Endogenous Erythroid Colony Formation in Patients with Retinal Vein Occlusion

Héron, Emmanuel; Marzac, Christophe; Feldman–Billard, S.; Girmens, Jean-François; Pâques, M.; Delarue, Richard; Piette, Jean‐Charles; Casadevall, Nicole; Hermine, Olivier

doi:10.1016/j.ophtha.2007.08.014

Cited by 9 publications

(9 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In SCD and PV a relationship between abnormal erythropoiesis and abnormal RBC behaviour has been proposed [16,31]. Seven patients who participated in a previous study of in vitro bone marrow culture in CRVO patients [15] have been studied for RBC adhesion and PS expression. Five of them showed endogenous erythroid progenitor growth; their results in the present study did not differ from those of the other patients.…”

Section: Discussionmentioning

confidence: 99%

“…Several blood viscosity parameters have been shown to be increased in RVO patients compared with normal subjects, including a higher hematocrit, higher whole blood viscosity, reduced red cell deformability, and enhanced index of erythrocyte aggregation [7,10–14]. We recently reported that about 27% of patients with CRVO exhibit spontaneous in vitro growth of erythroid precursors in the absence of any detectable myeloproliferative disorder [15]. Red blood cells (RBCs) from patients with polycythemia vera have an abnormal CD239 (Lu/BCAM) phosphorylation, which is responsible for abnormal interactions with endothelial cells [16].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion

Wautier

Héron

Picot

et al. 2011

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

) compared with RAO RBC (63 ± 5 · 10 2 mm )2 ) (P < 0.01) and normal control RBC (37 ± 3 · 10 2 mm )2 ) (P < 0.001). Under flow conditions, CRVO RBC adhered in greater numbers than normal RBC (P < 0.001). Phosphatidylserine (PS) expression on CRVO RBC was 2.4-fold higher than controls and correlated with RBC adhesion (P = 0.001). In static conditions, specific antibodies against PS receptor and annexin V inhibited RBC adhesion. In flow conditions, the inhibitory effect was in the same range with antibodies but was 2-fold higher with annexin V. Conclusion: Increased CRVO RBC adhesion is mediated by PS RBC and endothelial PS receptor. This phenomenon may be one of the factors responsible for CRVO.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion

Wautier

Héron

Picot

et al. 2011

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

show abstract

“…21,24,40,41,45,51 One of 153 patients with RVO had JAK2V617F mutation, for a mean prevalence of 0.99% (95% CI, 0.05%-3.20%). 21,31,40,41,47,48 Discussion This is the first systematic review and meta-analysis that assessed the role of JAK2 mutation in patients with venous thrombosis. The results of this study indicate that the prevalence of this mutation is high in patients with SVT.…”

Section: Patients With Vte In Other Sitesmentioning

confidence: 99%

“…Studies ranged in size from 11 to 560 patients; a total of 3508 patients were included. Six case-control studies 10,23,25,27,35,40 and 18 retrospective cohort studies 21,24,30,31,34,36,37,[41][42][43][44][45][46][47][48][49]51,52 were included in our systematic review. Five studies enrolled patients consecutively.…”

Section: Study Characteristicsmentioning

confidence: 99%

“…35,42,44,46,51 A few studies differentiated between patients with homozygote and heterozygote JAK2V617F mutation, 24,34,35,41,43,44,49 and 2 studies provided data on patients with homozygote mutation JAK2V617F. [24][25][26][27][28][29][30][31][32][33][34][35] Sixteen studies, 10,21,[23][24][25]30,[35][36][37]40,43,44,46,47,49,53 including a total 831 patients, assessed the prevalence of JAK2V617F mutation in patients with SVT. Eight studies, 21,27,34,37,[40][41][42]47 …”

Section: Study Characteristicsmentioning

confidence: 99%

See 1 more Smart Citation

JAK2V617F mutation for the early diagnosis of Ph− myeloproliferative neoplasms in patients with venous thromboembolism: a meta-analysis

Dentali

Squizzato

Brivio

et al. 2009

Blood

161

143

View full text Add to dashboard Cite

Recent studies suggested that JAK2V617F mutation is frequent in patients with splanchnic vein thrombosis (SVT) but not in patients with other venous thromboembolic events (VTE). However, whether screening for the JAK2V617F mutation in VTE patients is justified remains unclear. Therefore, we performed a systematic review to assess the frequency of JAK2 mutation in VTE patients and the role of JAK2V617F mutation in the diagnosis of myeloproliferative neoplasms. MEDLINE and EMBASE databases were searched. Two reviewers independently performed study selection and extracted study characteristics. Pooled odds ratios of case-control studies and weighted mean proportion of the prevalence of JAK2V617F mutation of uncontrolled series were calculated. Twenty-four studies involving 3123 patients were included. Mean prevalence of JAK2 mutation was 32.7% (95% confidence interval, 25.5%-35.9%) in SVT patients. JAK2 mutation was associated with increased risk of SVT (odds ratio, 53.98; 95% confidence interval, 13.10-222.45). Mean prevalence of JAK2 mutation in other VTE patients was low (range, 0.88%-2.57%). Presence of JAK2V617F mutation in SVT patients was associated with a subsequent diagnosis of myeloproliferative neoplasm in many patients. JAK2 mutation is strongly associated with SVT, and routine screening of JAK2 mutation appears to be indicated in these patients. (Blood. 2009;113:5617-5623)

show abstract

Retinal Vascular Disease

2010

The Retinal Atlas

View full text Add to dashboard Cite

Endogenous Erythroid Colony Formation in Patients with Retinal Vein Occlusion

Cited by 9 publications

References 42 publications

Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion

Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion

JAK2V617F mutation for the early diagnosis of Ph− myeloproliferative neoplasms in patients with venous thromboembolism: a meta-analysis

Retinal Vascular Disease

Contact Info

Product

Resources

About