Fibrinolytic Behavior in Long-Standing Branch Retinal Vein Occlusion

Abstract

The aim of our study was to evaluate the fibrinolytic system in patients with retinal branch vein occlusion (RVO). The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, α₂-antiplasmin and α₂-macroglobulin. Comparing the results of patients with those of normal controls, only the fibrinogen increase and PTT shortening were significantly different. All other tests taken into account were within normal limits. Only the patients without other associated diseases (diabetes or hypertension) showed a significant activation of fibrinolysis (either with respect to normal or to other RVO patient groups). In conclusion, no important fibrinolytic impairment was seen in our longstanding RVO patients. Fibrinolytic activation seen in patients without verified associated diseases may be related to the presence of a sound endothelium, still able to release plasminogen activators in response to RVO. The fibrinogen and PTT changes in RVO were probably due to other associated diseases.

Protein C, protein S and antithrombin III deficiencies in retinal vein occlusion

“…Trope demonstrated decreased levels of AT III in the retinal vein occlusion group (Trope et al 1983). Patrassi found nor-mal AT III levels in patients with long standing branch retinal vein occlusion (Patrassi et al 1987) and Gottlieb found normal PC, PS and AT III levels in young adults with CRVO (Gottlieb et al 1998). Williamson reported increased mean AT III and decreased mean activated protein C in patients with CRVO than in controls (Williamson et al 1996).…”

Prothrombotic states associated with retinal venous occlusion in young adults

“…Increased blood viscosity measured as increases in hematocrit, plasma fibrinogens, and immunoglobulins was implicated in the etiology of venous occlusions [9,10,[43][44][45]. Appiah and Trempe [46] found an association between the elevated erythrocyte sedimentation rate and CRVO.…”

Retinal Vein Occlusion Induced by a MEK Inhibitor - Impact of Oxidative Stress on the Blood-Retinal Barrier

“…Hematological dysfunction, such as increased plasma fibrinogen and disruption of the thrombosis-fibrinolysis balance, have been implicated in the development of RVO . Increased fibrinogen has been associated with RVO in several clinical reports (Lip et al, 1998;Patrassi et al, 1987;Peduzzi et al, 1986). An increasing number of studies have sought to establish an association between RVO and thrombophilic abnormalities.…”