Vascular Endothelial Growth Factor Levels in Aqueous, Vitreous and Subretinal Fluid in Patients With Retinopathy of Prematurity Stage V.

Vascular Endothelial Growth Factor (VEGF) is a dimeric glycoprotein, naturally expressed in epithelial and tumor cells (1). In conditions of hypoxia it is secreted by the pericytes, the Retina Pigmented epithelium (RPE)and glial cells, including a the Müller cells (1,2,4,5) favoring the formation of new abnormal vessels (1). Its activity is mediated by two high affinity receptors: the receptor VEGF 1 (FLT-1) and VEGF 2 (FLT-2) (1,9). The FLT-1 promotes cellular proliferation whereas FLT-2 the migration and cell- extracellular matrix interaction (9). The VEGF is essential as much for the normal retinal vascularization as for pathological (5,14).

Normal Retinal vascularization has two phases: In the first fase, cells of mesenquimatous origin form the first superficial plexus (14-21 weeks of gestation). In the second phase, denominated "angiogenesis phase", the superficial and deep capillary plexus are formed (15,20). The second phase is highly dependent of VEGF induced by hypoxia (15,20). In the normal retina the growth occurs from the optical nerve to the periphery (17).

The scientific progress in the neonatal intensive care units in the last years has allowed the survival of a larger number of premature newborns(15).

The Retinopathy of Prematurity (ROP)(ROP) was described for the first time in 1942 (4), at the present moment it is a public health problem in the developing countries. Of each 100.000 blind child in Latin America, 24.000 are due to ROP (240/1000 blind child) (17). It is the main cause of blindness in premature new born (1,4,5). It is of multifactorial etiology (17) but it has been related to a short gestational age (smaller to 32 weeks of gestation) (4), to low birth weight (less of 1500gr) or very low birth weight (less 1250gr)(1,4,5,17,18,20), to the administration of high oxygen concentration immediately after birth (1,3,18), low levels of the Insulin-like growth factor(IGF-I) and excessive production of VEGF (3,17).

All this, combined with large periods of hyperoxia-hypoxia, Produces that the normal vascularization of the retina stops. This also produces vascular-occlusive changes, arteriovenous anastomoses in the edge of the vascularized with the none-vascularized retina (18), begins the formation of abnormal vessels towards the vitreous, finally lead to retina detachment in the most severe cases (2,3,4,5).