Retinal vein occlusion signals a significant risk of mortality in the Beijing eye study

2007 ◽  
Vol 85 ◽  
pp. 0-0
Author(s):  
T LIBONDI ◽  
L XING ◽  
W LIU ◽  
Y WANG ◽  
H YANG ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Christina L. Ryu ◽  
Adrian Elfersy ◽  
Uday Desai ◽  
Thomas Hessburg ◽  
Paul Edwards ◽  
...  

Purpose. Ischemic central retinal vein occlusion (CRVO) eyes are at high risk of developing neovascular glaucoma (NVG). Our purpose is to investigate the effect of anti-VEGF therapy for macular edema after CRVO on the development of neovascular glaucoma (NVG) in ischemic CRVO eyes.Methods. This is a retrospective case series of 44 eyes from 44 patients with CRVO treated with anti-VEGF therapy for macular edema. The primary outcome was the development of NVG.Results. Of the 44 eyes, 14 eyes had ischemic CRVO, and 30 eyes had nonischemic CRVO. Nonischemic eyes received a mean of 8.4 anti-VEGF doses, over mean follow-up of 24 months. One nonischemic eye (3.3%) developed NVD but not NVG. The 14 ischemic eyes received a mean of 5.6 anti-VEGF doses, with mean follow-up of 23 months. Of these 14 ischemic eyes, two eyes (14%) developed iris neovascularization and 3 eyes (21%) developed posterior neovascularization. Three of these 5 eyes with neovascularization progressed to NVG, at 19.7 months after symptom onset, on average.Conclusion. Anti-VEGF therapy for macular edema may delay, but does not prevent, the development of ocular NV in ischemic CRVO. Significant risk of NVG still exists for ischemic CRVO eyes.


2020 ◽  
pp. 112067212096033
Author(s):  
Tony Y. Chen ◽  
Aditya Uppuluri ◽  
Marco A. Zarbin ◽  
Neelakshi Bhagat

Purpose: Several risk factors have been identified for central retinal vein occlusion (CRVO) in older population. CRVO in young is uncommon, and the risk factors for this group are unclear. This large retrospective, cross-sectional study used the National Inpatient Sample (NIS) database to evaluate the risk factors for CRVO in patients 18 to 40 years of age. Methods: The 2002 to 2014 NIS database was used. All patients 18 to 40 years of age with a primary diagnosis of CRVO were identified. Age- and gender-matched non-CRVO controls were randomly selected. The primary outcome was identification of risk factors for CRVO. Chi-square analysis and Firth logistic regression were performed with IBM SPSS 23 and R packages versions 3.4.3, respectively. p < 0.05 was considered significant. Results: A total of 95 weighted young CRVO patients were identified. The average age was 31.44 ± 6.41 years with no gender predilection. Systemic and ocular conditions found to have statistically significant associations with CRVO included primary open-angle glaucoma (POAG) (OR 836.72, p < 0.001), retinal vasculitis (OR 705.82, p < 0.001), pseudotumor cerebri (OR 35.94, p < 0.001), hypercoagulable state (OR 25.25, p < 0.001), history of deep vein thrombosis/pulmonary embolism (DVT/PE) (OR 21.88, p < 0.001), and hyperlipidemia (OR 3.60, p = 0.003). Conclusion: The most significant risk factors for CRVO in young adults were POAG, retinal vasculitis, and pseudotumor cerebri. Hypercoagulable states and DVT/PE were also associated with CRVO in this population. Systemic inflammatory conditions were not associated with CRVO. Traditional risk factors such as hypertension and diabetes did not pose significant risks, whereas hyperlipidemia was deemed a significant risk factor.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5242-5242
Author(s):  
Katerina Zoi ◽  
Christine Zoi ◽  
Andreas Giannopoulos ◽  
Argyri Gialeraki ◽  
Kassiani Giannaki ◽  
...  

