K. Ozoran et al., PLASMA VON-WILLEBRAND-FACTOR, TISSUE-PLASMINOGEN ACTIVATOR, PLASMINOGEN-ACTIVATOR INHIBITOR, AND ANTITHROMBIN-III LEVELS IN BEHCETS-DISEASE, Scandinavian journal of rheumatology, 24(6), 1995, pp. 376-382
Sixty-three patients with Behcet's disease (ED), 30 patients with recu
rrent oral ulcer and 30 healthy individuals as control group were incl
uded in the study. ISG criteria was used for the diagnosis of ED and p
atients were classified as active and inactive and evaluated according
ly. In the patient and control groups, von Willebrand factor (vWF), ti
ssue plasminogen activator (tPA), and plasminogen activator inhibitor
(PAI) levels were determined using ELISA method and antithrombin III (
AT-III) by nephelometric methods. High levels of endothelial product,
vWF in the active Behcet patient group (p<0.005) supports endothelial
destruction due to vasculitis related with ED. In the active patient g
roup tPA levels were significantly lower (p<0.05) than the inactive an
d control groups with higher levels of PAI (p<0.05 and p<0.01 respecti
vely). In Behcet disease, besides the decrease in tPA synthesis, high
PAI levels also can affect tPA decrease and lead to inhibition of fibr
inolytic activity. In active Behcet group, levels of AT-III were low a
nd no significant difference was observed in recurrent oral ulcer and
control groups. This situation may arise from the excessive use of AT-
III in active disease. In conclusion, high levels of VWF in Behcet pat
ients is thought to arise from vasculitis and high levels of PAI from
the accumulation of thrombocytes on the damaged surface of endothelium
leading to a decrease in tPA levels and inhibition of fibrinolytic ac
tivity.