI antigen/activity or thrombin generation. When data were corrected for age, TNF no longer differentiated CAOD patients from controls and RP subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Fourth Internal Medicine Department, S. Carlo Borromeo General Hospital, Milan, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Cimminiello
authors.forename: G
authors.initials: G
authors.lastname: Arpaia
authors.forename: V
authors.initials: V
authors.lastname: Toschi
authors.forename: F
authors.initials: F
authors.lastname: Rossi
authors.forename: M
authors.initials: M
authors.lastname: Aloisio
authors.forename: A
authors.initials: A
authors.lastname: Motta
authors.forename: G
authors.initials: G
authors.lastname: Bonfardeci
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D000991:Antithrombins / Q000378:metabolism; D001157:Arterial Occlusive Diseases / Q000097:blood* / Q000150:complications / Q000201:enzymology; D001779:Blood Coagulation Factors / Q000378:metabolism*; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000201:enzymology / Q000378:metabolism*; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000097:blood*; D007383:Intermittent Claudication / Q000209:etiology; D007871:Leg Ulcer / Q000209:etiology; D008297:Male; D008875:Middle Aged; D015849:Plasminogen Inactivators / Q000097:blood; D011928:Raynaud Disease / Q000097:blood* / Q000201:enzymology / Q000209:etiology; D012044:Regression Analysis; D013917:Thrombin / Q000378:metabolism; D010959:Tissue Plasminogen Activator / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D000991:Antithrombins; D001779:Blood Coagulation Factors; D007375:Interleukin-1; D015849:Plasminogen Inactivators; D014409:Tumor Necrosis Factor-alpha; D014841:von Willebrand Factor; D013917:Thrombin; D010959:Tissue Plasminogen Activator