Related Experiment Video
Updated: Jun 29, 2026

08:10
An Ex Vivo Tissue Culture Model for Fibrovascular Complications in Proliferative Diabetic Retinopathy
Published on: January 25, 2019
7.9K
Identifying Clinical Predictors of Proliferative Sickle Cell Retinopathy.
Rita Serras-Pereira1, Luísa Vieira1, Christopher J Saunders2
1Ophthalmology Department, Centro Hospitalar Universitário de Lisboa Central, Lisbon, Portugal.
Current Eye Research
|July 26, 2023
Summary
Mean corpuscular volume and fetal hemoglobin levels are key predictors of proliferative sickle retinopathy. Reduced lactate dehydrogenase also indicates potential hypoxia as a driver of this condition.
Area of Science:
- Ophthalmology
- Hematology
- Medical Research
Background:
- Sickle cell retinopathy is a significant complication of sickle cell disease.
- Proliferative sickle retinopathy (PSR) can lead to vision loss.
- Identifying predictors of PSR is crucial for early intervention.
Purpose of the Study:
- To determine systemic and ophthalmologic predictors of proliferative sickle retinopathy.
- To compare clinical, laboratory, and structural features in patients with and without PSR.
Main Methods:
- Cross-sectional study involving 45 sickle cell disease patients.
- Comprehensive systemic and ophthalmologic evaluations.
- Optical coherence tomography angiography (OCTA) and enhanced depth spectral domain OCT were used to analyze retinal and choroidal vascularization.
Main Results:
- 29% of patients had proliferative retinopathy.
- Mean corpuscular volume (MCV), lactate dehydrogenase (LDH), and fetal hemoglobin were significantly lower in patients with PSR.
- MCV was the best predictor of PSR (AUC=0.842), followed by fetal hemoglobin (AUC=0.763) and LDH (AUC=0.706).
- No significant differences in retinal or choroidal vascularization were observed between groups via OCTA and OCT.
Conclusions:
- Mean corpuscular volume and fetal hemoglobin are potential predictors of proliferative sickle retinopathy.
- Reduced LDH and MCV in PSR patients suggest hypoxia, not hemolysis, may drive the condition's pathophysiology.

