scholarly journals Anterior ischaemic optic neuropathy associated with central retinal vein occlusion

Eye ◽  
2000 ◽  
Vol 14 (4) ◽  
pp. 560-562 ◽  
Author(s):  
Ahmed M Abu El-Asrar ◽  
Saba A Al Rashaed ◽  
Abdel Galil M Abdel Gader
Keyword(s):  
Retinal Vein Occlusion ◽  
Optic Neuropathy ◽  
Central Retinal Vein Occlusion ◽  
Vein Occlusion ◽  
Ischaemic Optic Neuropathy ◽  
Anterior Ischaemic Optic Neuropathy ◽  
Central Retinal Vein

Central Retinal Vein Occlusion and Nonarteritic Ischemic Optic Neuropathy in 2 Patients with Mild Iron Deficiency Anemia

2001 ◽  
Vol 215 (2) ◽  
pp. 128-131 ◽  
Author(s):  
Boris Kacer ◽  
Lars-Olof Hattenbach ◽  
Steffen Hörle ◽  
Inge Scharrer ◽  
Peter Kroll ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Retinal Vein Occlusion ◽  
Iron Deficiency Anemia ◽  
Optic Neuropathy ◽  
Central Retinal Vein Occlusion ◽  
Deficiency Anemia ◽  
Ischemic Optic Neuropathy ◽  
Vein Occlusion ◽  
Central Retinal Vein

Hypercoagulability and High Lipoprotein(a) Levels in Patients with Central Retinal Vein Occlusion

1994 ◽  
Vol 72 (01) ◽  
pp. 039-043 ◽  
Author(s):  
Francesco Bandello ◽  
Silvana Vigano’ D’Angelo ◽  
Mariella Parlavecchia ◽  
Alessandra Tavola ◽  
Patrizia Della Valle ◽  
...  
Keyword(s):  
Retinal Vein Occlusion ◽  
Central Retinal Vein Occlusion ◽  
Specific Treatment ◽  
Fibrin Deposition ◽  
Heparin Cofactor Ii ◽  
Lipoprotein A ◽  
Vein Occlusion ◽  
Acute Event ◽  
D Dimer ◽  
Central Retinal Vein

SummaryA series of coagulation parameters and lipoprotein(a) (Lp(a)) were explored in plasma from 40 patients with central retinal vein occlusion (CRVO, non-ischemic type n = 12; ischemic type n = 28) free of local and systemic predisposing factors, 1 to 12 months after the acute event. Forty age- and sex-matched patients with cataract served as controls. Prothrombin fragment 1.2 (FI.2), D-dimer, FVII:C - but not FVII: Ag - were higher and fibrinogen was lower in CRVO patients than in controls. Patients with non-ischemic CRVO had higher FI .2 and FVII:C and lower heparin cofactor II than patients with ischemic CRVO. Lp(a) levels greater than 300 mg/1 were observed in 12 patients with CRVO and in 4 controls (30% vs 10%, p <0.025). Patients with high Lp(a) - consistently associated with the S2 phenotype - had higher FVII:C, FVII:C/Ag ratio, and fibrinogen than the remaining CRVO patients. Plasma FI.2 and D-dimer correlated fairly in controls (r = 0.41) and patients with normal Lp(a) levels (r = 0.55), but they did not in the group of patients with high Lp(a) (r = 0.19), where the latter parameter was negatively related to D-dimer (r = −0.55). There was no dependence of the abnormalities observed on the time elapsed from vein occlusion. The findings of activated FVII and high FI.2, D-dimer, and Lp(a) are not uncommon in patients with CRVO. Increased thrombin formation with fibrin deposition and impaired fibrinolysis may play a role in the pathophysiology of CRVO and require specific treatment

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