Abstract Background Myeloproliferative neoplasms (MPNs) have been associated with a high incidence of thrombosis and bleeding episodes, which significantly contribute to disease-related morbidity and mortality. Clinical data indicate an association of the JAK2V617F mutation, seen in nearly all polycythemia vera (PV) cases and almost 60% of those with essential thrombocythemia (ET) and myelofibrosis (MF). The mutation is also seen in 37% of patients with in splachnic vein thrombosis (SVT) and its presence was associated with an increased risk for SVT. However, the prevalence of JAK2V617 seems to be low in patients with other thromboembolic events in unusual sites such as cerebral sinus, upper limb deep venous thrombosis (DVT). Additionally, activating mutations of MPL gene, seen in 3% of ET and 5% of MF patients, are considered as a significant risk factor for microvessel disturbances and have been associated with an increased risk of arterial thrombosis. Retinal vein occlusion (RVO) is a thrombotic complication in an uncommon site that may result in sight threatening disease. In this study we investigated the prevalence of JAK2V617F and MPLW515L/K mutations in a prospectively assembled cohort of patients with RVO, hypothesizing that some cases may be associated with an underlying undiagnosed MPN. Patients and Methods We studied 52 (23 males and 29 females) consecutive patients with no evidence of an underlying MPN who had been diagnosed with RVO confirmed with fluorangiography from January 2007 to September 2011. The mean age was 70 years (range: 49-85) Twenty eight patients (53.8%) presented with central RVO and 24 patients with branched RVO (46.5%). DNA was extracted from peripheral blood samples by standard procedures. The JAK2V617F mutation was detected using a tetra-primer amplification refractory mutation system (ARMS) polymerase chain reaction (PCR) assay with a sensitivity of 1% and the allele burden was estimated with a semi-quantitative method. MPLW515L/K were detected using allele-specific PCR (AS-PCR) assays with a sensitivity of 1%. Results Overall, MPN associated mutations were detected in 5/52 cases. JAK2V617F was detected in 2/52 cases (3.8%; 95%CI-1.4%-9%), while MPL exon 10 mutations were detected in 3/52 (5.7%; 95%CI-0.6%-12%). The JAK2V617F allele burden in the two positive patients was 45% and 52% respectively. Both patients who carried the JAK2V617F mutation were female. The first patient had been already diagnosed with ET according to the WHO criteria at the time of RVO screening. She was receiving hydroxyurea and aspirin and her platelet count was normal. The second patient who also carried the JAK2V617F mutation had a PLT count of 850.000/μl at the time of screening and was diagnosed with ET within the 3 following months. The patients with MPL mutations presented with normal blood counts. Conclusions Our findings indicate that a latent MPN could underlie RVO even in the absence of conventional diagnostic criteria. Our results represent the first report that MPL mutations could underlie RVO cases and suggest that routine screening of RVO cases for MPN mutations may be useful, especially in older patients. Disclosures: No relevant conflicts of interest to declare.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Avnish Deobhakta ◽  
Louis K. Chang

Retinal vein occlusion is a common, vision-threatening vascular disorder. The role of inflammation in the pathogenesis and clinical consequences of retinal vein occlusion is a topic of growing interest. It has long been recognized that systemic inflammatory disorders, such as autoimmune disease, are a significant risk factor for this condition. A number of more recent laboratory and clinical studies have begun to elucidate the role inflammation may play in the molecular pathways responsible for the vision-impairing consequences of retinal vein occlusion, such as macular edema. This improved understanding of the role of inflammation in retinal vein occlusion has allowed the development of new treatments for the disorder, with additional therapeutic targets and strategies to be identified as our understanding of the topic increases.


1977 ◽  
Vol 38 (02) ◽  
pp. 0399-0406 ◽  
Author(s):  
Peter N. Walsh ◽  
Richard E. Goldberg ◽  
Richard L. Tax ◽  
Larry E. Magargal

SummaryTo determine whether platelets play a role in the pathogenesis of retinal vein occlusion (RVO), platelets and coagulation were evaluated in 28 patients with RVO. Platelet coagulant activities concerned with the initiation and early stages of intrinsic coagulation were 2–4 fold increased in 9 patients with acute primary RVO but not in patients with acute secondary (10 patients) or chronic (9 patients) RVO. Platelet factor 3 activity, platelet aggregation, serotonin release by platelets and plasma coagulation were normal in all patients. Platelets may provide a trigger mechanism for venous thrombosis in the eye when local conditions permit.


1994 ◽  
Vol 72 (01) ◽  
pp. 039-043 ◽  
Author(s):  
Francesco Bandello ◽  
Silvana Vigano’ D’Angelo ◽  
Mariella Parlavecchia ◽  
Alessandra Tavola ◽  
Patrizia Della Valle ◽  
...  

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


1997 ◽  
Vol 77 (01) ◽  
pp. 214-216 ◽  
Author(s):  
Tuuli Linna ◽  
Antti Ylikorkala ◽  
Kimmo E Kontula ◽  
Päivi Puska ◽  
Timo Tervo

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