Deficit of somatostatin-like immunoreactivity in the vitreous fluid of diabetic patients: possible role in the development of proliferative diabetic retinopathy.
OBJECTIVE
To evaluate the vitreous levels of somatostatin-like immunoreactivity (SLI) in patients with proliferative diabetic retinopathy (PDR).


METHODS
A total of 14 diabetic patients with PDR, in whom a vitrectomy was performed, were included in the study. Sixteen nondiabetic patients, with other conditions requiring vitrectomy, served as a control group. Both venous blood and vitreous samples were collected at the time of vitreoretinal surgery. Patients in whom intravitreous hemoglobin was detectable were excluded. In addition, a correction for plasma levels of SLI and intravitreal proteins was performed. SLI was measured by radioimmunoassay and vitreous hemoglobin by spectrophotometry.


RESULTS
SLI in the vitreous fluid was significantly lower in diabetic patients than in the control group (68 +/- 18.7 vs. 193.6 +/- 30.8 pg/ml, P < 0.01). The vitreous SLI-to-plasma SLI ratio was strikingly higher in nondiabetic subjects than in diabetic patients with PDR (5.3 [1.2-71.1] vs. 0.6 [0.03-4.1], P < 0.01). After correcting for total vitreous protein concentration, SLI (pg/mg of proteins) remained significantly higher in nondiabetic control subjects than in diabetic patients with PDR (186 [51-463] vs. 7.5 [0.8-82], P < 0.0001). Remarkably, intravitreous levels of SLI were higher than those obtained in plasma in nondiabetic control subjects (193.6 +/- 30.8 vs. 43.5 +/- 10.7 pg/ml, P < 0.0001). Finally, a lack of relationship between plasma and vitreous levels of SLI was observed in both diabetic patients with PDR and nondiabetic control subjects.


CONCLUSIONS
The significantly higher SLI in the vitreous fluid than in plasma detected in nondiabetic control subjects supports the concept that somatostatin plays a relevant role in retinal homeostasis. In addition, the intravitreous deficit of SLI observed in diabetic patients with PDR suggests that it might contribute to the process of retinal neovascularization.
Simó
Rafael
R
Diabetes Unit, Division of Endocrinology, Hospital General Universitari Vall d'Hebron, Barcelona, Spain. rsimo@hg.vhebron.es
Lecube
Albert
A
Sararols
Laura
L
García-Arumí
José
J
Segura
Rosa M
RM
Casamitjana
Roser
R
Hernández
Cristina
C
D017668:Age of Onset; D003920:Diabetes Mellitus / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D003930:Diabetic Retinopathy / Q000503:physiopathology* / Q000601:surgery; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D013004:Somatostatin / Q000032:analysis* / Q000172:deficiency*; D014821:Vitrectomy; D014822:Vitreous Body / Q000737:chemistry*
D006442:Glycated Hemoglobin; D013004:Somatostatin