Analysis of Thrombophilic Risk Factors in Patients Suffering from Ocular Thrombotic Complications

Analysis of Thrombophilic Risk Factors in Patients Suffering from Ocular Thrombotic Complications

H.H. Wolf, A. Frühauf, C. Grünauer-Kloevekorn, A. Krause and H.-J. Schmoll

Objective

Non-arthritic ischemic optic neuropathy or ocular venous thrombosis may cause sudden unilateral loss of vision sometimes complicated by contralateral thrombotic events some years later. Retinal hemorrhages may occur due to thrombosis, but hemodilution, administration of corticosteroids and inhibitors of platelet aggre- gation is standard therapy prior to effective anticoagulation [1].

Effectivity of the therapy has been discussed controversially. Minor therapeutic results of this regimen could be related to the patients` underlying hypercoagulable state and impaired plasmatic coagulation.

We report preliminary results of hemostaseologic screening for thrombophilic risk factors in 12 consecutive patients suffering from acute ocular thrombotic com- plications.

Patients Characteristics

12 patients (17 to 78 years old) suffered from acute, almost complete loss of vision due to thrombotic occlusions either of central vein (n=6), minor ocular veins(n=3), ischemic optical neuropathy(n=2), or arterial thrombosis(n=1), respectively. In 4 patients, loss of vision had been recognized more than 72 hours prior to admission.

We performed the following hemostaseologic examinations for thrombophilic risk factors: coagulation factor analysis, lupus anticoagulant, anticardiolipin anti- bodies, procoagulant factors (protein C, protein S, antithrombin), and indicators of fibrinolysis (PAI-1, tissue factor, D-dimers).

Molecular analysis was done for MTHFR C677T, Factor V Leiden G1691A, or prothrombin gene G20210A mutations. The patients were checked for autoimmune vasculitis, diabetes mellitus, and hyperlipoproteinemia.

Hemostaseologic Results

Thrombophilic diathesis was diagnosed in almost all patients: MTHFR gene muta- tion C677T was found in patients, one of them homozygous; Factor V Leiden G1691A in 2; and prothrombin gene mutation G20210A in 2 patients. We found dia-

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34^thHemophilia Symposium Hamburg 2003

” Springer Medizin Verlag Heidelberg 2005

betes mellitus in 4 patients, hyperlipoproteinemia in 2 patients. Anticardiolipin antibodies were seen in 4 patients (Fig. 1).

Conclusions

Concerning our hemostaseologic data ocular thrombosis seems to resemble hyper- coagulable state due to plasmatic disorders of coagulation [2]. Therefore, anti- coagulation with low-molecular weight heparin additional to standard therapy might be a useful therapy in patients suffering from acute ocular complications.

References

1. Tripodi A, Mannucci PM. Clinical investigation of thrombophilia. Clin Chem. 2001;47:1597- 1606

2. Nagy V, Facsko A, Takacs L, Balazs E, Berta A, Balogh I, Edes I, Czuriga I, Pfliegler G.

Activated protein C resistance in anterior ischaemic optic neuropathy. Acta Ophthalmol Scand. 2004;82:140-143

Analysis of Thrombophilic Risk Factors in Patients Suffering from OT Complications 303

0 1 2 3 4 5 6 7 8

MTHFR

Factor V Leiden

Prothrombin

Anticardiolipin antibodies

Diabetes mellitus

Hyperlipoproteinemia

Fig. 1. Hypercoagulable state, characterization of risk factors