Deficit of Somatostatin in the Vitreous Fluid of Patients With Diabetic Macular Edema
- Rafael Simó, MD1,
- Esther Carrasco, PHD1,
- Alex Fonollosa, PHD2,
- Josep García-Arumí, MD2,
- Roser Casamitjana, MD3 and
- Cristina Hernández, MD1
- 1Diabetes Research Unit, Endocrinology Division, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain
- 2Department of Ophthalmology, Hospital Universitari Vall d’Hebron, Barcelona, Spain
- 3Department of Hormonology, Hospital Clínic, Barcelona, Spain
- Address correspondence and reprint requests to Dr. Rafael Simó, Diabetes Research Unit, Endocrinology Division, Hospital Universitari Vall d’Hebron, Pg. Vall d’Hebron 119-129, 08035 Barcelona, Spain. E-mail: rsimo{at}ir.vhebron.net
Although diabetic macular edema (DME) is the main cause of visual loss in type 2 diabetic patients (1), its pathogenic mechanisms have been much less studied than proliferative diabetic retinopathy (PDR). The production of both somatostatin (SST) and its receptors by the retina suggests an autocrine action. However, the functional roles of this peptidergic system in retinal physiology are far from being fully elucidated. In recent years we have demonstrated that SST is decreased in the vitreous fluid from patients with PDR, SST-28 being the main molecular variant accounting for this deficit (2,3). Apart from angiostatic properties, SST has anti-inflammatory and anti-edema effects (4–9). Therefore, it is possible that its deficit can be involved not only in PDR but also in DME development.
The aim of the present study was to determine whether, as occurs in PDR, a deficit of intravitreous SST also exists in DME, thus allowing us to identify a new potential pathogenic contributor to this devastating complication of diabetes. Since SST-28 is the main molecular variant in the vitreous fluid, it has been selected as the ideal candidate to be explored.
RESEARCH DESIGN AND METHODS—
The study included 35 type 2 diabetic patients (15 with DME and 20 with PDR), in whom a classic three port pars plana vitrectomy was performed. Vitreous from 30 age-matched nondiabetic patients (18 with macular hole and 12 with idiopathic epiretinal membrane) served as the control group. The exclusion criteria were as follows: 1) previous vitreoretinal surgery, 2) recent vitreous hemorrhage or intravitreous hemoglobin >5 mg/ml, or 3) photocoagulation in the preceding 3 months. Fluorescein angiography was performed in all patients with DME in order to assess …
