Central retinal vein occlusion and thrombophilia

Fegan, Chris

doi:10.1038/sj.eye.6700040

Cited by 74 publications

(65 citation statements)

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“…24 Our study confirms the earlier reports suggesting that isolated FVL, prothrombin gene mutation, and MTHFR are not major risk factors for RVO. 7 It is however the first study identifying that the GpIa/IIa genotype(s) leading to an increased receptor density is a very common abnormality in this patient group. The 37.5% incidence of the low GpIa/IIa density (CC/GG) seen in our normal population is similar (33-49%) to that reported in other normal European populations.…”

Section: Discussionmentioning

confidence: 93%

“…Interestingly, the acquired thrombophilia conditions, hyperhomocysteinaemia, and antiphospholipid syndrome, which cause both arterial and venous thrombosis, are most associated with RVO. 7 The platelet GpIa/IIa complex initiates platelet adhesion to collagen at low and high shear rates (50-1500/s), ultimately leading to thrombus formation. 31,32 Recent studies have shown that a common polymorphism with two silent linked point mutations in the GpIa/IIa complex determines the density of receptor expression and therefore platelet adhesion.…”

Section: Discussionmentioning

confidence: 99%

“…The frequencies of the various GpIa/IIa polymorphisms and the common thrombophilic conditions vary between ethnic groups, which may partly explain the conflicting results as to the role of FVL and MTHFR in RVO. 7,23,30,39 Other types of platelet glycoprotein polymorphisms exist. Larsson and Hillarp 40 recently reported, however, that another polymorphism of glycoprotein IIIa played no role in RVO.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly therefore, the major thrombophilic risk factors for RVOFhyperhomocysteinaemia and antiphospholipid syndromeFcause both arterial and venous thrombosis whereas the hereditary thrombophilic risk factors usually only cause venous thrombosis. 7 While there are consistent clinical risk factors underlying RVO, to date there has been no abnormality identified in the majority of patients, that is, suggesting causality, and no report of any possible genetic marker.…”

Section: Introductionmentioning

confidence: 99%

“…Studies looking at both rarer causes of thrombophilia (protein C, protein S, and antithrombin III deficiency) and the three more common Factor V Leiden (FVL), prothrombin gene G20210A (PT), and homozygosity for C677T methylene tetrahydrofolate reductase enzyme mutation (MTHFR) have given conflicting results with regard to their exact role(s) in RVO. 7 Homozygous MTHFR C677T mutations can cause mildly elevated homocysteine levels, but this effect is neutralised if there is a high folate content in the diet. 8 Thus, many patients homozygous for this abnormality have normal homocysteine levels.…”

Section: Introductionmentioning

confidence: 99%

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The platelet glycoprotein Ia/IIa gene polymorphism C807T/G873A: a novel risk factor for retinal vein occlusion

Dodson

Haynes

Starczynski

et al. 2003

Eye

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Retinal vein occlusion (RVO) is associated with hyperhomocysteinaemia and the antiphospholipid syndromeFdisorders known to contribute to both arterial and venous thrombosis. In both of these conditions and RVO, platelet activation occurs. Aspirin, not warfarin, is the most effective antithrombotic agent in RVO and, taken together, these observations suggest an important role for platelets in this common ocular thrombotic condition. Platelet glycoprotein Ia/IIa (GpIa/IIa) is an adhesion molecule mediating platelet-collagen interactions and is key to the initiation of thrombosis. Recently, the cellular density of this molecule was shown to be determined by two silent, linked polymorphisms (C807T/ G873A) within the GpIa/IIa gene. There is evidence that some of the resulting genotypes are associated with thrombo-embolic disease. This study therefore aimed to establish the prevalence of the GpIa/IIa polymorphisms and the three commonest hereditary thrombophilic disorders (prothrombin gene G20210A (PT) mutation, Factor V Leiden (FVL), and the thermolabile methylene tetrahydrofolate reductase C677T (MTHFR) mutation) in patients with RVO and normal controls. The GpIa/IIa polymorphisms and thrombophilic abnormalities were all identified using the polymerase chain reaction. Our results show that the frequency of the GpIa/IIa polymorphisms was similar in our normal control population to previously published series. Patients with RVO, however, had only a 10% (4/40) frequency of the lowest risk subtype (CC/GG) compared to 37.5% (15/40) in the control groupFP 0.0039.The incidence of the PT, FVL, and MTHFR thrombophilic mutations was not different between the two groups, but interestingly none of the 7/40 RVO cases with a PT, FVL, or MTHFR mutation had the low-risk GpIa/IIa genotype while all but one of the controls didFPo0.05. Thus, 17.5% of RVO patients harboured more than one prothrombotic abnormality. The principal difference between the RVO and control group was the very high incidence of the intermediate-risk GpIa/IIa subtype (CT/GA)F82.5 vs 50%, Po0.05. These results suggest a major role for GpIa/IIa polymorphisms in the pathogenesis of RVO.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%