Corneal hydration control in diabetes mellitus.
OBJECTIVE
To assess the effects of diabetes mellitus on corneal structure and function.


METHODS
The authors measured endothelial permeability to fluorescein and corneal deswelling for 7.5 hours after 2 hours of hypoxic contact lens wear in 20 patients with diabetes who had nonproliferative retinopathy and 21 age-matched control subjects. Central corneal endothelial photographs were also taken. Corneal deswelling rates, expressed as percent recovery per hour (PRPH), and open eye steady state (OESS) thickness were estimated by nonlinear regression techniques.


RESULTS
The OESS thickness was greater in patients with diabetes than in controls (562 +/- 35 microns versus 539 +/- 24 microns, P = 0.02). During hypoxia, the diabetic corneas swelled less (7.7% +/- 1.8% versus 9.9% +/- 1.6%, P < 0.001) and had less endothelial permeability (3.55 +/- 0.83 x 10(-4) cm/min versus 4.14 +/- 0.68 x 10(-4) cm/min, P = 0.02) than the controls. During normoxia after contact lens removal, however, diabetic and control corneas had similar deswelling rates and permeabilities. Corneal autofluorescence was increased in the patients with diabetes (8.1 +/- 3.1 versus 6.0 +/- 1.9 ng/ml fluorescein equivalents, P = .005). The endothelial cells of the two groups were morphologically similar. Within the group with diabetes, however, those with moderate nonproliferative retinopathy had larger coefficients of variation of cell area and smaller percentages of hexagonal cells than those with mild nonproliferative retinopathy.


CONCLUSIONS
Although the diabetic corneas were thicker and more autofluorescent than control corneas, during hypoxia they swelled less and had decreased endothelial permeability. During normoxia, however, no difference was found in endothelial permeability or deswelling rate. The effects of diabetes on endothelial cell morphologic features appear to be related to the severity of the diabetes.
Weston
B C
BC
Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota 55905.
Bourne
W M
WM
Polse
K A
KA
Hodge
D O
DO
D000328:Adult; D000368:Aged; D001693:Biological Transport, Active / Q000502:physiology; D002463:Cell Membrane Permeability / Q000502:physiology*; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D003930:Diabetic Retinopathy / Q000503:physiopathology; D004728:Endothelium, Corneal / Q000473:pathology / Q000502:physiology*; D005260:Female; D019793:Fluorescein; D005452:Fluoresceins; D015590:Fluorophotometry; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D014882:Water-Electrolyte Balance / Q000502:physiology
D005452:Fluoresceins; D019793:Fluorescein